Journal of Cellular Physiology最新文献_第5页

Dysregulation of Non-Muscle Myosin IIA Assembly and Phosphorylation in S100A4 Null Mouse Lens S100A4小鼠晶状体非肌球蛋白IIA组装和磷酸化失调。

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-06-18 DOI: 10.1002/jcp.70202

Rupalatha Maddala, Levi K. Lankford, Nikolai P. Skiba, Ponugoti V. Rao

{"title":"Dysregulation of Non-Muscle Myosin IIA Assembly and Phosphorylation in S100A4 Null Mouse Lens","authors":"Rupalatha Maddala, Levi K. Lankford, Nikolai P. Skiba, Ponugoti V. Rao","doi":"10.1002/jcp.70202","DOIUrl":"10.1002/jcp.70202","url":null,"abstract":"Non-muscle myosin IIA (NMIIA), a motor protein plays a critical role in regulating cell morphology, adhesion, migration, contractility, and mechanotransduction across various tissues, including the ocular lens. S100A4, a known NMIIA-interacting protein, is abundantly expressed and exhibits a discrete spatial distribution in lens fibers. Loss of S100A4 has previously been shown to associate with late-onset lens opacification in mice. However, its role in regulating NMIIA activity, assembly, and actin cytoskeletal organization in the lens remains unclear. Using S100A4-null mice, this study reveals that S100A4 co-immunoprecipitates with NMIIA and that its absence leads to decreased NMIIA (Ser1943) phosphorylation, impaired NMIIA filament assembly, and disruption in actin cytoskeletal organization and polymerization in the lens. Quantitative proteomic analysis further identified decreased levels of CLIC5 and RNA binding protein-SERBP1 in cytoskeletal- and membrane-enriched fractions from S100A4-null versus wild-type lenses. Moreover, treatment of wild-type mouse lenses in ex-vivo with trifluoperazine, a known S100A4 inhibitor, induced lens opacification in association with increased insolubilization of S100A4, NMIIA and actin. Collectively, these findings demonstrate that S100A4 plays a critical role in regulating NMIIA activity and assembly, and maintaining actin cytoskeletal organization in the ocular lens, thereby contributing to lens transparency and homeostasis.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 6","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70202","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148271784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to “A Probiotic Combination of Limosilactobacillus reuteri and Clostridium butyricum Ameliorates 5-Fluorouracil-Induced Intestinal Mucositis in Rats by Strengthening Barrier Integrity and Modulating Immuno-Microbial Homeostasis” “罗伊氏乳酸杆菌和丁酸梭菌的益生菌组合通过加强屏障完整性和调节免疫微生物稳态来改善5-氟尿嘧啶诱导的大鼠肠道黏膜炎”的更正。

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-06-15 DOI: 10.1002/jcp.70200

Chu-Chyn Ou

{"title":"Corrigendum to “A Probiotic Combination of Limosilactobacillus reuteri and Clostridium butyricum Ameliorates 5-Fluorouracil-Induced Intestinal Mucositis in Rats by Strengthening Barrier Integrity and Modulating Immuno-Microbial Homeostasis”","authors":"Chu-Chyn Ou","doi":"10.1002/jcp.70200","DOIUrl":"10.1002/jcp.70200","url":null,"abstract":"Leong, P. Y., W. C. Chuang, J. L. Ko, et al. 2026. “A Probiotic Combination of Limosilactobacillus reuteri and Clostridium butyricum Ameliorates 5-Fluorouracil-Induced Intestinal Mucositis in Rats by Strengthening Barrier Integrity and Modulating Immuno-Microbial Homeostasis.” Journal of Cellular Physiology 241, no. 5: e70183. doi/10.1002/jcp.70183In Section 2.3 (Probiotic Strain and Mixture Preparation) of the Materials and Methods section, the description of Clostridium butyricum MIYAIRI 588 was incomplete.The text:C. butyricum MIYAIRI 588 (CBM588), originally isolated from a soil sample in Japan in 1963 and developed as a pharmaceutical-grade probiotic (Isa et al. 2016), was purchased as a lyophilized powder from Miyarisan Pharmaceutical Co. (Nagano, Japan) via Asia Bio-Med Management Limited (Taichung, Taiwan).Should have read:C. butyricum MIYAIRI 588 (CBM588), originally isolated from a soil sample in Japan in 1963 and developed as a pharmaceutical-grade probiotic (Isa et al. 2016), was obtained in the form of Miyarisan BM (manufactured by Miyarisan Pharmaceutical Co., Ltd., Tokyo, Japan).In addition, the text:In contrast, C. butyricum MIYAIRI 588 was reconstituted directly from the pharmaceutical-grade lyophilized powder in PBS (pH 7.2) without prior subculturing.Should have read:In contrast, C. butyricum MIYAIRI 588 was prepared directly from the commercial finished product in PBS (pH 7.2) without prior subculturing.We apologize for this error.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 6","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70200","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148251684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sexually Dimorphic Regulation of MiR-29a/c-3p in Human Endothelial Cells: Cell Functions and Transcriptome 人内皮细胞中MiR-29a/c-3p的两性二态调节：细胞功能和转录组。

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-06-14 DOI: 10.1002/jcp.70199

Si-yan Zhang, Colman I. Freel, Chi Zhou, Jing Zheng

{"title":"Sexually Dimorphic Regulation of MiR-29a/c-3p in Human Endothelial Cells: Cell Functions and Transcriptome","authors":"Si-yan Zhang, Colman I. Freel, Chi Zhou, Jing Zheng","doi":"10.1002/jcp.70199","DOIUrl":"10.1002/jcp.70199","url":null,"abstract":"Preeclampsia (PE) is a major cause of maternal and fetal morbidity and mortality during pregnancy. PE is characterized by widespread endothelial dysfunction in mothers and fetuses. The etiology of PE remains elusive, but the dysregulation of microRNAs (miRNAs) in endothelial cells may contribute to the pathogenesis of PE. We have reported that PE downregulates expression of two miRNAs, miR-29a-3p and miR-29c-3p (miR-29a/c-3p), and knockdown of miR-29a/c-3p impairs functions of human umbilical vein endothelial cells (HUVECs). Herein, we tested the hypothesis that knockdown of miR-29a/c-3p sex-specifically impairs cellular responses to vascular endothelial growth factor-A (VEGFA) and fibroblast growth factor 2 (FGF2) via disrupting the transcriptome in HUVECs. MiR-29a/c-3p were knocked down using miR-29c-3p inhibitors in male and female HUVECs. Chemotactic and proliferative responses to VEGFA and FGF2 were assessed. RNA-seq was performed to identify miR-29a/c-3p regulated genes and pathways. Knockdown analysis demonstrated that miR-29c-3p inhibitors decreased miR-29a/c-3p levels by over 95% in male and female HUVECs. Functionally, miR-29c-3p inhibitors suppressed VEGFA-, but not FGF2-stimulated chemotaxis by 26% in male, but not female HUVECs. RNA-seq revealed that miR-29a/c-3p inhibitors dysregulated 47 and 118 genes in male and female HUVECs, respectively. Bioinformatics analyses showed that miR-29a/c-3p-regulated genes were differently associated with hypertension, heart, angiogenesis, and immunology in male and female HUVECs. These data demonstrate that knockdown of miR-29a/c-3p sex-specifically affects cellular responses to VEGFA and FGF2 in HUVECs, possibly via disrupting the transcriptome and relevant pathways. These miR-29a/c-3p-regulated genes might represent promising sex-specific therapeutic targets for PE-associated endothelial dysfunction pending further in vivo and clinical verification.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 6","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70199","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148251712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immune Evasion in Ovarian Cancer Peritoneal Metastasis: Mechanisms and Biomarker-Guided Therapeutic Matching 卵巢癌腹膜转移的免疫逃避：机制和生物标志物引导的治疗匹配

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-06-07 DOI: 10.1002/jcp.70197

Xiaodong Wang, Junjie Wang, Di Xiong, Songli Cui, Qianqian Wang, Yiping Huang, Gouping Ding, Yixuan Tang, Yeqian Feng

{"title":"Immune Evasion in Ovarian Cancer Peritoneal Metastasis: Mechanisms and Biomarker-Guided Therapeutic Matching","authors":"Xiaodong Wang, Junjie Wang, Di Xiong, Songli Cui, Qianqian Wang, Yiping Huang, Gouping Ding, Yixuan Tang, Yeqian Feng","doi":"10.1002/jcp.70197","DOIUrl":"https://doi.org/10.1002/jcp.70197","url":null,"abstract":"Ovarian cancer peritoneal metastasis remains a major cause of recurrence and death despite advances in cytoreductive surgery, platinum-based chemotherapy, PARP inhibition, and immune checkpoint blockade. The limited activity of immunotherapy in this setting reflects layered immune resistance shaped by impaired antigen visibility, redundant inhibitory receptor networks, suppressive myeloid and regulatory circuits, and metabolic-epigenetic constraints within ascites and multicellular spheroids. These compartment-specific features distinguish peritoneal disease from anatomically confined tumors and help explain why systemic immune reinvigoration alone rarely produces durable benefit. Here, we synthesize current evidence on the mechanisms that govern immune escape in ovarian cancer peritoneal dissemination, with emphasis on antigen presentation defects, checkpoint-driven T-cell exhaustion, anti-phagocytic signaling, soluble suppressive mediators, and metabolic remodeling of the ascites microenvironment. We further examine how DNA damage response states intersect with innate immune sensing and discuss the translational implications of homologous recombination deficiency for combination treatment design. Finally, we propose a biomarker-guided framework that links antigen-presentation competence, immune engagement, dominant suppressive axes, and ascites-specific biology to rational therapeutic matching. This mechanism-centered view supports more precise trial design and provides a roadmap for combination immunotherapy in advanced ovarian cancer.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 6","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70197","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148194129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IF 4 2区生物学

Journal of Cellular Physiology Pub Date : 2026-05-28