European Journal Of Histochemistry[JOURNAL]
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200 papers
Proceedings of the 69th Congress of the Italian Embryological Group-Italian Society of Development and Cell Biology (GEI-SIBSC) - Naples, 11-14 June 2024.
Committee TS
Eur J Histochem · 2024 Jun · PMID 40488581 · Publisher ↗
Proceedings of the 69th Congress of the Italian Embryological Group-Italian Society of Development and Cell Biology (GEI-SIBSC) - Naples, 11-14 June 2024.
Proceedings of the 69th Congress of the Italian Embryological Group-Italian Society of Development and Cell Biology (GEI-SIBSC) - Naples, 11-14 June 2024.
Proceedings of the 70th Congress of the Italian Embryological Group-Italian Society of Development and Cell Biology (GEI-SIBSC).
Committee TS
Eur J Histochem · 2025 Jun · PMID 40488575 · Publisher ↗
Proceedings of the 70th Congress of the Italian Embryological Group-Italian Society of Development and Cell Biology (GEI-SIBSC) - Modena, 10-13 June 2025.
Proceedings of the 70th Congress of the Italian Embryological Group-Italian Society of Development and Cell Biology (GEI-SIBSC) - Modena, 10-13 June 2025.
E-cadherin inhibits the proliferation and migration of human colorectal cancer cells through Hippo signaling pathway.
Wang Z, Qin X, Liu S … +4 more , Wen Y, Lan B, Liao H, Wei H
Eur J Histochem · 2025 Apr · PMID 40421484 · Full text
E-cadherin (E-cad) is a crucial regulatory factor in rescue Epithelial-mesenchymal transition and is involved in the occurrence of various malignant tumor. However, the mechanisms by which E-cadherin regulates tumor meta...
E-cadherin (E-cad) is a crucial regulatory factor in rescue Epithelial-mesenchymal transition and is involved in the occurrence of various malignant tumor. However, the mechanisms by which E-cadherin regulates tumor metastasis in CRC remain unclear. We established sh-E-cad (silenced by short hairpin RNA) and rescue-E-cad (overexpressed by E-cad plasmid transfection) CRC cell lines to investigate the role of E-cad in CRC in vitro. Immunohistochemistry, clonogenic assays, scratch wound healing assays, CCK-8 assays, flow cytometry, Transwell assay, real time-PCR and Western blot were employed to investigate the underlying mechanisms by which E-cad involve the progression of CRC. In CRC tissues, E-cad expression was significantly reduced, while YAP expression was markedly elevated. Silencing E-cad induced a significant increase of clonogenic ability in CRC cells, which was reduced upon rescue of E-cad expression. Transwell assays indicate that low expression of E-cad enhances the cell migration, a finding corroborated by scratch wound healing experiments. CCK-8 results demonstrate that silencing E-cad promotes the proliferation of CRC cells. Importantly, we found that E-cad influences apoptosis rather than the cell cycle. Analysis of Hippo signaling pathway-related factors revealed that silencing E-cad resulted in significantly decreased expression of MST1/2 and LATS1/2, as well as reduced phosphorylation levels of YAP, while YAP expression was significantly increased. Additionally, immunofluorescence confirmed the nuclear translocation of YAP. Our study indicates that E-cad regulates the malignant progression of CRC via the Hippo signaling pathway, offering a potential new strategy for CRC treatment.
Erratum - Effect of CDX2 on proliferation, invasion, migration, and apoptosis of duodenal cancer cells.
Pan J, Zhao Y, Zhang Y … +4 more , Zhou Y, Zhang F, Chen Y, Chu X
Eur J Histochem · 2025 Apr · PMID 40391518 · Full text
This corrects the article published in the European Journal of Histochemistry 2025;69:4203.
This corrects the article published in the European Journal of Histochemistry 2025;69:4203.
Anatomical insights into the proximal aponeurosis of the long head of the biceps femoris.
Mantecón-Tagarro CJ, Nanizawa E, Naito M … +3 more , Otsuka S, Maas H, Kawakami Y
Eur J Histochem · 2025 Apr · PMID 40357529 · Full text
The biceps femoris long head (BFlh) is prone to strain injuries, but its reasons remain unclear. This study analyzed the BFlh proximal intramuscular aponeurosis in donor samples (n=4) through morphometric, microscopic, a...
The biceps femoris long head (BFlh) is prone to strain injuries, but its reasons remain unclear. This study analyzed the BFlh proximal intramuscular aponeurosis in donor samples (n=4) through morphometric, microscopic, and histological methods. Cross-sections were taken every 5% of the muscle belly to differentiate connective, adipose, and muscle tissues. The aponeurosis extended from the muscle surface, becoming intramuscular from 40-70% of the muscle belly, and ended distally. Quantitative analysis revealed significant reductions of size in both the cross-sectional area (CSA) and width of the aponeurosis at 50% of muscle length, with CSA ranging from 4.9 mm² to 13.4 mm² and widths from 6.8 mm to 12.4 mm across subjects. Dense connective tissue bundles were separated by adipose or loose connective tissues. The aponeurosis shape varied along the muscle, with T- and hook-shaped configurations, and small branches were observed distally. These findings reveal the BFlh proximal aponeurosis as a complex structure, potentially influencing its injury susceptibility.
MiR-122-5p inhibits the epithelial mesenchymal transition of liver cancer cells by inducing hiPSCs to differentiate into hepatocyte-like cells.
Xing Q, Xu Y, Luo Y … +4 more , Li C, Wang P, Kang B, Lu C
Eur J Histochem · 2025 Apr · PMID 40336362 · Full text
Epithelial-mesenchymal transition (EMT) is closely linked to liver cancer prognosis, invasiveness, and aggressiveness. One promising treatment for liver cancer is cell therapy, where stem cells are stimulated to develop...
Epithelial-mesenchymal transition (EMT) is closely linked to liver cancer prognosis, invasiveness, and aggressiveness. One promising treatment for liver cancer is cell therapy, where stem cells are stimulated to develop into functional liver cells. This study aimed to investigate the effect of miR-122-5p on the differentiation of human induced pluripotent stem cells (hiPSCs) into hepatocyte-like cells and its impact on the EMT process in liver cancer cells. MiR-122-5p was overexpressed or silenced in hiPSCs to analyze the expression of liver-specific markers, including AFP, ALB and ASGPR, to confirm hepatocyte-like differentiation. A co-culture system with HepG2 liver cancer cells was also used to evaluate the effect of miR-122-5p-overexpressing hiPSCs or miR-122-5p-silencing hiPSCs on the expression of EMT markers. Results revealed that overexpression of miR-122-5p in hiPSCs induced hepatocyte-like characteristics, as evidenced by increased levels of AFP, ALB, and ASGPR. However, knockdown of miR-122-5p had the opposite effect. In the co-culture system, hiPSCs overexpressing miR-122-5p inhibited the EMT process of HepG2 cells, resulting in increased levels of mesenchymal markers and decreased levels of epithelial markers. Taken together, miR-122-5p promotes the differentiation of hiPSCs into hepatocyte-like cells and inhibits EMT process of liver cancer cells. Targeting miR-122-5p may be a novel approach to prevent liver cancer progression through cell therapy.
Knockdown of miR-411-3p induces M2 macrophage polarization and promotes colorectal cancer progression by regulation of MMP7.
Bai T, Li P, Liu Y … +6 more , Cai B, Li G, Wang W, Yan R, Zheng X, Du S
Eur J Histochem · 2025 Apr · PMID 40322788 · Full text
Colorectal cancer (CRC) is prone to metastasis, leading to a poor prognosis. miR-411-3p exhibits a tumor-suppressive function in CRC, but its exact mechanism is unclear. The malignant biological properties of CRC cells w...
Colorectal cancer (CRC) is prone to metastasis, leading to a poor prognosis. miR-411-3p exhibits a tumor-suppressive function in CRC, but its exact mechanism is unclear. The malignant biological properties of CRC cells were detected by Carboxyfluorescein diacetate succinimidyl ester (CFSE) staining, scratch-wound and transwell assay. Levels of markers associated with macrophage polarization were evaluated by flow cytometry and ELISA kits. Bioinformatics analysis to screen whether the downstream target mRNA of miR-411-3p is matrix metalloproteinase 7 (MMP7), and Dual-Luciferase reporter assay verified the targeting relationship between the two. qRT-PCR tested miR-411-3p and MMP7 levels. MMP7 level was quantified by Western blot. Additionally, a nude mouse subcutaneous graft tumor model was constructed, Ki-67 expression was detected by immunohistochemistry, and the impact of miR-411-3p/MMP7 on the polarization of M2 macrophages was explored. miR-411-3p expression is downregulated in CRC. Knockdown of miR-411-3p elevated the amount of CFSE-positive, migrating, and invading cells, decreased apoptosis, and elevated the levels of M2 macrophage polarization markers. After overexpression of miR-411-3p, all of the above metrics were reversed in CRC cells. miR-411-3p targeted negative regulation of MMP7 expression, and MMP7 overexpression further enhanced the promotional effect of knockdown of miR-411-3p on the malignant progression of CRC and M2 macrophage polarization. Furthermore, knockdown of miR-411-3p upregulated the MMP7 level, elevated Ki-67-positive cells count, and induced M2 macrophage polarization in vivo. Knockdown of miR-411-3p upregulates MMP7 and induces M2 macrophage polarization, which in turn promotes malignant biological progression of CRC.
Effect of CDX2 on proliferation, invasion, migration, and apoptosis of duodenal cancer cells.
Pan J, Zhao Y, Zhang Y … +4 more , Zhou Y, Zhang F, Chen Y, Chu X
Eur J Histochem · 2025 Apr · PMID 40272258 · Full text
This study investigates the expression and biological role of caudal homologous transcription factor 2 (CDX2) in duodenal carcinoma. Paraffin-embedded samples from 40 duodenal carcinoma cases were analyzed using immunohi...
This study investigates the expression and biological role of caudal homologous transcription factor 2 (CDX2) in duodenal carcinoma. Paraffin-embedded samples from 40 duodenal carcinoma cases were analyzed using immunohistochemistry on a tissue microarray to assess CDX2 expression and its prognostic significance. CDX2 overexpression plasmids and CDX2-siRNA were transfected into colon and duodenal cancer cells. Transfection efficiency was confirmed by RT-PCR and Western blotting. Cell proliferation was assessed using CCK8 assay, migration via scratch assay, and cell cycle and apoptosis by flow cytometry. CDX2 staining was primarily nuclear, with a positive rate of 65% in duodenal carcinoma tissues, significantly lower than in adjacent non-tumor tissues (p<0.05). CDX2-positive patients had better prognoses than negative patients (p<0.05). Reduced CDX2 expression significantly enhanced the proliferation of CaCO2 and HuTu-80 cells (p<0.001), whereas CDX2 overexpression suppressed proliferation (p<0.001). CDX2 knockdown increased migration, while its overexpression reduced migration (p<0.05). CDX2 overexpression led to a significant increase in G0/G1 phase cells and a decrease in S phase cells (p<0.05), whereas knockdown reduced G0/G1 phase cells and increased S and G2/M phase cells (p<0.05). Apoptosis was significantly increased following CDX2 overexpression (p<0.001) and decreased after CDX2 knockdown (p<0.001). CDX2 expression is downregulated or lost in duodenal carcinoma, acting as a tumor suppressor. CDX2 may serve as a crucial biomarker for predicting the onset, progression, and treatment of duodenal carcinoma.
Cancer cell-derived exosomal miR-34a inhibits the malignant progression of pancreatic adenocarcinoma cells by restraining the M2 polarization of macrophages.
Long K, Kui X, Zeng Q … +1 more , Dong W
Eur J Histochem · 2025 Apr · PMID 40244037 · Full text
This study aimed to investigate the crosstalk mechanism between pancreatic cancer (PAC) cells and M2 tumor-associated macrophages induced by tumor-derived exosomal miR-34a. MicroRNA and mRNA expression levels were detect...
This study aimed to investigate the crosstalk mechanism between pancreatic cancer (PAC) cells and M2 tumor-associated macrophages induced by tumor-derived exosomal miR-34a. MicroRNA and mRNA expression levels were detected using RT-qPCR. Cell Counting Kit-8, wound-healing, transwell assays and flow cytometry were respectively employed to assess cell proliferation, migration, invasion and apoptosis. Enzyme-linked immunosorbent assay was utilized to determine cytokine secretion. Transmission electron microscopy and nanoparticle tracking analyses were performed to detect the exosome morphology and particle size. Phagocytosis of exosomes by macrophages was verified by PKH26 labeling. The effects of exosome-treated macrophages on the epithelial-mesenchymal transition, invasion, and migration of PANC-1 cells were investigated using coculture experiments. The identification of miR-34a's potential targets were determined with TargetScan and validated by a dual-luciferase reporter assay. miR-34a was expressed at low levels in PAC tissues, cells, and exosomes. The overexpression of miR-34a restrains the malignant progression of PANC-1 cells. After miR-34a-overexpressed PANC-1-derived exosomes were phagocytosed by macrophages, the process of M2 polarization in macrophages was obstructed, leading to the suppression of epithelial-mesenchymal transition, migration, and invasion of the cocultured PANC-1 cells. Suppressor of cytokine signaling 3 is a direct target of miR-34a. MiR-34a negatively modulates the suppressor of cytokine signaling 3 to prevent the M2 polarization of macrophages by engaging the Janus kinase/signal transducers and activators of the transcription pathway and influencing the malignancy of PAC cells. miR-34a in cancer cell-derived exosomes inhibits the malignant progression of pancreatic cancer cells by restraining M2 polarization of macrophages.
Downregulation of S100 calcium-binding A4 (S100A4) ameliorates hepatic fibrosis regulating Wnt/β-catenin signaling pathway.
Zhang C, Bai K, Li D
Eur J Histochem · 2025 Apr · PMID 40223805 · Full text
S100 calcium-binding protein A4 (S100A4), a fibrosis-associated calcium-binding protein, has been implicated in fibrotic progression across multiple organs. Activation of the Wnt/β-catenin signaling pathway is a critical...
S100 calcium-binding protein A4 (S100A4), a fibrosis-associated calcium-binding protein, has been implicated in fibrotic progression across multiple organs. Activation of the Wnt/β-catenin signaling pathway is a critical driver of hepatic fibrosis, yet the mechanistic role of S100A4 in this context remains poorly defined. This study investigated the regulatory role of S100A4 in hepatic fibrosis in vitro and in vivo. Hepatic stellate cells (HSCs) were treated with TGF-β to induce fibrotic activation, and S100A4 expression was silenced using shRNA. A carbon tetrachloride (CCl₄)-induced murine hepatic fibrosis model was employed for in vivo validation. Fibrotic markers, including collagen I, fibronectin, and α-smooth muscle actin (α-SMA), were assessed via qRT-PCR, Western blotting, immunofluorescence, and immunohistochemistry. Liver histopathology and function were evaluated using Masson trichrome staining, hematoxylin-eosin staining, and serum ALT/AST assays. In vitro experiments demonstrated that TGF-β treatment upregulated S100A4 expression in HSCs, while S100A4 silencing suppressed HSC activation, extracellular matrix (ECM) deposition, and Wnt/β-catenin signaling. In vivo, S100A4 downregulation attenuated CCl₄-induced hepatic fibrosis, reduced collagen accumulation, improved liver histology, and normalized serum ALT/AST levels. These findings indicate that S100A4 promotes hepatic fibrosis by activating the Wnt/β-catenin pathway, highlighting its potential as a therapeutic target.
Independent and interactive roles of hirudin and HMGB1 interference in protecting renal function by regulating autophagy, apoptosis, and kidney injury in chronic kidney disease.
Li Y, Gao X, Chen Y … +3 more , Li H, Tang J, Sun W
Eur J Histochem · 2025 Apr · PMID 40191929 · Full text
Chronic kidney disease (CKD) is a progressive disorder characterized by renal fibrosis, inflammation, and dysregulated autophagy and apoptosis. High-mobility group box 1 (HMGB1) plays a crucial role in regulating autopha...
Chronic kidney disease (CKD) is a progressive disorder characterized by renal fibrosis, inflammation, and dysregulated autophagy and apoptosis. High-mobility group box 1 (HMGB1) plays a crucial role in regulating autophagy in CKD. Hirudin, a potent thrombin inhibitor, has demonstrated antifibrotic and anti-inflammatory properties, but its effects on autophagy and apoptosis in CKD remain unclear. In this study, a rat model of renal interstitial fibrosis (RIF) and an HK-2 cell culture model were established to assess the effects of varying doses of hirudin and HMGB1 interference. Molecular and histological analyses, including RTqPCR, Western blot, TUNEL staining, hematoxylin-eosin (H&E) staining, immunofluorescence, and immunohistochemistry (IHC), were performed to assess renal injury, fibrosis, apoptosis, and autophagy-related markers. Hirudin treatment significantly reduced the expression of LC3, ATG12, ATG5, α-SMA, COL1A1, caspase-3, and caspase-9 while increasing P62 levels (p<0.05). It also lowered the renal coefficient (p<0.001) and apoptosis levels. The optimal effective concentration of hirudin in vitro was determined to be 4.8 ATU/mL (p<0.001). HMGB1 interference suppressed autophagy and apoptosis, as indicated by decreased LC3-II/LC3-I, ATG12, ATG5, caspase-3, and caspase-9 levels, increased P62 expression (p<0.001), and reduced apoptosis. However, simultaneous HMGB1 interference in hirudin-treated cells weakened the therapeutic effects of hirudin, leading to increased autophagy and apoptosis markers, decreased P62 levels, and a higher renal coefficient. These findings indicate that hirudin exerts protective effects in CKD by modulating autophagy and apoptosis, potentially through HMGB1 regulation. These findings highlight the therapeutic potential of targeting these mechanisms in renal dysfunction and underscore the necessity for further research to support clinical applications.
miR-627-5p inhibits malignant progression of cervical cancer by targeting ANGPTL4.
Wu X, Lin K, Gao C … +4 more , Ni Y, Zhang L, Yang T, Chen J
Eur J Histochem · 2025 Apr · PMID 40191921 · Full text
In recent years, accumulating evidence has highlighted the critical role of miR-627-5p in the occurrence and progression of various cancers. However, its specific role and mechanism in cervical cancer (CC) remain unclear...
In recent years, accumulating evidence has highlighted the critical role of miR-627-5p in the occurrence and progression of various cancers. However, its specific role and mechanism in cervical cancer (CC) remain unclear. This study aimed to elucidate the mechanism by which miR-627-5p inhibits the malignant progression of CC and assess its potential clinical implications. In C33A cells, the mRNA expression levels of ANGPTL4 and miR-627-5p were analyzed using qRT-PCR. The miR-627-5p mimics and their control (miR-NC) were transfected into C33A cells to determine whether miR-627-5p directly regulates ANGPTL4 expression. A comprehensive suite of assays, including CCK-8, migration, transwell, flow cytometry, and Western blotting, was conducted to evaluate how miR-627-5p modulates the malignant biological behavior of CC cells. Rescue experiments were performed by overexpressing ANGPTL4. In C33A cells, miR-627-5p expression was reduced, whereas ANGPTL4 expression was elevated. Further analysis confirmed that miR-627-5p negatively regulates ANGPTL4 by directly targeting its 3'-UTR. Functional assays demonstrated that miR-627-5p inhibits proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) while promoting apoptosis and S-phase arrest in C33A cells, effects that were reversed by ANGPTL4 overexpression. These findings highlight the potential of miR-627-5p as both a biomarker and a therapeutic target for CC. By inhibiting EMT and regulating ANGPTL4 expression, miR-627-5p may provide a novel avenue for improving therapeutic strategies, particularly in advanced or metastatic CC. Moreover, miRNA-based therapies, supported by advanced delivery systems such as nanoparticle carriers, could enhance the stability and precision of miR-627-5p applications. This study lays the groundwork for future research integrating miR-627-5p into precision medicine approaches for CC treatment.
Co-expression of MyHC-15 with other known isoforms in rat muscle spindles.
Smerdu V, Ugwoke CK, Šink Ž
Eur J Histochem · 2025 Jan · PMID 40126372 · Full text
Muscle spindles are skeletal muscle sensory receptors composed of intrafusal fibres, partially encapsulated by connective tissue capsule. This capsule encloses the central A and B regions while leaving the distal C regio...
Muscle spindles are skeletal muscle sensory receptors composed of intrafusal fibres, partially encapsulated by connective tissue capsule. This capsule encloses the central A and B regions while leaving the distal C region extracapsular. Several past studies in rat have shown that muscle spindles typically contain a single bag1 fibre, a single bag2 fibre, and two smaller chain fibres. Intrafusal fibres co-express multiple myosin heavy chain (MyHC) isoforms: -slow or -1, -slow-tonic, -α, -2a, -2b, -embryonic, and -neonatal. While MyHC-2x was previously thought absent, the recently discovered MyHC-15 isoform has been identified in the C region of rat bag fibres. Using antibodies specific for nine MyHC isoforms and analyzing four different rat skeletal muscles-soleus, extensor digitorum longus, and the lateral and medial heads of gastrocnemius-we aimed to further characterize the co-expression pattern of MyHC-15 with other known isoforms and to determine whether MyHC-2x is expressed in rat intrafusal fibres. While rodents are widely used as animal models in skeletal muscle research, notable species-specific differences in MyHC isoform expression exist. Our findings revealed that MyHC-15 expression in rat intrafusal fibres is less abundant than in human fibres. MyHC-15 was primarily observed in bag fibres but was not detected in the C region, contrary to previous reports in both rat and human. We confirmed the absence of MyHC-2x in rat intrafusal fibres. Similarly, MyHC-embryonic and -neonatal were not detected in the analyzed spindles, suggesting that previously used antibodies may have cross-reacted with MyHC-2a and -2b. While our results partially corroborate previous extensive studies, discrepancies suggest that MyHC expression in intrafusal fibres varies not only along the fibre length but also across muscles.
Reliable hexokinase 3 protein detection in human cell lines and primary tissue.
Mady YH, Kalbermatter CG, Khan M … +5 more , Schläfli AM, Mehmeti R, Zlobec I, Christe L, Tschan MP
Eur J Histochem · 2025 Jan · PMID 40071468 · Full text
Accurate differentiation of homologous proteins that share high sequence identity remains a significant challenge in biomedical research, as conventional antibodies often lack sufficient specificity, leading to potential...
Accurate differentiation of homologous proteins that share high sequence identity remains a significant challenge in biomedical research, as conventional antibodies often lack sufficient specificity, leading to potential misinterpretations. This issue is particularly evident in the study of hexokinases, a family of isoenzymes that catalyze the first step of glycolysis by phosphorylating glucose. Beyond their canonical metabolic roles, hexokinases play critical non-glycolytic functions, especially in cancer biology. However, their unique tissue distributions and context-dependent roles are often obscured by the overlapping specificities of commercially available antibodies, which can produce misleading results. In this study, we rigorously evaluated a panel of antibodies targeting hexokinase isoenzyme 3 (HK3), highlighting the widespread issue of cross-reactivity and insufficient validation. Through this process, we identified and validated a highly specific antibody for HK3, demonstrating its reliability in western blot and immunohistochemistry applications. Using this validated tool, we reveal the distinct localization of HK3 in myeloid cell populations, providing new insights into its potential functional roles in these cells. This work addresses a critical gap in antibody specificity and establishes HK3 as a uniquely expressed gene in myeloid and immune cells and is absent in other cell types under basal conditions. Providing a foundation for future investigations into its context-dependent functions.
Expression of S100β during mouse cochlear development.
Liu W, Zhang Y, Liang C … +1 more , Su L
Eur J Histochem · 2025 Jan · PMID 40066753 · Full text
In the present study, the expression of S100β was examined in the mouse cochlea from embryonic day 17 (E17) to postnatal day 32 (P32) using immunofluorescence, aiming to explore its possible role in auditory system. At E...
In the present study, the expression of S100β was examined in the mouse cochlea from embryonic day 17 (E17) to postnatal day 32 (P32) using immunofluorescence, aiming to explore its possible role in auditory system. At E17, S100β expression was not detected, except in the external cochlear wall. Starting at E18.5, S100β staining appeared in the organ of Corti and the stria vascularis. In the E18.5 and P1 organ of Corti, S100β was confined to the developing pillar cells. By P6, cytoplasmic staining of S100β was evident in the inner and outer pillar cells, forming the tunnel of Corti. Additionally, S100β expression extended medially into the three rows of Deiter's cells, with labeling of their phalangeal processes. At P8, S100β continued to be expressed in the heads, bodies, and feet of the two pillar cells, as well as in the soma and phalangeal processes of the three rows of Deiter's cells. In the lateral wall of the P8 cochlea, S100β was expressed not only in the stria vascularis but also in the spiral ligament. Between P10 and P12, S100β expression was maintained in the Deiter's cells and pillar cells of the organ of Corti, as well as in the lateral wall, and spiral limbus. From P14 onwards, S100β expression ceased in the stria vascularis, though it persisted in the spiral ligament and spiral limbus into adulthood. Within the P14 and P21 organ of Corti, S100β remained in the Deiter's and pillar cells. S100β immunostaining was not observed in the phalangeal processes of Deiter's cells but was specifically present in the Deiter's cell cups at P21. In the adult cochlea (P28 and P32), S100β expression declined in both Deiter's and pillar cells. The dynamic spatiotemporal changes in S100β expression during cochlear ontogeny suggest its role in cochlear development and hearing function.
Immunohistochemistry of carbonic anhydrases I, II and VI in the rat lingual serous salivary glands of von Ebner.
Redman RS
Eur J Histochem · 2025 Jan · PMID 40034043 · Full text
Carbonic anhydrase (CA) has been localized to many structures involved in ion transport including the acini and ducts of the major (parotid, sublingual and submandibular) salivary glands of humans and rodents. It also ha...
Carbonic anhydrase (CA) has been localized to many structures involved in ion transport including the acini and ducts of the major (parotid, sublingual and submandibular) salivary glands of humans and rodents. It also has been localized by enzyme histochemistry and by immunohistochemistry for CA isoenzyme VI (CA VI) to the acini and ducts of rat serous lingual glands of von Ebner. The purpose of this study was to explore the intracellular distribution by cell type of three CA isoenzymes in these glands. Immunohistochemistry was undertaken with antibodies to human CAs I, II and VI in paraffin sections of rat tongues that had been fixed in Helly's fluid. The density of the reaction product was scored as 0 (none) to 5 (strongest). Reactions in the acini with CA I and II antibodies were weak luminally to moderate basally and generally moderate, respectively, moderate in the intercalated ducts, and moderate basally to strong luminally in the excretory ducts. Weak to moderate CA VI reactions occurred in the acini and ducts. The stronger luminal reactions to CAs I and II in the excretory ducts suggest that they contribute to pH regulation in the saliva of von Ebner's glands via HCO3- transport.
Exploring the efficacy of AMACR, ERG, and AR immunostains in prostatic adenocarcinoma and their association with novel grade groups.
Andarawi MO, Otifi H, Hassan H … +6 more , Yousif AA, Mustafa SA, Elsiddig SA, Babker AM, Ali EI, Elhag OO
Eur J Histochem · 2025 Feb · PMID 39931952 · Full text
The study examines the utility of AMACR, ERG, and AR immunostains in diagnosing prostatic adenocarcinoma (PCa) and assessing prognosis in comparison to the Gleason score and new WHO grading groups. Seventeen PCa biopsies...
The study examines the utility of AMACR, ERG, and AR immunostains in diagnosing prostatic adenocarcinoma (PCa) and assessing prognosis in comparison to the Gleason score and new WHO grading groups. Seventeen PCa biopsies and five benign prostatic hyperplasia (BPH) biopsies were analyzed. Immunoreactivity, scored from 1 to 3 based on percentage of positive cells and intensity of expression, was assessed, revealing 76.47% positivity for AMACR, 35.29% for ERG, and 94.12% for AR in PCa cases, with variable scores and intensity among markers and grade groups. AMACR sensitivity and ERG specificity were noted. Higher-grade PCa exhibited increased positivity for both markers, indicating prognostic significance. In BPH cases, AMACR showed positivity in 2 cases, ERG in 1, and AR in all cases, albeit with lower expression. Differential expression was observed among immunomarkers and grade groups of malignancy. AMACR and ERG stains serve as sensitive and specific markers for PCa diagnosis and prognosis. Their increasing positivity with higher-grade groups underscores prognostic value. These findings highlight the importance of immunostains in refining PCa diagnosis and prognostication.
Erratum - Effect of Danggui Buxue decoction on hypoxia-induced injury of retinal Müller cells .
Ge X, Huang C, Chen W … +4 more , Yang C, Huang W, Li J, Yang S
Eur J Histochem · 2025 Jan · PMID 39836115 · Full text
This corrects the article published in European Journal of Histochemistry 2024;68:4140 doi: 10.4081/ejh.2024.4140 IF: 2.1 Q4 B4 IF: 2.1 Q4 B4.
This corrects the article published in European Journal of Histochemistry 2024;68:4140 doi: 10.4081/ejh.2024.4140 IF: 2.1 Q4 B4 IF: 2.1 Q4 B4.
Restorative effects of camellia oil on the skin-barrier function in a model of DNCB-induced atopic dermatitis.
Jiao S, Deng L, Niu M … +1 more , Yang J
Eur J Histochem · 2025 Jan · PMID 39836107 · Full text
This study aimed to evaluate the therapeutic efficacy of camellia oil on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD) in mice, as well as its effect on the expression of skin-barrier-related proteins. A...
This study aimed to evaluate the therapeutic efficacy of camellia oil on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD) in mice, as well as its effect on the expression of skin-barrier-related proteins. A mouse model of AD was created via topical application of DNCB; subsequently, the animals were randomly divided into four groups: the blank control (Control), model (Model), moisturizing cream (Moisturizer), and camellia oil (Camellia) groups. The Camellia group received camellia oil, whereas the Moisturizer group was treated with moisturizing cream, as a positive control. Skin lesions, ear and back tissue morphology, and the serum levels of IgE, IL-4, and IFN-γ were analyzed. Compared with the Control group, AD mice exhibited erythema, papules, dryness, peeling, and significantly higher serum IgE and IL-4 levels. Compared with the Model group, treatment with camellia oil and moisturizing cream considerably reduced skin inflammation, ear thickness, and scratching frequency. A histopathological analysis revealed that camellia oil reduced inflammatory-cell infiltration and edema in the AD-affected skin. Furthermore, camellia oil upregulated filaggrin (FLG), thus aiding in skin-barrier repair. These findings suggest that camellia oil significantly improves AD symptoms, enhances FLG expression, and restores the damaged skin barrier in AD mouse models.
Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathway.
Yang M, Xu W, Yue C … +7 more , Li R, Huang X, Yan Y, Yan Q, Liu S, Liu Y, Li Q
Eur J Histochem · 2025 Jan · PMID 39836101 · Full text
Intestinal barrier damage causes an imbalance in the intestinal flora and microbial environment, promoting a variety of gastrointestinal diseases. This study aimed to explore the mechanism by which adipose-derived stem c...
Intestinal barrier damage causes an imbalance in the intestinal flora and microbial environment, promoting a variety of gastrointestinal diseases. This study aimed to explore the mechanism by which adipose-derived stem cells (ADSCs) repair intestinal barrier damage. The human colon adenocarcinoma cell line Caco-2 and rats were treated with lipopolysaccharide (LPS) to establish in vitro and in vivo models, respectively, of intestinal barrier damage. The expression of inflammatory cytokines (TNF-α, HMGB1, IL-1β and IL-6), antioxidant enzymes (iNOS, SOD and CAT), and oxidative products (MDA and 8-iso-PGF2α) was detected using ELISA kits and related reagent kits. Apoptosis-related proteins (Bcl-2, Bax, Caspase-3 and Caspase-9), tight junction proteins (ZO-1, Occludin, E-cadherin, and Claudin-1) and p38 MAPK pathway-associated protein were detected by Western blotting. In addition, cell viability and apoptosis was determined by a CCK-8 kit and flow cytometry, respectively. Cell permeability was assayed by the transepithelial electrical resistance value and FITC-dextran concentration. The homing effect of ADSCs was detected by fluorescence labeling, and intestinal barrier tissue was observed by HE staining. After ADSC treatment, the level of phosphorylated p38 MAPK protein decreased, the expression of inflammatory factors, oxidative stress and cell apoptosis decreased, the expression of tight junction proteins increased, and cell permeability decreased in Caco-2 cells stimulated with LPS. In rats, ADSCs are directionally recruited to damaged intestinal tissue. ADSCs significantly decreased the levels of D-lactate, diamine oxidase (DAO) and FITC-dextran induced by LPS. ADSCs promoted tight junction proteins and inhibited oxidative stress in intestinal tissue. These effects were reversed after the use of a p38 MAPK activator. ADSCs can be directionally recruited to intestinal tissue, upregulate tight junction proteins, and reduce apoptosis and oxidative stress by inhibiting the p38MAPK signaling pathway. This study provides novel insights into the treatment of intestinal injury.
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