Acta Histochem. [JOURNAL]
Sun
200 papers
Three-dimensional human germinal centers of different sizes in patients diagnosed with lymphadenitis show comparative constant relative volumes of B cells, T cells, follicular dendritic cells, and macrophages.
Schemel CM, Wurzel P, Scharf S … +4 more , Schäfer H, Hartmann S, Koch I, Hansmann ML
Acta Histochem · 2023 Oct · PMID 37459798 · Publisher ↗
Germinal centers (GCs) are some of the most important structures in the human immune system. As such, their cell types and functions have been thoroughly investigated. B cells, T cells, follicular dendritic cells (FDCs),...
Germinal centers (GCs) are some of the most important structures in the human immune system. As such, their cell types and functions have been thoroughly investigated. B cells, T cells, follicular dendritic cells (FDCs), and macrophages have widely been found to typically be aggregated in GCs. However, the amount of space occupied by each of these cell types has yet to be investigated. In this study, we conducted confocal laser-based 3D cell-volume quantification of typical GC cells under reactive conditions in lymphadenitis and investigated how volume proportions change during GC development. For this investigation, we used anti-CD3 (T cells), anti-CD20 and anti-Pax5 (B cells), anti-CD23 (FDCs), anti-CD68 (macrophages), and DAPI (nuclear staining). We detected average proportions of about 11% CD3, 9% CD20, 6% CD23, and 2% CD68 in the largest possible regions of interest within GCs. Interestingly, these values remained steady relatively independent of GC size. The remarkably low B cell proportion can be attributed to technical constraints given the use of the CD20 antibody in 3D. Applying the B cell marker Pax5, we found that about 44% of the volume was occupied by B cells after extrapolating the volume of B cell nuclei to that of whole B cells. We concluded that Pax5 is more suitable than anti-CD20 for 3D B cell quantification in GCs. The substantial unstained volume in GCs raises the question of whether other cell types fill these open spaces. Our 3D investigation enabled a unique morphological and volumetric evaluation of GC cells that balance their overall volumes in GCs.
Corrigendum to "Hypoxia activates the PI3K/AKT/HIF-1α pathway to promote the anti-inflammatory effect of adipose mesenchymal stem cells" [Acta Histochem.125(4) (2023) 152042].
Ren H, Liu M, Jihu Y … +3 more , Zeng H, Yao C, Yan H
Acta Histochem · 2023 Aug · PMID 37451944 · Publisher ↗
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The CellProfiler pipeline analysis of cell migration.
Ariffin NS
Acta Histochem · 2023 Oct · PMID 37437311 · Publisher ↗
We demonstrate herein a refined method to evaluate the migration capacity of monolayer cells using the CellProfiler pipeline. We used MDA-MB-231 cells, a triple-negative breast cancer cell line, as a model to perform the...
We demonstrate herein a refined method to evaluate the migration capacity of monolayer cells using the CellProfiler pipeline. We used MDA-MB-231 cells, a triple-negative breast cancer cell line, as a model to perform the wound healing assay and proceeded with the pipeline analysis. In order to see a contrast in our analysis of cell migration, we treated the cells with 10 µM kartogenin for 48 h and compared the result to the control cells treated with 0.1 % dimethyl sulfoxide (DMSO). The migration rate of MDA-MB-231 cells could be measured precisely using this method whereby in the presence of 10 µM kartogenin, the cells migrated at 6.3 ± 1.7µmh whilst the vehicle control migrated at 9.1 ± 3.2 µmh (p < 0.05). The small changes in the rate of migration could be significantly differentiated and we believe that this method is accurate in analyzing data of scratch assays as it is of high precision and therefore can be used for high-throughput screenings.
LSD1 knockdown confers protection against osteoclast formation by reducing histone 3 lysine 9 monomethylation and dimethylation in ITGB3 promoter.
Yu D, Li Z, Cao J … +2 more , Wei G, Shen F
Acta Histochem · 2023 Oct · PMID 37422927 · Publisher ↗
ITGB3, an osteoclast marker, is involved in osteoclast formation. Nevertheless, its related mechanism remains poorly characterized. Herein, this study examines the mechanisms affecting osteoclast formation with the invol...
ITGB3, an osteoclast marker, is involved in osteoclast formation. Nevertheless, its related mechanism remains poorly characterized. Herein, this study examines the mechanisms affecting osteoclast formation with the involvement of ITGB3. Osteoclast formation was induced with macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B ligand (RANKL), followed by measurement of the mRNA and protein expression of ITGB3 and LSD1. After gain- and loss-of-function assays, cell viability and the expression of osteoclast marker genes (NFATc1, ACP5, and CTSK) were assessed, and osteoclast formation was evaluated with TRAP staining. ChIP assays were used to examine histone 3 lysine 9 (H3K9) monomethylation (H3K9me1) and H3K9 dimethylation (H3K9me2) modifications and LSD1 protein enrichment in the ITGB3 promoter. During osteoclast formation, ITGB3 and LSD1 were gradually augmented. Knockdown of LSD1 or ITGB3 curbed cell viability, the expression of osteoclast marker genes, and osteoclast formation. Moreover, overexpression of ITGB3 nullified the suppressive impact of LSD1 knockdown on osteoclast formation. Mechanistically, LSD1 promoted ITGB3 expression by reducing H3K9 levels in the ITGB3 promoter. LSD1 enhanced ITGB3 expression by decreasing H3K9me1 and H3K9me2 levels in ITGB3 promoter to boost osteoclast formation.
MCM5 is an oncogene of colon adenocarcinoma and promotes progression through cell cycle control.
Mao J, Shen J, Lu X … +6 more , Cai Y, Tao R, Deng Y, Zhang Y, Wu Y, Chen W
Acta Histochem · 2023 Aug · PMID 37385108 · Publisher ↗
Many patients with colon adenocarcinoma (COAD) are diagnosed at an advanced stage, and the molecular mechanism of COAD progression is intricate and controversial. Therefore, there is an urgent need to identify more novel...
Many patients with colon adenocarcinoma (COAD) are diagnosed at an advanced stage, and the molecular mechanism of COAD progression is intricate and controversial. Therefore, there is an urgent need to identify more novel prognosis biomarkers for COAD and elucidate the molecular mechanism of this disease. The present study aimed to screen out key genes correlated with COAD prognosis. In this study, a key module was identified and four hub genes (MCM5 (encoding minichromosome maintenance complex component 5), NOLC1 (encoding nucleolar and coiled-body phosphoprotein 1), MYC (encoding MYC proto-oncogene, BHLH transcription factor), and CDK4 (encoding cyclin dependent kinase 4)) were selected that correlated with COAD prognosis, based on the GSE9348 dataset in Gene Expression Omnibus database. Gene ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that MCM5 correlated with the cell cycle. Furthermore, MCM5 expression was upregulated in tumor tissues of patients with COAD compared with that in adjacent tissues, based on various databases, including The Cancer Genome Atlas, the Clinical Proteomic Tumor Analysis Consortium database, and the Human Protein Atlas database. Small interfering RNA-mediated knockdown of MCM5 inhibited the cell cycle and migration of colorectal cancer cells in vitro. And western blotting results indicated that factors correlated with cell cycle (CDK2/6, Cyclin D3, P21) were downregulated after knockdown of MCM5 in vitro. Besides, downregulation of MCM5 was demonstrated to inhibit lung metastasis of COAD in nude mice model. In conclusion, MCM5 is an oncogene of COAD that promotes COAD progression via cell cycle control.
The role of vascular endothelial cells in tumor metastasis.
Feng Y, Luo S, Fan D … +2 more , Guo X, Ma S
Acta Histochem · 2023 Aug · PMID 37348328 · Publisher ↗
Vascular endothelial cells (VECs) are an integral component of the inner lining of blood vessels, and their functions are essential for the proper functioning of the vascular system. The tight junctions formed by VECs ac...
Vascular endothelial cells (VECs) are an integral component of the inner lining of blood vessels, and their functions are essential for the proper functioning of the vascular system. The tight junctions formed by VECs act as a significant barrier to the intravasation and extravasation of tumor cells (TCs). In addition to that, the proliferation, activation, and migration of VECs play a vital role in the growth of new blood vessels, a process known as tumor angiogenesis, which is closely related to the malignant progression of tumors. However, during tumor progression, VECs undergo endothelial-to-mesenchymal transition (EndMT), which further promotes tumor progression. Furthermore, VECs act as the first line of defense against effector immune cells and help prevent immune cells from infiltrating into tumor tissues. VECs also secrete various cytokines that can contribute to regulating the stemness of tumor stem cells. Thus, it has been increasingly recognized that dysfunction of VECs is one of the key driving forces behind tumor metastasis, and therapeutic strategies targeting VECs have the potential to be an effective means of antitumor therapy. This review aims to present a comprehensive overview of the role and mechanisms of VECs in regulating tumor progression and metastasis, providing insights into the possibilities for the development of novel antitumor therapies that target VECs.
Phospholysine phosphohistidine inorganic pyrophosphate phosphatase suppresses human esophageal cancer cell growth by inducing mitotic catastrophe through the P27/cyclin A/CDK2 signaling pathway.
Ruifang D, Changqing Y, Chenxia R … +2 more , Ji L, Zibai W
Acta Histochem · 2023 Aug · PMID 37348327 · Publisher ↗
Esophageal cancer (ESCA) is a global dead malignancy with poor prognosis. However, its underlying molecular mechanism remains to be elucidated. Phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) ha...
Esophageal cancer (ESCA) is a global dead malignancy with poor prognosis. However, its underlying molecular mechanism remains to be elucidated. Phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) has been reported as a tumor suppressor in multisystem cancer but its function in ESCA has not been reported. We analyzed LHPP expression between normal and tumor tissues of ESCA patients and performed LHPP overexpression on the ESCA cells KYSE-150 (K150). We did not observe significant differences in the expression level of LHPP between ESCA and normal tissue, and noticed that LHPP expression was not related to ESCA patient survival rate. However, increased expression of LHPP in K150 cells induced mitochondrial dysfunction, inhibited cell proliferation, migration, and cell cycle, and simultaneously increased cell apoptosis. Besides, we found that K150 cells underwent mitotic catastrophe after overexpressing LHPP, which may be regulated through the P27/cyclin A/cdk2 signaling pathway. Although the expression of LHPP may not be related to the progression and prognosis of ESCA, mitotic catastrophe, a new mechanism of tumor suppressor function of LHPP was found after overexpressing LHPP in ESCA cells. DATA AVAILABILITY: The data used to support the findings of this study are included within the article.
Astaxanthin inhibits oxidative stress and apoptosis in diabetic retinopathy.
Fang J, Bai W, Yang L
Acta Histochem · 2023 Aug · PMID 37343496 · Publisher ↗
BACKGROUND: The pathophysiology of diabetic retinopathy (DR) is thought to be influenced by oxidative stress. Astaxanthin (ASX) is a natural product with antioxidant effect, but it is not clear whether its mechanism of i...
BACKGROUND: The pathophysiology of diabetic retinopathy (DR) is thought to be influenced by oxidative stress. Astaxanthin (ASX) is a natural product with antioxidant effect, but it is not clear whether its mechanism of inhibiting the development of DR is related to anti-oxidation. METHODS: Rats were intraperitoneally injected with streptozotocin (60 mg/kg) to create DR rat models followed by ASX (20 mg/kg) for 45 days. Retinal tissue was examined by Hematoxylin and Eosin staining. By using Enzyme-linked immunosorbent assay (ELISA), 2,7-Dichlorodrhydrofluorescein diace (DCFH-DA) probes, immunohistochemistry and western blot, it was feasible to evaluate the contents of inflammation-related factors (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and macrophage inhibitory cytokine-1 (MIC-1)), oxidative stress-related indicators (glutathione (GSH), malonic dialdehyde (MDA), glutathione peroxidase (GPx), reactive oxygen species (ROS) and Total antioxidant capacity (T-AOC)), antioxidant enzymes (hemoxgenase-1(HO-1) and Quinone Oxidoreductase 1 (NQO1)), and apoptosis-related proteins (Bcl-2, Bcl2 Associated X Protein (BAX), and cleaved-caspase-3). Additionally, antioxidant proteins downstream of the nuclear factor E2 related factors (Nrf-2) pathway, expression levels of Nrf2/ Kelch-like ECH-associated protein 1(Keap 1) pathway-associated proteins, and nuclear and cytoplasmic levels of Nrf2 were assessed using immunohistochemistry, western blot, or quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: ASX alleviated retinal tissue damage by increasing overall retina thickness and ganglion cell layer (GCL) cell numbers and exerted the anti-inflammatory, anti-oxidative stress, and anti-apoptosis effects in DR rats. Additionally, ASX could inhibit the expression of Keap1, promote the transport of Nrf2 from cytoplasm to nucleus and facilitate the expressions of HO-1, NQO1, γ-glutamylcysteine synthetase, (γ-GCS) and GPx. CONCLUSION: ASX exerted antioxidant effects through Nrf2/keap1 pathway, thereby alleviating apoptosis, inflammation, and oxidative stress in retinal tissues of DR rats.
Resveratrol as an antitumor agent for glioblastoma multiforme: Targeting resistance and promoting apoptotic cell deaths.
Karkon-Shayan S, Aliashrafzadeh H, Dianat-Moghadam H … +7 more , Rastegar-Pouyani N, Majidi M, Zarei M, Moradi-Vastegani S, Bahramvand Y, Babaniamansour S, Jafarzadeh E
Acta Histochem · 2023 Aug · PMID 37336070 · Publisher ↗
Glioblastoma multiforme (GBM) is one of the most aggressive brain and spinal cord tumors. Despite the significant development in application of antitumor drugs, no significant increases have been observed in the survival...
Glioblastoma multiforme (GBM) is one of the most aggressive brain and spinal cord tumors. Despite the significant development in application of antitumor drugs, no significant increases have been observed in the survival rates of patients with GBM, as GBM cells acquire resistance to conventional anticancer therapeutic agents. Multiple studies have revealed that PI3K/Akt, MAPK, Nanog, STAT 3, and Wnt signaling pathways are involved in GBM progression and invasion. Besides, biological processes such as anti-apoptosis, autophagy, angiogenesis, and stemness promote GBM malignancy. Resveratrol (RESV) is a non-flavonoid polyphenol with high antitumor activity, the potential of which, regulating signaling pathways involved in cancer malignancy, have been demonstrated by many studies. Herein, we present the potential of RESV in both single and combination therapy- targeting various signaling pathways- which induce apoptotic cell death, re-sensitize cancer cells to radiotherapy, and induce chemo-sensitizing effects to eventually inhibit GBM progression.
PRSS2 regulates EMT and metastasis via MMP-9 in gastric cancer.
Wang F, Yi J, Chen Y … +4 more , Bai X, Lu C, Feng S, Zhou X
Acta Histochem · 2023 Aug · PMID 37331089 · Publisher ↗
Serine protease 2 (PRSS2) is upregulated in gastric cancer tissues, correlates with poor prognosis and promotes migration and invasion of gastric cancer cells. However, the exact mechanism by which PRSS2 promotes metasta...
Serine protease 2 (PRSS2) is upregulated in gastric cancer tissues, correlates with poor prognosis and promotes migration and invasion of gastric cancer cells. However, the exact mechanism by which PRSS2 promotes metastasis in gastric cancer is unclear. We examined serum PRSS2 levels in healthy controls and gastric cancer patients by enzyme linked immunosorbent assay (ELISA) and analyzed the correlation between PRSS2 serum level with the clinicopathological characteristics of gastric cancer patients and matrix metalloproteinase-9 (MMP-9) expression. A lentiviral MMP-9 overexpression vector was constructed and used to transfect gastric cancer cells with stable silencing of PRSS2, and migration, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer cells were examined. High serum PRSS2 levels were detected in gastric cancer patients and associated with lymphatic metastasis and TNM stage. Serum PRSS2 was positively correlated with serum MMP-9 level. PRSS2 silencing inhibited EMT, and knock-down of PRSS2 partially abrogated cell metastasis and EMT caused by overexpression of MMP-9. These results suggest that PRSS2 promotes the migration and invasion of gastric cancer cells through EMT induction by MMP-9. Our findings suggest that PRSS2 may be a potential early diagnostic marker and therapeutic target of gastric cancer.
Study of platelet-rich fibrin promoting endothelial cell differentiation and angiogenesis induced by transplantation of adipose-derived stem cells.
Ma Z, Ding J, Wang Y … +3 more , Zhang T, Chen G, Huang J
Acta Histochem · 2023 Aug · PMID 37329849 · Publisher ↗
Diabetic patients are characterized by long wound healing time, and adipose stem cells (ADSCs) can secrete growth factors to promote angiogenesis and improve diabetic wound healing. In this research, we attempted to inte...
Diabetic patients are characterized by long wound healing time, and adipose stem cells (ADSCs) can secrete growth factors to promote angiogenesis and improve diabetic wound healing. In this research, we attempted to interrogate the impact of platelet-rich fibrin (PRF) on ADSCs in diabetic wound healing. ADSCs were harvested from human adipose tissues and identified through flow cytometry. After pretreatment with cultured medium supplemented with different concentrations of PRF (2.5%, 5%, and 7.5%), proliferation and differentiation capacity of ADSCs were assessed by CCK-8 assay, qRT-PCR and immunofluorescence (IF), respectively. Tube formation assay measured angiogenesis. Western blot analysis analyzed expression of endothelial markers and the extracellular signal-regulated kinase (ERK) and serine/threonine kinase (Akt) pathways in PRF-induced ADSCs. The CCK-8 experiment indicated that PRF enhanced proliferation of ADSCs in dose-dependent manner, relative to normal control group. The expression of endothelial markers and the capacity of tube formation were significantly promoted by 7.5% PRF. The release of growth factors containing vascular endothelial grow factor (VEGF) and insulin-like growth factor-1 (IGF-1) from PRF was increased with the extension of detection time. When the receptors of VEGF or/and IGF-1 were neutralized, ADSCs differentiation into endothelial cells were obviously inhibited. Additionally, PRF stimulated ERK and Akt pathways, and the inhibitors of ERK and Akt attenuated PRF-induced differentiation of ADSCs into endothelial cells. In conclusion, PRF promoted endothelial cell differentiation and angiogenesis induced by ADSCs in diabetic wound healing, which appears to give guidance for treating patients.
Impacts of iron on ultrastructural features of NCI-H295R cell line related to steroidogenesis.
Duranova H, Fialkova V, Simora V … +4 more , Bilcikova J, Massanyi P, Lukac N, Knazicka Z
Acta Histochem · 2023 Aug · PMID 37321134 · Publisher ↗
The current study was intended to evaluate impacts of both iron (Fe) enrichment and overload (in the form of ferrous sulphate heptahydrate, FeSO.7HO) on ultrastructural characteristics of human adrenocarcinoma NCI-H295R...
The current study was intended to evaluate impacts of both iron (Fe) enrichment and overload (in the form of ferrous sulphate heptahydrate, FeSO.7HO) on ultrastructural characteristics of human adrenocarcinoma NCI-H295R cell line. Here, the NCI-H295R cells were treated with 0, 3.90, and 1000 µM FeSO.7HO, and consequently proceeded for purposes of ultrastructural studies. Micrographs taken under transmission electron microscope (TEM) were investigated from the qualitative and quantitative (unbiased stereological approaches) aspects, and obtained findings were compared among the three groups of the cells. The ultrastructural features related to the steroidogenic process were found to be similar between the untreated and both Fe-exposed cell populations, with conspicuous mitochondria with well-defined lamellar cristae (creating clusters of varying sizes in the regions of increased energy demands) and concentric whorls of smooth endoplasmic reticulum (SER) being the most noticeable characteristics. The precise estimates of the component (volume, surface) fractions of the nucleus, mitochondria, and lipid droplets (LDs), as well as of the nucleus/cytoplasm (N/C) ratio have revealed close similarities (P > 0.05) in all cell groups investigated. Nonetheless, the low concentration of FeSO.7HO exhibited beneficial action on ultrastructural organization of the NCI-H295R cells. In effect, these cells were distinguished by mitochondria with smoother surfaces and clearer outlines, higher density of thin, parallel lamellar cristae (deeply extending into the mitochondrial matrix), and more widespread distribution of fine SER tubules as compared to the control ones, all of them suggesting higher level of energy requirements and metabolic activity, and more intensive rate of steroidogenesis. Interestingly, no obvious ultrastructural modifications were observed in the NCI-H295R cells treated with high FeSO.7HO concentration. This finding can be linked to either an adaptive ultrastructural machinery of these cells to cope with the adverse effect of the element or to insufficient dose of FeSO.7HO (1000 µM) to induce ultrastructural signs of cytotoxicity. Purposefully, the results of the current study complement our previous paper dealing with impacts of FeSO.7HO on the NCI-H295R cell viability and steroidogenesis at the molecular level. Hence, they fill a knowledge gap considering structure-function coupling in this cellular model system upon the metal exposure. This integrated approach can enhance our understanding of the cellular responses to Fe enrichment and overload which can be helpful for individuals with reproductive health concerns.
Classification of colorectal cancer consensus molecular subtypes using attention-based multi-instance learning network on whole-slide images.
Xu H, Wu A, Ren H … +3 more , Yu C, Liu G, Liu L
Acta Histochem · 2023 Aug · PMID 37300984 · Publisher ↗
Colorectal cancer (CRC) is the third most common and second most lethal cancer globally. It is highly heterogeneous with different clinical-pathological characteristics, prognostic status, and therapy responses. Thus, th...
Colorectal cancer (CRC) is the third most common and second most lethal cancer globally. It is highly heterogeneous with different clinical-pathological characteristics, prognostic status, and therapy responses. Thus, the precise diagnosis of CRC subtypes is of great significance for improving the prognosis and survival of CRC patients. Nowadays, the most commonly used molecular-level CRC classification system is the Consensus Molecular Subtypes (CMSs). In this study, we applied a weakly supervised deep learning method, named attention-based multi-instance learning (MIL), on formalin-fixed paraffin-embedded (FFPE) whole-slide images (WSIs) to distinguish CMS1 subtype from CMS2, CMS3, and CMS4 subtypes, as well as distinguish CMS4 from CMS1, CMS2, and CMS3 subtypes. The advantage of MIL is training a bag of the tiled instance with bag-level labels only. Our experiment was performed on 1218 WSIs obtained from The Cancer Genome Atlas (TCGA). We constructed three convolutional neural network-based structures for model training and evaluated the ability of the max-pooling operator and mean-pooling operator on aggregating bag-level scores. The results showed that the 3-layer model achieved the best performance in both comparison groups. When compared CMS1 with CMS234, max-pooling reached the ACC of 83.86 % and the mean-pooling operator reached the AUC of 0.731. While comparing CMS4 with CMS123, mean-pooling reached the ACC of 74.26 % and max-pooling reached the AUC of 0.609. Our results implied that WSIs could be utilized to classify CMSs, and manual pixel-level annotation is not a necessity for computational pathology imaging analysis.
Localization of alpha 2,6-linked sialic acid residues in gastrointestinal tract compartments of some tetrapod's representatives: Comparative histochemical study.
Awaad A, Rushdy A, Adly MA
Acta Histochem · 2023 Jul · PMID 37262962 · Publisher ↗
Epithelial mucins composed mainly of glycoproteins and play a vital role as protective barrier against a variety of harmful molecules and microbial infection. Additionally sialic acids, like glycoproteins, are considered...
Epithelial mucins composed mainly of glycoproteins and play a vital role as protective barrier against a variety of harmful molecules and microbial infection. Additionally sialic acids, like glycoproteins, are considered as a main component of epithelial mucins and play an important role in mucosal immunity. For example, alpha 2,6-linked galactose/N-acetyl-galactosamine (Gal/GalNAc) sialic acid residues can recognize and mask different biological sites in some intermolecular or intercellular interactions. In this study, the localization sites relationship between general mucins and alpha 2,6-linked Gal/GalNAc sialic acid residues in different compartments in gastrointestinal tract (GIT) of tetrapod representatives were investigated using lectin histochemistry. The toad (Bufo regularis), lizard (Trachylepis quinquetaeniata), pigeon (Columba livia domestica) and mouse (Mus musculus) were used as amphibian, reptilian, avian and mammalian representatives respectively. In general, the biodistribution sites of mucins are localized in most compartment sites and partially overlapped with the sites of sialic acid residues in some compartment in each animal representative. Additionally, the localization sites of both mucins and sialic acid in the GIT regions differ based on the tissue type in each tetrapod representative. The mucosa of oesophagus in the toad and lizard showed higher positive signal of general mucins compared with other tetrapod representatives. However, the mucosa of the oesophagus in the toad revealed a positive signal of sialic acid in the tubular glands only, whereas the lizard's mucosa showed a positive signal of sialic acid in the goblet cells. Additionally, the pigeon's oesophagus showed no localization of the sialic acid or mucins while, all layers of the mouse's oesophagus showed a positive localization of the sialic acid residues. In the stomach, all stomach mucosa compartments in all representatives showed positive signal of mucins, while the gastric glands in the toad, pigeon (proventricular glands) and mouse showed signals of sialic acid residues localization but in different trends. While the lizard showed a localization of the sialic acid in the mucosal lamina propria only. Furthermore, the mucosa of the ileum showed positive signal of mucin in the goblet cells and some absorptive cells brush borders in all tetrapod animals. While a higher signal of the sialic acid residues in the absorptive cells but not the goblet cells in the case of the toad and mouse. While the lizard's ileum showed a higher localization of sialic acid in the goblet cells only. Mucin localization in the rectum was similar to those in ileum. Specifically, the toad and lizard showed signals of the sialic acid residues in the goblet cells only, while the mouse's rectum showed a higher signal of sialic acids in the absorptive cells and lamina propria but not in the goblet cells. The present study introduces important data about the biodistribution and localization profiles of general mucins and sialic acids residues in the GIT different compartments in each representative of tetrapoda animals. Further studies are needed to investigate the important role of sialic acid residues localization in different compartments of GIT mucosa.
Immunohistochemical analysis of the vimentin filaments in Sertoli cells is a powerful tool for the prediction of spermatogenic dysfunction.
Saito H, Yokota S, Kitajima S
Acta Histochem · 2023 Jul · PMID 37224719 · Publisher ↗
The close interaction between male germ cells and Sertoli cells, a type of somatic cell found in the seminiferous tubules of mammalian testis, is essential for the normal progression of spermatogenesis in mammals. Viment...
The close interaction between male germ cells and Sertoli cells, a type of somatic cell found in the seminiferous tubules of mammalian testis, is essential for the normal progression of spermatogenesis in mammals. Vimentin is an intermediate filament protein that primarily provides mechanical support, preserves cell shape, and maintains the nuclear position, and it is often used as a marker to identify Sertoli cells. Vimentin is known to be involved in many diseases and aging processes; however, how vimentin is related to spermatogenic dysfunction and the associated functional changes is still unclear. In a previous study, we reported that vitamin E deficiency affected the testes, epididymis, and spermatozoa of mice, accelerating the progression of senescence. In this study, we focused on the Sertoli cell marker vimentin and explored the relationship between the cytoskeletal system of Sertoli cells and spermatogenic dysfunction using testis tissue sections that caused male reproductive dysfunction with vitamin E deficiency. The immunohistochemical analysis showed that the proportion of the vimentin-positive area in seminiferous tubule cross-sections was significantly increased in testis tissue sections of the vitamin E-deficient group compared with the proportion in the control group. The histological analysis of testis tissue sections from the vitamin E-deficient group showed that vimentin-positive Sertoli cells were greatly extended from the basement membrane, along with an increased abundance of vimentin. These findings suggest that vimentin may be a potential indicator for detecting spermatogenic dysfunction.
KCCs, NKCCs, and NCC: Potential targets for cardiovascular therapeutics? A comprehensive review of cell and region specific expression and function.
Modi AD, Khan AN, Cheng WYE … +1 more , Modi DM
Acta Histochem · 2023 May · PMID 37201245 · Publisher ↗
Cardiovascular diseases, the leading life-threatening conditions, involve cardiac arrhythmia, coronary artery disease, myocardial infarction, heart failure, cardiomyopathy, and heart valve disease that are associated wit...
Cardiovascular diseases, the leading life-threatening conditions, involve cardiac arrhythmia, coronary artery disease, myocardial infarction, heart failure, cardiomyopathy, and heart valve disease that are associated with the altered functioning of cation-chloride cotransporters. The decreased number of cation-chloride cotransporters leads to reduced reactivity to adrenergic stimulation. The KCC family is crucial for numerous physiological processes including cell proliferation and invasion, regulation of membrane trafficking, maintaining ionic and osmotic homeostasis, erythrocyte swelling, dendritic spine formation, maturation of postsynaptic GABAergic inhibition, and inhibitory/excitatory signaling in neural tracts. KCC2 maintains intracellular chlorine homeostasis and opposes β-adrenergic stimulation-induced Cl- influx to prevent arrhythmogenesis. KCC3-inactivated cardiac tissue shows increased vascular resistance, aortic distensibility, heart size and weight (i.e. hypertrophic cardiomyopathy). Due to KCC4's high affinity for K+, it plays a vital role in cardiac ischemia with increased extracellular K+. The NKCC and NCC families play a vital role in the regulation of saliva volume, establishing the potassium-rich endolymph in the cochlea, sodium uptake in astrocytes, inhibiting myogenic response in microcirculatory beds, regulation of smooth muscle tone in resistance vessels, and blood pressure. NKCC1 regulates chlorine homeostasis and knocking it out impairs cardiomyocyte depolarization and cardiac contractility as well as impairs depolarization and contractility of vascular smooth muscle rings in the aorta. The activation of NCC in vascular cells promotes the formation of the abdominal aortic aneurysm. This narrative review provides a deep insight into the structure and function of KCCs, NKCCs, and NCC in human physiology and cardiac pathobiology. Also, it provides cell-specific (21 cell types) and region-specific (6 regions) expression of KCC1, KCC2, KCC3, KCC4, NKCC1, NKCC2, and NCC in heart.
Geniposide alleviates pressure overload in cardiac fibrosis with suppressed TGF-β1 pathway.
Yao Y, Lin L, Tang W … +3 more , Shen Y, Chen F, Li N
Acta Histochem · 2023 May · PMID 37196380 · Publisher ↗
BACKGROUND: Cardiac fibrosis is one of the main contributors to the pathogenesis of heart failure. Geniposide (GE), a major iridoid in gardenia fruit extract, has recently been reported to improve skeletal muscle fibrosi...
BACKGROUND: Cardiac fibrosis is one of the main contributors to the pathogenesis of heart failure. Geniposide (GE), a major iridoid in gardenia fruit extract, has recently been reported to improve skeletal muscle fibrosis through the modulation of inflammation response. This investigation aimed to illuminate the cardio-protective effect and the potential mechanism of GE in cardiac fibrosis. MATERIAL AND METHODS: A transverse aortic contraction (TAC) induction mice model was established and GE (0 mg/kg; 10 mg/kg; 20 mg/kg; 40 mg/kg) was administered by oral gavage daily for 4 weeks. Hemodynamic parameters, Masson's trichrome stain, and hematoxylin-eosin (HE) staining were estimated and cardiomyocyte fibrosis, interstitial collagen levels, and hypertrophic markers were analyzed using qPCR and western blot. In vitro, H9C2 cells were exposed to the Ang II (1 μM) pretreated with GE (0.1 μM, 1 μM, and 10 μM). Cardiomyocyte apoptosis was detected. Moreover, the transforming growth factor β1 (TGF-β1)/Smad2 pathway was assessed in vivo and in vitro. RESULTS: GE significantly ameliorated TAC-induced cardiac hypertrophy, ventricular remodeling, myocardial fibrosis, and improved cardiac function in vivo, and it inhibited Ang II-induced cardiomyocyte apoptosis in vitro. We further observed that the inflammatory channel TGF-β1/Smad2 pathway was suppressed by GE both in vivo and in vitro. CONCLUSION: These results indicate that GE inhibited myocardial fibrosis and improved hypertrophic cardiomyocytes with attenuated the TGF-β1/Smad2 pathway and proposed to be an important therapeutic of cardiac fibrosis reduced by TAC.
Advantages of mesenchymal stem cell over the other stem cells.
Gopalarethinam J, Nair AP, Iyer M … +2 more , Vellingiri B, Subramaniam MD
Acta Histochem · 2023 May · PMID 37167794 · Publisher ↗
A stem cell is a particular group of cells that has the extraordinary potential to convert within the body into particular cell types. They are used to regenerate tissues and cells in the body that have been damaged or d...
A stem cell is a particular group of cells that has the extraordinary potential to convert within the body into particular cell types. They are used to regenerate tissues and cells in the body that have been damaged or destroyed by the disease. Stem cells come in three different varieties: adult stem cells, embryonic stem cells and induced pluripotent stem cells (iPSCs). Embryonic stem cells have a high chance of immune rejection and also have ethical dilemmas and iPSCs have genetic instability. Adult stem cells are difficult to analyze and extract for research since they are frequently insufficient in native tissues. However, mesenchymal stem cells (MSC) one of the categories of adult stem cells are stromal cells with a variety of potentials that can differentiate into a wide range of cell types. MSCs can be transplanted into a variety of people without worrying about rejection because they have demonstrated the ability to prevent an adverse reaction from the immune system. These transplants have powerful anti-inflammatory and immunosuppressive effects and greatly enhance the body's inherent healing capacity. While MSCs do not offer treatment for illnesses, the idea behind them is to enable the body to recover sufficiently for a protracted reduction in symptoms. In many cases, this is sufficient to significantly enhance the patient's well-being. Inspite of several advantages some potential long-term concerns connected to MSC therapy are maldifferentiation, immunosuppression and cancerous tumor growth. In this review, we will compare the mesenchymal stem cells with other stem cells with respect to the source of origin, their properties and therapeutic applications, and discuss the MSC's disadvantages.
Hypoxia activates the PI3K/AKT/HIF-1α pathway to promote the anti-inflammatory effect of adipose mesenchymal stem cells.
Ren H, Liu M, Jihu Y … +3 more , Zeng H, Yao C, Yan H
Acta Histochem · 2023 May · PMID 37137202 · Publisher ↗
This study aimed to investigate the effect of hypoxia on the anti-inflammatory effect of adipose-derived mesenchymal stem cells (AMSCs) in vitro and its possible mechanism. AMSCs were cultured in vitro in a hypoxic envir...
This study aimed to investigate the effect of hypoxia on the anti-inflammatory effect of adipose-derived mesenchymal stem cells (AMSCs) in vitro and its possible mechanism. AMSCs were cultured in vitro in a hypoxic environment with 3% O, and a normoxic (21% O) environment was used as the control. The cells were identified by in vitro adipogenic and osteogenic differentiation and cell surface antigen detection, and the cell viability were detected. The effect of hypoxic AMSCs on macrophage inflammation was analyzed by co-culture. The results showed that under hypoxia, AMSCs had better viability, significantly downregulated the expression of inflammatory factors, alleviated macrophage inflammation, and activated the PI3K/AKT/HIF-1α pathway.
Immunohistochemical distribution of Ca/calmodulin-dependent protein kinase II subunits in the rat carotid body.
Saito H, Yokoyama T, Nakamuta N … +1 more , Yamamoto Y
Acta Histochem · 2023 May · PMID 37126880 · Publisher ↗
Carotid body (CB) activity stimulated by a lower partial oxygen pressure in rats is enhanced by exposure to chronic intermittent hypoxia. However, the mechanisms that modulate CB activity remain unclear. In the present s...
Carotid body (CB) activity stimulated by a lower partial oxygen pressure in rats is enhanced by exposure to chronic intermittent hypoxia. However, the mechanisms that modulate CB activity remain unclear. In the present study, the expression and distribution of one of the candidate molecules to modulate reactivity, Ca/calmodulin-dependent protein kinase II (CaMKII) were examined in the rat CB using reverse transcriptional polymerase chain reaction and immunofluorescence with isoform-specific antibodies. CaMKIIγ and CaMKIIδ were distributed in CB chemoreceptor cells, and exhibited intense immunoreactivity in dopamine β-hydroxylase-positive chemoreceptor cells. CaMKIIβ and CaMKIIγ were distributed in sensory nerve endings attached to chemoreceptor cells of the CB. In the petrosal ganglion, immunoreactivities for CaMKIIα, CaMKIIβ, CaMKIIγ, and CaMKIIδ were detected in the perinuclear region of ganglion cells. The present results indicate that CaMKIIγ and CaMKIIδ in chemoreceptor cells and CaMKIIβ and CaMKIIγ in sensory nerve endings enhanced reciprocal synaptic transmission, i.e., noradrenaline and ATP for cells to neurons and glutamate for neurons to cells.
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