J. Cell. Physiol. [JOURNAL]
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200 papers
PIEZO1 Channels Modulate the Small Extracellular Vesicle Release in C2C12 Cells.
Annalisa B, Ru ZW, Laura SS … +9 more , Alessia N, Anna F, Marianna L, Marina S, Griffoni A, William RK, Giulio T, Paola L, Agenor L
J Cell Physiol · 2026 Mar · PMID 41834672 · Full text
PIEZO1 are mechanically-activated ion channels expressed in many cell types. Their pharmacological activation by the selective agonist Yoda1 has been reported to favor skeletal muscle regeneration by controlling the fate...
PIEZO1 are mechanically-activated ion channels expressed in many cell types. Their pharmacological activation by the selective agonist Yoda1 has been reported to favor skeletal muscle regeneration by controlling the fate of myogenic precursors cells, but the underlying mechanisms remain largely unknown. Hereby, we investigated the possibility that PIEZO1 could control the release of small extracellular vesicles in myogenic C2C12 cells. Myoblasts and differentiated myotubes were treated with the PIEZO1 agonist Yoda1 (5 μM) for 24 hours. Released small extracellular vesicles were isolated by ultracentrifugation methods, and characterized by Western blotting, Nano Tracking and proteomic analysis. Pharmacological activation of PIEZO1 showed cell-type-specific effects: In myoblasts, Yoda1 treatment did not significantly affect the size or release of the small extracellular vesicles and resulted in only minor alterations to their proteomic profile. In myotubes Yoda1 treatment significantly increased small extracellular vesicles release and caused subtsantial alterations to the proteomic cargo. Notably, small extracellular vesicles released from both myoblasts and myotubes under PIEZO1 activation promoted myotube formation, though they did so through different capacities. Interestingly, in myotubes, Yoda1 also increased the expression of PIEZO1 protein of the vesicles suggesting a different biogenesis in undifferentiated and differentiated myogenic cells. Here, we propose PIEZO1 as a key element in controlling the release of small extracellular vesicles in myogenic precursors. Given the critical role of small extracellular vesicles in intercellular communication during muscle regeneration, our findings contribute to a better understanding of the role of PIEZO1 in the physiopathology of skeletal muscle tissue.
TMEM16A Contributes to Calcium-Activated Chloride Currents and Membrane Potential Changes in the Mouse Oocyte.
Dalati S, Jones VJ, Day ML
J Cell Physiol · 2026 Mar · PMID 41806302 · Full text
Oscillations in intracellular Ca [Ca] are essential for mouse oocyte activation following fertilization. These [Ca] oscillations also induce repetitive hyperpolarizations in the membrane potential (Em). The present study...
Oscillations in intracellular Ca [Ca] are essential for mouse oocyte activation following fertilization. These [Ca] oscillations also induce repetitive hyperpolarizations in the membrane potential (Em). The present study aimed to identify the channels underlying the Em hyperpolarizations. Sulfhydryl reagents such as thimerosal, that oxidize the IP3-R channel, mimic the physiological changes at fertilization by eliciting simultaneous Em changes and [Ca] oscillations. Thimerosal-induced Em and [Ca] changes were prevented by the non-specific Ca-activated Cl channel (CaCC) inhibitors DIDS and NFA, as well as the TMEM16A/Anoctamin 1 CaCC specific inhibitor, T16Ainh-01. The K channel blocker TEA, and voltage-gated Cl channel blocker 9AC failed to inhibit the Em or [Ca] changes. TMEM16A protein was expressed in all stages of mouse preimplantation development, being localized at the plasma membrane in oocytes. Culture of zygotes in the TMEM16A inhibitor prevented development to the blastocyst stage. In summary, we present the first evidence for CaCC channels, namely TMEM16A, being critical for the initiation of Em hyperpolarisations in mouse oocytes.
Distinct Thromboxane A₂-Dependent Pathways Regulate Arachidonic Acid-Triggered VASP Phosphorylation at Ser239 and Ser157 in Human Platelets: Real-Time Visualization Reveals Superior Antithrombotic Efficacy by Targeting Thromboxane A₂ Signaling over Cyclooxygenase Inhibition.
Sheu JR, Huang WC, Chang CC … +4 more , Hsia CW, Hsia CH, Jayakumar T, Hou SM
J Cell Physiol · 2026 Mar · PMID 41800570 · Full text
Platelets, as anucleate blood cells, play a pivotal role in the pathogenesis of cardiovascular diseases (CVDs), making antiplatelet therapy essential for preventing thrombotic events such as myocardial infarction. Thromb...
Platelets, as anucleate blood cells, play a pivotal role in the pathogenesis of cardiovascular diseases (CVDs), making antiplatelet therapy essential for preventing thrombotic events such as myocardial infarction. Thromboxane A₂ (TXA₂) is a key pro-aggregatory mediator that drives platelet activation. Phosphorylation of vasodilator-stimulated phosphoprotein (VASP) at Ser157 and Ser239 serves as a marker of cyclic nucleotide-mediated inhibitory signaling. The crosstalk between TXA₂ signaling and site-specific VASP phosphorylation in arachidonic acid (AA)-stimulated human platelets remains unclear and requires further investigation. In this study, AA at 60 µM induced maximal platelet activation, as evidenced by ultrastructural changes and increased P-selectin expression. Picotamide, a thromboxane synthase (TXS) inhibitor, effectively reversed AA-induced alterations, including ultrastructural remodeling, P-selectin expression, TXA₂ production, adenosine triphosphate (ATP)-release, mobilization of [Ca²⁺]ᵢ, and integrin αβ activation. Importantly, picotamide's inhibition of platelet aggregation was unaffected by adenylate or guanylate cyclase inhibitors, suggesting a mechanism independent of cyclic nucleotide signaling. AA selectively increased VASP phosphorylation at Ser239, but not Ser157. While picotamide alone had no effect, its sequential administration with AA significantly enhanced Ser157 phosphorylation without altering Ser239 levels. These findings suggest that AA differentially regulates VASP phosphorylation sites via distinct mechanisms: Ser239 via a TXA₂-independent pathway associated with inhibitory signaling, and Ser157 via a TXA₂-dependent pathway linked to platelet activation. Finally, picotamide demonstrated superior antithrombotic efficacy compared to aspirin at an equivalent dose, as evidenced by real-time intravital imaging of thrombotic platelet plug formation in vivo. These results highlight TXS inhibition as a promising strategy for modulating platelet activation and thrombosis.
Extracellular pH and NHE1 Regulate Ductal Branching Morphogenesis in Organotypic Cultures of Human Pancreatic Duct Epithelial Cells.
Molfetta DD, Ardone M, Fracasso F … +8 more , Greco MR, Tamma G, Centrone M, Barile M, Tolomeo M, Nisco A, Reshkin SJ, Cardone RA
J Cell Physiol · 2026 Mar · PMID 41773348 · Full text
Branching morphogenesis is a key process for constructing the tree-like architecture of multiple organs. The mechanisms regulating pancreatic ductal morphogenesis are still poorly understood, especially in the context of...
Branching morphogenesis is a key process for constructing the tree-like architecture of multiple organs. The mechanisms regulating pancreatic ductal morphogenesis are still poorly understood, especially in the context of the particular pH dynamics of this organ. Indeed, ductal cells periodically release an alkaline juice to balance stomach acidity during digestion. This leads to a drop in extracellular pH (pHe) in the extracellular matrix (ECM) to maintain intracellular pH (pHi) homeostasis. Among the transporters involved in pH regulation, NHE1 also regulates epithelial branching morphogenesis in various tissues/organs. However, neither the effect of the changing pHe nor the role of NHE1 in branching morphogenesis has been investigated in a physiomimetic model in the human pancreas. Here, using 3D organotypic cultures of human pancreatic ductal cells (HPDE), we found that cells seeded on a Matrigel rich-ECM resembling normal ECM formed branched duct-like structures, which did not form on a more fibrotic Collagen I-rich ECM. Further, these cells overexpressed NHE1 mainly at the basolateral membrane. Ductal morphogenesis was affected by acidic pHe (pHe 6.7), which determined a hyper-branched network, and this was further increased by the inhibition of NHE1. We conclude that ECM composition and extracellular acidosis modulate branching morphogenesis in pancreatic ductal HPDE cells via NHE1 activity.
Induction of Cellular Senescence by Pesticide Exposure in Human Umbilical Vein Endothelial Cells (HUVECs): Impacts on Telomerase Length, Cellular Morphology, and mtDNA Variation.
Mazzone A, Konstantinidou F, Lamanna D … +10 more , Rocca YD, Gatta V, Marconi GD, Bello DG, Falcone R, Mattioli-Belmonte M, Nanci A, Trubiani O, Diomede F, Pizzicannella J
J Cell Physiol · 2026 Feb · PMID 41749052 · Full text
Chronic exposure to pesticides represents a substantial risk to human health; however, their role in promoting cellular senescence remains poorly understood. It's well known that endothelial dysfunction is an early hallm...
Chronic exposure to pesticides represents a substantial risk to human health; however, their role in promoting cellular senescence remains poorly understood. It's well known that endothelial dysfunction is an early hallmark of aging-related vascular damage. We employed Human Umbilical Vein Endothelial Cells (HUVECs) as an in vitro model for vascular endothelium to investigate whether pesticide exposure accelerates cellular senescence. The pesticides Boscalid (B), Pyraclostrobin (PY), Propamocarb (PR), and Lambda-cyhalothrin (LC) were tested individually and in combination. Following pesticide exposure, we evaluated cell viability through MTS assay, Endothelial Tube Formation by Scanning Electron Microscopy (SEM), alteration in mitochondria through Mitochondrial DNA Copy Number (mtDNA) variation, and TOM20 evaluation, Telomere Length reduction, expression of p21, reduced Ki67, and TERT through Immunofluorescence. Our findings suggest that pesticides accelerate senescence in endothelial cells.
HMGB-1 Mediates The Exacerbation of Anaphylactic Shock Under Hyperlipidemic Conditions.
Liu Z, Ding T, Wan J … +7 more , Fan Z, Yue Z, Pang K, Jin Z, Yang W, Zhang W, Chen H
J Cell Physiol · 2026 Feb · PMID 41738381 · Publisher ↗
Coronary heart disease (CHD) may worsen anaphylactic shock, but the exact mechanism is unknown. This study aimed to investigate the mechanisms by which coronary heart disease exacerbates anaphylaxis.C57BL/6 (WT) mice and...
Coronary heart disease (CHD) may worsen anaphylactic shock, but the exact mechanism is unknown. This study aimed to investigate the mechanisms by which coronary heart disease exacerbates anaphylaxis.C57BL/6 (WT) mice and LDLR mice were fed a high-fat diet for 20 weeks to develop atherosclerosis. Anaphylaxis was then induced using ovalbumin (OVA). Compared to WT mice, LDLR mice showed lower body temperature, worse pulmonary edema and higher mortality. Pulmonary endothelial cell CD31 (PECAM-1) expression decreased, but serum HMGB-1 levels increased. In vitro experiments found that ox-LDL exposure led to more HMGB-1 release from HUVECs. Moreover, ox-LDL induced mast cells release of histamine, upregulating the expression of more H1 receptors (H1R) in HUVECs, thereby further promoting HMGB-1 release. Pretreatment with an H1R inhibitor (chlorpheniramine) or an HMGB-1 neutralizing antibody improved survival and attenuated hypothermia in mice. In summary, ox-LDL exacerbates endothelial cell damage, resulting in increased HMGB-1 release and vascular permeability, which may worsen anaphylaxis to anaphylactic shock. The mechanisms are not fully understood, but HMGB-1 could be a potential target for future alleviation of anaphylactic shock.
Acetyl-CoA Homeostasis via Mitochondrial Pyruvate Oxidation Governs Survival, Transcriptional Fidelity and Neural Specification in Primed Human Embryonic Stem Cells.
Zhong N, Liu Y, Shao M … +7 more , Zhao H, Wang Y, Gu J, Chen Q, Yin H, Jin Y, Liao B
J Cell Physiol · 2026 Feb · PMID 41705723 · Publisher ↗
Human embryonic stem cells (hESCs) hold immense promises for regenerative medicine and exhibit two distinct pluripotency states: primed and naïve. However, metabolic regulation underlying these states remains incompletel...
Human embryonic stem cells (hESCs) hold immense promises for regenerative medicine and exhibit two distinct pluripotency states: primed and naïve. However, metabolic regulation underlying these states remains incompletely understood. In particular, mitochondrial pyruvate oxidation in pluripotency regulation has not been documented. Here, we combined an inducible dihydrolipoamide S-acetyltransferase (DLAT) knockout model and pharmacological inhibition of mitochondrial pyruvate uptake (via the mitochondrial pyruvate carrier inhibitor UK5099) to dissect the state-specific effects of mitochondrial pyruvate oxidation in isogenic naïve and primed hESCs. Primed hESCs lacking DLAT or treated with UK5099 displayed pronounced cell death, reduced global protein acetylation levels, and transcriptional dysregulation. These defects were partially rescued by sodium acetate supplementation, implicating a reduction in acetyl-CoA abundance as a key mechanism. Notably, a set of neural lineage genes was specifically downregulated by disrupted mitochondrial pyruvate oxidation in primed hESCs, revealing the importance of mitochondrial pyruvate oxidation-mediated acetyl-CoA production in priming neural differentiation. In line with this, disruption of mitochondrial pyruvate oxidation impaired the differentiation process of primed hESCs towards neuroectoderm. In contrast, DLAT depletion in naïve hESCs did not affect cell growth and the naïve pluripotency state, highlighting the pluripotency state-dependent function of mitochondrial pyruvate oxidation. Our study uncovers the pivotal roles of mitochondrial pyruvate oxidation-mediated acetyl-CoA production for sustaining survival and transcriptional fidelity as well as facilitating neural differentiation in primed hESCs. Moreover, we emphasize that the function of mitochondrial pyruvate oxidation in hESCs is pluripotency state-dependent. These findings provide new cues for optimizing hESC maintenance and differentiation through targeted metabolic manipulation.
Epigenetic Silencing of Primary Cilia Genes by PRAME and ETS2 in Melanoma Cells.
Heo HH, Youn H, Moon EY … +1 more , Um SJ
J Cell Physiol · 2026 Feb · PMID 41700497 · Publisher ↗
Primary cilia are sensory organelles that regulate key signaling pathways essential for cell growth and differentiation. Loss of primary cilia is a common feature of melanoma and contributes to tumor progression, yet the...
Primary cilia are sensory organelles that regulate key signaling pathways essential for cell growth and differentiation. Loss of primary cilia is a common feature of melanoma and contributes to tumor progression, yet the underlying regulatory mechanisms remain poorly understood. In this study, we identify a transcriptional repression mechanism involving Preferentially Expressed Antigen in Melanoma (PRAME) and the transcription factor ETS2 as key modulators of ciliogenesis. We demonstrate an inverse correlation between PRAME expression and primary cilia formation in melanoma cells (R = -0.83, p = 0.042), and show that PRAME knockdown significantly promotes ciliogenesis, underscoring its role as a negative regulator. Integrative analyses combining our RNA-seq data with publicly available ChIP-seq data (GSE26439) and promoter motif analysis revealed that both PRAME and ETS2 are recruited to shared promoter regions of intraflagellar transport (IFT) genes, which are essential for cilia assembly. Notably, PRAME specifically interacts with ETS2, but not ETS1, indicating a selective and functionally relevant interaction. Similar to PRAME, ETS2 overexpression suppresses ciliogenesis and downregulates IFT gene expression. Mechanistically, the PRAME-ETS2 complex recruits histone deacetylase 1 (HDAC1) to IFT gene promoters, leading to epigenetic silencing via histone deacetylation. Together, these findings suggest that PRAME and ETS2 cooperatively suppress ciliogenesis in melanoma cells, proposing a previously unrecognized epigenetic mechanism of ciliary loss. This mechanism broadens our understanding of melanoma progression and highlights the role of the PRAME-ETS2-HDAC1 axis in regulating ciliogenesis.
The Functions and Mechanisms of TGF-β3 Signalling in Controlling the Fate Determinations of Various Types of Stem Cells.
Kuang L, Xiang J, He Z
J Cell Physiol · 2026 Feb · PMID 41700496 · Publisher ↗
The fate determinations of stem cells are governed by signalling molecules and pathways, and notably, the TGF-β superfamily members play pivotal roles in mediating these decisions. Significantly, TGF-β3 participates in a...
The fate determinations of stem cells are governed by signalling molecules and pathways, and notably, the TGF-β superfamily members play pivotal roles in mediating these decisions. Significantly, TGF-β3 participates in affecting the development of stem cells and their microenvironment. In this review, we address the functions and regulatory networks of TGF-β3 in the fate decisions of several types of stem cells, including neural stem cells, haematopoietic stem cells, odontogenic stem cells, hair-follicle stem cells, adipose-derived stem cells, and mesenchymal stem cells. Specifically, we discuss the biosynthesis, activation, the roles, and mechanisms of TGF-β in influencing the proliferation, differentiation, and cell death of these stem cells, and we further highlight the perspective in this field. TGF-β signalling in stem cells begins with the activation of either integrin-dependent or integrin-independent pathways by binding to cell surface receptors TbRII and TbRI and co-receptor Betaglycan (TR3). TGF-β acts via both classical Smad signalling pathways and a variety of non-classical pathways. Notably, the biological functions of TGF-β3 depend primarily on specific cell type and the existing conditions of stem cells, reflecting the integration of multiple factors including the concentration, duration of action, interactions with other genes and/or non-coding RNAs. This review provides in-depth analyses of the molecular mechanisms through which TGF-β3 affects the fate decisions of adult stem cells, which lays a basis for identifying potential targets and developing future interventions for treating human diseases.
Correction to "Blocking Sphingosine 1-phosphate Metabolism With Fingolimod Prevents the Progression of Vascular Smooth Muscle Cells Calcification in Chronic Kidney Disease".
J Cell Physiol · 2026 Feb · PMID 41661693 · Full text
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Calpain-1 and Cholesterol Regulate the Dynamics of the Lipid Membrane Domains Essential for Suitable Capacitation and Acrosomal Reactions.
Muñoz-Sánchez AA, Salgado-Lucio ML, Jorge-Cruz CY … +3 more , Roa-Espitia AL, Baltiérrez-Hoyos R, Hernández-González EO
J Cell Physiol · 2026 Feb · PMID 41661664 · Publisher ↗
Calpain-1 and -2 are calcium-dependent cysteine proteases associated with sperm processes, such as capacitation, the acrosomal reaction, and motility, making them important for the acquisition of fertilizing capacity amo...
Calpain-1 and -2 are calcium-dependent cysteine proteases associated with sperm processes, such as capacitation, the acrosomal reaction, and motility, making them important for the acquisition of fertilizing capacity among spermatozoa. Moreover, their inhibition significantly reduces in vitro fertilization. Guinea pig spermatozoa express only calpain-1, which has been implicated in spectrin cytoskeletal remodeling and NOX2 and NOX4 activation during capacitation. However, little is known about the mechanisms by which calpains participate in capacitation and the acrosomal reaction. The interaction of spectrin with phospholipids maintains the asymmetry of the plasma membrane. Since spectrin is a significant target of calpain, calpain may be involved in the dynamics of phospholipids and other membrane lipids during the capacitation process. Therefore, this work aims to elucidate the role of calpain in capacitation and acrosomal reactions, as well as its relationship with the dynamics of different membrane lipids related to capacitation and the acrosomal reaction. The results show that calpain-1 inhibition by calpeptin significantly reduced the number of spermatozoa that underwent capacitation and acrosomal reactions. Inhibition of calpain-1 also blocked protein phosphorylation at Tyr, as well as calcium influx and actin polymerization, which required for successful capacitation. Calpain inhibition also prevented phosphatidylserine translocation and the dynamics of caveolin-1, both processes associated with capacitation and the acrosome reaction. Sperm capacitation in the presence of cholesterol prevented the dynamics of phosphatidylserine, GM1 and caveolin-1. However, calpain-1 inhibition did not prevent cholesterol or GM1 ganglioside dynamics. The results of this investigation provide strong evidence for the mechanisms by which calpain-1 regulates capacitation and the acrosome reaction in guinea pig spermatozoa, suggesting that calpain-1 is a key player in optimal capacitation and the acrosome reaction.
RETRACTION: CircFUT10 Reduces Proliferation and Facilitates Differentiation of Myoblasts by Sponging miR-133a.
J Cell Physiol · 2026 Feb · PMID 41661660 · Publisher ↗
H. Li, J. Yang, X. Wei, C. Song, D. Dong, Y. Huang, X. Lan, M. Plath, C. Lei, Y. Ma, X. Qi, Y. Bai, and H. Chen, "CircFUT10 Reduces Proliferation and Facilitates Differentiation of Myoblasts by Sponging miR-133a," Journa...
H. Li, J. Yang, X. Wei, C. Song, D. Dong, Y. Huang, X. Lan, M. Plath, C. Lei, Y. Ma, X. Qi, Y. Bai, and H. Chen, "CircFUT10 Reduces Proliferation and Facilitates Differentiation of Myoblasts by Sponging miR-133a," Journal of Cellular Physiology 233, no. 6 (2018): 4643-4651, https://doi.org/10.1002/jcp.26230. The above article, published online on 18 October 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed upon following concerns raised by a third party regarding data presented in the article. An investigation identified duplication between the two MyoD bands shown in Figure 3B and two MyhC bands in Figure 3H. All MyhC bands in Figure 3H were also found to be identical to western blot bands published in another article by the same authors, where they were presented as representing a different protein. Furthermore, overlaps were identified between images in Figure 6 A and images published in another article by the same authors, which were also used to represent different material. Finally, the miR-133a flow cytometry data shown in Figure 6B was also found to be identical to a dot plot found in another article published by the same authors, again representing different material. The authors cooperated with the investigation and provided some supporting data; however, this was not sufficient to restore the editors' confidence in the results. The editors consider the results and conclusions unreliable. The authors did not respond when asked to agree to the final wording of the retraction.
Dose-Dependent Biphasic Effect of Palmitic Acid on Oligodendrocyte Function: Impacts on Viability, Differentiation, and Myelination.
Palmiero A, Pipicelli L, Rosa G … +10 more , Sozio C, Punziano C, Raia M, Faraonio R, Vitolo G, Cammarota M, Boscia F, Menale C, Santillo M, Damiano S
J Cell Physiol · 2026 Feb · PMID 41661646 · Full text
Palmitic acid (PA), the most abundant saturated fatty acid (SFA) in humans, plays a key role in energy metabolism, membrane synthesis, and signaling. Oligodendrocyte precursor cells (OPCs), which generate mature oligoden...
Palmitic acid (PA), the most abundant saturated fatty acid (SFA) in humans, plays a key role in energy metabolism, membrane synthesis, and signaling. Oligodendrocyte precursor cells (OPCs), which generate mature oligodendrocytes (OLs) forming the myelin sheath, are responsive to metabolic and redox signals. Despite increasing interest in lipid metabolism and mitochondrial dynamics as regulators of OPC fate, the effects of PA remain unclear. This study investigates the biphasic, dose-dependent effects of PA on OPCs using the oligodendrocyte precursor MO3.13 cell line and employs rat organotypic slice cultures to evaluate the effects of non-toxic PA doses under pathological conditions and on axonal (re)-myelination. In MO3.13 cells, high-dose PA (100 µM) induces mitochondrial fragmentation and caspase-7 activation, accompanied by reduced mitofusin-2 (MFN2) and phosphorylated dynamin-related protein 1 at Ser616 (p-DRP1), indicating altered fusion-fission balance and impaired reactive oxygen species (ROS) generation. In contrast, low-dose PA (25 µM) triggers a protective response involving nuclear factor erythroid 2-related factor 2 (Nrf2) activation and upregulation of antioxidant and lipid-regulatory genes (glutamate-cysteine ligase modifier subunit [GCLM], NAD(P)H dehydrogenase [quinone] 1 [NQO1], peroxisome proliferator-activated receptor gamma [PPARγ], and cluster of differentiation 36 [CD36]) resulting in reduced intracellular ROS and enhanced lipid mobilization. PA 25 µM promotes OPC differentiation by inhibiting migration and cell cycle progression and increasing myelin basic protein (MBP) and proteolipid protein (PLP) expression. Notably, early exposure (1 day) favors mitochondrial fusion, whereas prolonged exposure (4 days) shows a physiological shift to fission. PA 25 µM prevents neurodegeneration in hippocampal organotypic slice cultures exposed to a neuroinflammatory insult. In cerebellar organotypic slice cultures, PA 25 µM enhances axonal myelination and accelerates remyelination following lysolecithin-induced demyelination. These findings highlight the physiological relevance of low-dose PA in modulating OLs.
Correction to "PCTR1 Improves Pulmonary Edema Fluid Clearance Through Activating the Sodium Channel and Lymphatic Drainage in Lipopolysaccharide-Induced ARDS".
J Cell Physiol · 2026 Feb · PMID 41661645 · Publisher ↗
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RETRACTION: Epigallocatechin Gallate in Combination With Eugenol or Amarogentin Shows Synergistic Chemotherapeutic Potential in Cervical Cancer Cell Line.
J Cell Physiol · 2026 Feb · PMID 41655042 · Publisher ↗
D. Pal, S. Sur, R. Roy, S. Mandal, and C. Kumar Panda, "Epigallocatechin Gallate in Combination With Eugenol or Amarogentin Shows Synergistic Chemotherapeutic Potential in Cervical Cancer Cell Line," Journal of Cellular...
D. Pal, S. Sur, R. Roy, S. Mandal, and C. Kumar Panda, "Epigallocatechin Gallate in Combination With Eugenol or Amarogentin Shows Synergistic Chemotherapeutic Potential in Cervical Cancer Cell Line," Journal of Cellular Physiology 234, no. 1 (2019): 825-836, https://doi.org/10.1002/jcp.26900. The above article, published online on 4 August 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Figures 3A and 7B were found to contain duplicated image elements that were presented in different scientific contexts. Due to the time elapsed since publication, the authors were unable to retrieve the raw data underlying the article, and the clarification they provided was insufficient to address the concerns. Accordingly, the article has been retracted, as the editors have lost confidence in the accuracy and the integrity of the whole body of data presented. The authors have been informed of the retraction decision and disagree with it.
Calcium Signaling Pathways in Head and Neck Squamous Cell Carcinoma Therapy: A Review.
Yu Q, Jiang X
J Cell Physiol · 2026 Jan · PMID 41574451 · Publisher ↗
Calcium ion (Ca) is a crucial secondary messenger in cells and participates in multiple physiological activities, during which various calcium regulatory proteins regulate the Ca homeostasis. It has been verified that ca...
Calcium ion (Ca) is a crucial secondary messenger in cells and participates in multiple physiological activities, during which various calcium regulatory proteins regulate the Ca homeostasis. It has been verified that calcium signaling differs significantly between tumor and normal cells. Additionally, the heterogeneity in calcium signaling is found across head and neck squamous cell carcinoma (HNSCC) with different pathological subtypes and infection status of human papillomavirus. The abnormality of calcium signaling is related to the initiation, progression, therapeutic response, and clinical prognosis of HNSCC. Moreover, the calcium signaling plays a vital role in regulating the tumor microenvironment, which is closely related to the tumor cell and shares constant interaction with it, by metabolic reprogramming and immunosuppressive effects. Understanding the changes in calcium signaling may provide a potential target for the treatment of HNSCC.
MeHg-Induced Cytotoxicity Associated With Oxidative Stress and Early Calcium Mobility in Rat Cerebral Cortical Astrocytes.
Chen YT, Chen SH, Chen YJ … +6 more , Yao CJ, Bao BY, Saputra F, Tran NT, Chiu CC, Lin-Shiau SY
J Cell Physiol · 2026 Jan · PMID 41572590 · Publisher ↗
Methylmercury (MeHg) is a potent neurotoxin that can cross the blood-brain barrier and disrupt neurological function in animals. Emerging evidence suggests that MeHg neurotoxicity may originate from compromised astrocyte...
Methylmercury (MeHg) is a potent neurotoxin that can cross the blood-brain barrier and disrupt neurological function in animals. Emerging evidence suggests that MeHg neurotoxicity may originate from compromised astrocytes, as they are strategically positioned to metabolize and process substances that enter the central nervous system. Thus, a better characterization of the timely cellular responses of astrocytes upon MeHg exposure is key to delineating the toxicology of MeHg. Here, MeHg exposure caused a transient increase in reactive oxygen species (ROS) and intracellular calcium concentration ([Ca²⁺]i), which peaked within 3 h and 30 min, respectively, in astrocytes. Further analyses indicated that the increase in [Ca²⁺]i after MeHg exposure might involve both extracellular Ca²⁺ influx and Ca²⁺ release from intracellular stores, as evidenced by alteration of Ca²⁺ dynamics in cells by targeting specific Ca²⁺ channels with blockers. Further cytotoxicity analyses revealed that antagonizing Ca²⁺-dependent signaling pathways and ROS levels markedly protected astrocytes against MeHg-induced cell death. Treatment with lipopolysaccharide improved cell survival under MeHg exposure, suggesting a reciprocal interaction of proinflammatory signaling and MeHg on [Ca²⁺]i kinetics and nitric oxide production. Collectively, our findings indicated that transient alterations in free radical and Ca²⁺ levels in astrocytes may be associated with MeHg-induced cytotoxicity. Targeting oxidative stress and Ca²⁺ signaling in astrocytes may provide potential strategies for mitigating MeHg-induced neurotoxicity.
Pathological Degeneration of Disc and Bone Is Associated With Chronic Low Back Pain in a Rat Model With Intradiscal Monosodium Iodoacetate.
Cho YH, Choi C, Kwon M … +6 more , Kwon J, Ok H, Ryu D, Yang KS, Kim J, Park EH
J Cell Physiol · 2026 Jan · PMID 41572557 · Publisher ↗
This study aimed to determine whether degeneration of intervertebral discs and subchondral bone correlates with the development of persistent low back pain (LBP) in a rat model with intradiscal monosodium iodoacetate (MI...
This study aimed to determine whether degeneration of intervertebral discs and subchondral bone correlates with the development of persistent low back pain (LBP) in a rat model with intradiscal monosodium iodoacetate (MIA), focusing on structural alterations, neuronal sensitization, and pain-related behavior. Male Sprague Dawley rats received MIA injections (2 mg in 2 μl) into L4/5 and L5/6 lumbar discs to induce degeneration. LBP-related behaviors were assessed over 42 days via dynamic weight-bearing and hindpaw withdrawal thresholds. Neuronal sensitization was evaluated via electrophysiological recordings of mechanosensitive afferent nerves (MSAN) and calcium imaging of labeled dorsal root ganglia (DRG) neurons innervating discs. Structural alterations in subchondral bone and disc were analyzed using in vivo/ex vivo µCT imaging, along with immunohistochemistry for TRPV1 and CGRP expression. Intradiscal MIA induced long-term LBP behaviors, characterized by forelimb weight-bearing shifts and reduced hindpaw withdrawal thresholds. MSAN exhibited hyperexcitability and lowered firing thresholds to intradiscal pressure, while DRG neurons showed enhanced TRPV1- and TRPA1-mediated calcium influx. µCT imaging revealed decreased disc volume and deteriorated trabecular bone quality. Histology confirmed disc and subchondral bone degeneration, with upregulated TRPV1 and CGRP expression in subchondral bone, indicating nociceptive fiber ingrowth. Linear discriminant analysis identified weight-bearing asymmetry (HindFore AUC), trabecular thickness, connectivity, and trabecular pattern factor as strong predictors of LBP development. Pathological degeneration of disc and bone is associated with chronic LBP through structural remodeling and peripheral neuronal sensitization. These findings suggest that therapeutic strategies targeting both tissues can alleviate chronic pain in degenerative spine conditions.
Endoglin Regulates Pluripotency and Differentiation in Human Embryonic Stem Cells Through Wnt and TGF-β Signaling Crosstalk.
Kim MT, Kang M, Jeong S … +6 more , Koh H, Zhen X, Lee SJ, Kim DY, Hong SH, Lee JH
J Cell Physiol · 2026 Jan · PMID 41568654 · Publisher ↗
Although endoglin (ENG) is traditionally recognized as a coreceptor in TGF-β signaling, its role in human pluripotent stem cells (hPSCs) remains unexplored. Here, we report that ENG knockout (ENG) hPSCs maintain core plu...
Although endoglin (ENG) is traditionally recognized as a coreceptor in TGF-β signaling, its role in human pluripotent stem cells (hPSCs) remains unexplored. Here, we report that ENG knockout (ENG) hPSCs maintain core pluripotency markers yet undergo spontaneous differentiation and exhibit markedly reduced potential to form mesoderm, ectoderm, and endoderm lineages. Contrary to expectations, pharmacological inhibition of TGF-β signaling failed to replicate or rescue this phenotype, implicating pathways beyond TGF-β in governing the ENG phenotype. Instead, we observed aberrant WNT activation in ENG cells, which correlated with the emergence of peripherally localized differentiated cells and compromised multilineage commitment. Notably, blocking WNT secretion with IWP2 suppressed spontaneous peripheral differentiated cell formation and partially restored ectodermal and endodermal differentiation. These findings establish a novel regulatory role for ENG in balancing WNT signaling, to preserve hPSCs' developmental potential, thereby illuminating an unrecognized mechanism of stem cell fate control and revealing ENG as a critical mediator of hPSCs' self-renewal and lineage fidelity.
SPINK3-Sperm Interaction Determines a Stable Sperm Subpopulation With Intact CatSper Channel.
Nicolli AR, Huang X, Zalazar L … +8 more , Stival C, Gomez-Olivieri LR, Demare G, Romarowski A, Buffone MG, Krapf D, Chung JJ, Cesari A
J Cell Physiol · 2026 Jan · PMID 41568585 · Full text
Sperm capacitation involves proteolytic remodeling of membrane proteins, including components of the CatSper calcium channel, which is essential for hyperactivation and male fertility. Here, we identify the seminal prote...
Sperm capacitation involves proteolytic remodeling of membrane proteins, including components of the CatSper calcium channel, which is essential for hyperactivation and male fertility. Here, we identify the seminal protease inhibitor SPINK3, a known decapacitation factor that suppresses premature capacitation in the female tract, as the first physiological inhibitor of CATSPER1 processing. In mouse sperm, SPINK3 blocks capacitation-induced CATSPER1 cleavage, preserving a subpopulation with intact CatSper channels and lacking pTyr development in the flagellum. SPINK3 localizes to the outer surface of the sperm principal piece membrane in a CatSper-dependent but non-quadrilateral pattern, stabilizes membrane organization, and delays cholesterol efflux. These results reveal SPINK3 as a multifunctional regulator of capacitation, shaping sperm subpopulations in the female reproductive tract.
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