Journal of Cellular Physiology最新文献

{"title":"The Role of Transient Receptor Potential Canonical 3 (TRPC3) in Wound Healing","authors":"Rima Patel,&nbsp;Lily Waltz,&nbsp;Gemma Toogood,&nbsp;Wei Li,&nbsp;Junwang Xu","doi":"10.1002/jcp.70065","DOIUrl":"https://doi.org/10.1002/jcp.70065","url":null,"abstract":"<div>\u0000 \u0000 <p>Wound healing is a complex, highly orchestrated process involving distinct yet overlapping phases: hemostasis, inflammation, proliferation, and remodeling. Effective healing requires precise cellular and molecular interactions across these phases, with calcium signaling playing a pivotal role in modulating cellular responses such as migration, proliferation, and differentiation. Among the calcium channels involved, the Transient Receptor Potential Canonical (TRPC) family, particularly TRPC3, emerged as a key modulator of wound repair processes. In this review, we explore the dynamic contributions of TRPC3 to each phase of wound healing, highlighting its regulation of calcium fluxes and the downstream cellular responses critical for effective tissue repair. We will further discuss the altered role of TRPC3 in pathological conditions, such as chronic wounds and diabetic ulcers, where aberrant TRPC3 signaling disrupts normal wound healing, contributing to impaired resolution and fibrosis. By summarizing findings from recent studies, we underscore the potential of targeting TRPC3 as a therapeutic strategy to restore normal wound healing. Finally, we will discuss future directions in TRPC3-targeted interventions, including the development of selective modulators and the use of TRPC3-targeting therapy, to address unmet needs in wound care. This review aims to provide a comprehensive overview of TRPC3's multifaceted role in wound repair and its therapeutic potential in regenerative medicine.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Notum as a Crucial Regulator of Matrix Integrity in Dentinogenesis","authors":"Hwajung Choi,&nbsp;Ju-Kyung Jeong,&nbsp;Dinuka Adasooriya,&nbsp;Sung-Won Cho,&nbsp;Eui-Sic Cho","doi":"10.1002/jcp.70070","DOIUrl":"https://doi.org/10.1002/jcp.70070","url":null,"abstract":"<p>Dentinogenesis, the formation of dentin, requires precise coordination of cellular differentiation, extracellular matrix synthesis, and signaling regulation. Here, we elucidate the role of Notum, a secreted Wnt inhibitor, in orchestrating these processes during dentin formation. In <i>Notum</i>^{<i>−/−</i>} mice, dentin exhibited a thicker yet dysplastic structure with disrupted tubule organization and impaired mineralization, deviating from the functional architecture of healthy dentin. Loss of <i>Notum</i> led to excessive activation of Wnt/β-catenin signaling within the dentin-pulp complex and enhanced expression of odontogenic genes, including <i>dentin sialophosphoprotein</i> (<i>Dspp</i>), and <i>dentin matrix protein 1</i> (<i>Dmp1</i>). However, this upregulation was uncoupled from proper extracellular matrix composition and mineralization, indicating that initial odontoblast differentiation alone is insufficient for functional dentin formation. At the molecular level, <i>Notum</i> deficiency disrupted matrix integrity, characterized by reduced collagen organization and increased expression of non-collagenous matrix proteins such as bone sialoprotein (Bsp). Collectively, these findings highlight Notum as a critical modulator that fine-tunes Wnt/β-catenin signaling to coordinate cellular differentiation with matrix organization during dentinogenesis. Therapeutic targeting Notum may offer new strategies for restoring dentin integrity and enhancing regenerative outcomes.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666346","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}

{"title":"Correction to “Proteasome Subunit LMP2 Is Required for Matrix Metalloproteinase-2 and -9 Expression and Activities in Human Invasive Extravillous Trophoblast Cell Line”","authors":"","doi":"10.1002/jcp.70058","DOIUrl":"https://doi.org/10.1002/jcp.70058","url":null,"abstract":"<p>Wang HX, Wang HM, Lin HY, Yang Q, Zhang H, Tsang BK, Zhu C. <i>J. Cell. Physiol</i>. 2006; 206: 616–623 DOI: 10.1002/jcp.20508</p><p>We apologize for the errors. The new Figure 4 is shown below. These corrections do not affect the overall conclusions of the paper.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70058","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666607","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}

{"title":"ATP Mediates Pyroptosis in the Intestinal Mucosal System During Colitis","authors":"Sihyun Jeong,&nbsp;Soyeong Park,&nbsp;Doyeon Lee,&nbsp;Gwangbeom Heo,&nbsp;Yunna Lee,&nbsp;Sang Hoon Rhee,&nbsp;Eunok Im","doi":"10.1002/jcp.70071","DOIUrl":"https://doi.org/10.1002/jcp.70071","url":null,"abstract":"<p>Damage-associated molecular patterns (DAMPs) are molecules released from damaged or dying cells that contribute to inflammation and cell death. Extracellular ATP, a type of DAMP, has been studied primarily in the context of pyroptosis in monocytes. This study aimed to investigate the role of ATP as a DAMP in mediating pyroptosis within the intestinal mucosal system. Colitis was induced in mice by administering dextran sodium sulfate, followed by analysis of ATP levels and with the expression of pyroptosis-related proteins. Colonic epithelial cells were treated with ATP to assess cell death and pyroptosis levels. Mice with colitis exhibited elevated ATP levels in the colon and serum. Additionally, the expression of pyroptosis-related mediators was significantly upregulated in the colons of these mice. In vitro, ATP treatment increased cell death and mitochondrial dysfunction in colonic epithelial cells. ATP also enhanced inflammatory and pyroptosis responses in these cells, while the expression of apoptosis mediator proteins remained unchanged. Notably, ATP did not further enhance flagellin-induced inflammation. These findings demonstrate that ATP levels are elevated in colitis and that ATP functions as a DAMP to induce pyroptosis in intestinal epithelial cells. This study also highlights a self-propagating cycle where ATP released during pyroptosis triggers further pyroptosis in adjacent cells, exacerbating the condition. Importantly, this study extends our understanding of ATP-mediated pyroptosis to the context of the intestinal mucosal system.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70071","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666345","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}

{"title":"Metabolic Effects of Succinate Dehydrogenase Loss in Cancer","authors":"Adam Chatoff,&nbsp;Daniel S. Kantner,&nbsp;Nathaniel W. Snyder,&nbsp;Lori Rink","doi":"10.1002/jcp.70066","DOIUrl":"https://doi.org/10.1002/jcp.70066","url":null,"abstract":"<div>\u0000 \u0000 <p>Succinate dehydrogenase (SDH) is both Complex II in the electron transport chain (ETC) and a key metabolic enzyme in the tricarboxylic acid cycle. SDH is a heterotetrameric enzyme consisting of four subunits SDHA, SDHB, SDHC, and SDHD, all encoded in the nuclear genome. In addition, the SDH complex requires two assembly factors, SDHAF1 and SDHAF2, which are required for assembly of SDHA and SDHB onto the inner mitochondrial-embedded subunits SDHC and SDHD. Once assembled, SDH catalyzes the conversion of succinate to fumarate coupled to the reduction of ubiquinone to ubiquinol via FAD/FADH₂ and ultimately the generation of ATP via ATP synthase through a functioning ETC. Given the unique dual metabolic role of SDH, loss of activity results in major metabolic rewiring, potentially uncovering metabolic vulnerabilities that could be targeted for pharmacological manipulation in disease states. SDH is a tumor suppressor and SDH-loss is a driver of oncogenesis for cancers including pheochromocytomas, paragangliomas, gastrointestinal stromal tumors, and clear cell renal cell carcinomas. SDH deficiency also plays a role in the pathogenesis in non-neoplastic diseases, including Leigh syndrome and other neurometabolic disorders. Considering the implications of SDH function in both normal physiology and disease, understanding SDH function has fundamental and translational implications. This review seeks to summarize SDH deficiency, focusing on the role SDH plays in metabolism, the metabolic consequences of SDH deficiency, the proteomic consequences of SDH loss, thereby highlight potential therapeutic vulnerabilities in SDH-deficient cells.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of Myl2 Inspires Thermogenic Potential of BAT by Enhancing Adipogenic Differentiation of Brown Adipose Derived Stem Cells","authors":"Shenglu Jiang,&nbsp;Jian Li,&nbsp;Jingjing Li,&nbsp;Zhenxiong Zhao,&nbsp;Weiping Huang,&nbsp;Yuping Quan","doi":"10.1002/jcp.70068","DOIUrl":"https://doi.org/10.1002/jcp.70068","url":null,"abstract":"<div>\u0000 \u0000 <p>Obesity arises from a prolonged state of energy intake exceeding energy expenditure, leading to the “whitening” of brown adipose tissue (BAT) and a decline in metabolic function. To investigate factors contributing to BAT whitening in mice, we used microarray analysis to identify genes differentially expressed in brown adipose-derived stem cells (BADSCs) of wild-type (WT) and ob/ob mice. By intersecting differentially expressed genes between BADSCs and white adipose-derived stem cells (WADSCs) in WT mice, we identified <i>Myl2</i> as a key gene in BAT function. <i>Myl2</i> expression showed a 120.8-fold change between ob/ob and WT BADSCs, which was validated by in vivo BAT and in vitro BADSC experiments. Downregulation of <i>Myl2</i> expression by inhibitor administration significantly reduced the differentiation capacity of BADSCs. Furthermore, overexpression of <i>Myl2</i> in vitro through adeno-associated virus (AAV) transduction promoted the differentiation of obese mouse-derived BADSCs into brown adipocytes. We further demonstrated the therapeutic potential of <i>Myl2</i> by administering local injections of <i>Myl2</i>-expressing adeno-associated virus specifically for adipose tissue in ob/ob mice, resulting in improved brown adipose activity and energy metabolism. In summary, this study highlighted the crucial role of <i>Myl2</i> in BADSC differentiation and BAT function, providing a potential therapeutic target for obesity treatment.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “GTP-Binding Inhibitors Increase LRRK2-Linked Ubiquitination and Lewy Body-Like Inclusions”","authors":"","doi":"10.1002/jcp.70057","DOIUrl":"https://doi.org/10.1002/jcp.70057","url":null,"abstract":"<p>Thomas, J. M., Wang, X., Guo, G., et al. 2020. “GTP-Binding Inhibitors Increase LRRK2-Linked Ubiquitination and Lewy Body-Like Inclusions.” <i>Journal of Cellular Physiology</i> 235: 7309–7320.</p><p>The authors, by reviewing the records of the original western blots from this study, recently found that the anti-Flag (tagged LRRK2) blot in Figure 3A (the middle blot of right panel) had been duplicated in Figure 2A (the middle blot of right panel). It has been discovered that the wrong image was inadvertently selected for Figure 2A due to the similarity in the cropped blots. The authors have located the correct blot image for Figure 2A and provided the corrected Figure 2. The conclusions of this paper are not affected by this error.</p><p>The authors apologize for this error and any confusion.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647365","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}

{"title":"EXPRESSION OF CONCERN: Oldenlandia diffusa Extracts Exert Antiproliferative and Apoptotic Effects on Human Breast Cancer Cells Through ERα/Sp1-Mediated p53 Activation","authors":"","doi":"10.1002/jcp.70073","DOIUrl":"https://doi.org/10.1002/jcp.70073","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: G. Gu, I. Barone, L. Gelsomino, C. Giordano, D. Bonofiglio, G. Statti, F. Menichini, S. Catalano, and S. Andò, “<i>Oldenlandia diffusa</i> Extracts Exert Antiproliferative and Apoptotic Effects on Human Breast Cancer Cells Through ERα/Sp1-Mediated p53 Activation,” <i>Journal of Cellular Physiology</i> 227, no. 10 (2012): 3363–3372, https://doi.org/10.1002/jcp.24035.</p><p>This Expression of Concern is for the above article, published online on 21 June 2012 in Wiley Online Library (wileyonlinelibrary.com), and has been published by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The Expression of Concern has been published due to concerns raised by a third party regarding highly similar image sections between the subpanels of Figures 2B and 5A. The authors’ explanation was found to be insufficient to resolve these concerns, and due to the time elapsed since the original publication, the raw data could no longer be retrieved. In the absence of the original raw data, the journal team could not verify the authenticity of these figures and could not exclude that these concerns affect the related conclusions of the article. Therefore, the journal has decided to issue an Expression of Concern to inform and alert the readers.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647366","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}

{"title":"Cover Image, Volume 240, Number 4, April 2025","authors":"Paul G. DeCaen,&nbsp;Louise F. Kimura","doi":"10.1002/jcp.70075","DOIUrl":"https://doi.org/10.1002/jcp.70075","url":null,"abstract":"<p><b>Front Cover Caption:</b> The cover image is based on the article <i>Methods to assess neuronal primary cilia electrochemical signaling</i> by Paul G. DeCaen et al., https://doi.org/10.1002/jcp.70075.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144635093","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}

{"title":"Caveolin-1 Regulates Parathyroid Hormone (PTH)-Related Protein (PTHrP) Actions on PTH Receptor Type 1 in Bone Cells","authors":"Sara Heredero-Jiménez,&nbsp;Eduardo Martín-Guerrero,&nbsp;Joan Pizarro-Gómez,&nbsp;Irene Tirado-Cabrera,&nbsp;Luis Álvarez-Carrión,&nbsp;Teresita Bellido,&nbsp;Arancha R. Gortázar,&nbsp;Juan A. Ardura","doi":"10.1002/jcp.70067","DOIUrl":"https://doi.org/10.1002/jcp.70067","url":null,"abstract":"<p>Caveolin-1 (Cav1), a protein present in lipid raft invaginations known as caveolae, regulates the trafficking and signaling of some cell surface receptors. Current evidence suggests that the number of caveolae might increase with aging. The parathyroid hormone (PTH) receptor type 1 (PTH1R) regulates osteoblast and osteocyte actions after activation by PTH and PTH-related protein (PTHrP) peptides. PTH1R activation leads to defined biological effects depending on its association with different membrane or intracellular molecules. Since PTH1R exhibits a potential Cav1 binding domain, we hypothesized that PTH1R responses are regulated by Cav1 in cells of the osteoblastic lineage, conditioning PTHrP actions during aging. We report that Cav1 colocalizes with PTH1R at membrane microdomains in osteoblastic and osteocytic cells. Cav1 overexpression modifies PTHrP-dependent signaling in osteoblastic cells by decreasing intracellular calcium accumulation and increasing cAMP levels leading to upregulation of Runx2, osteocalcin, bone alkaline phosphatase, and OPG in a rapid and transient manner. Conversely, Cav1 silencing causes over-phosphorylation of ERK1/2 kinase and overproduction of calcium, which leads to reduced expression of Runx2, osteocalcin, and alkaline phosphatase. Further, the gene expression of Cav1 increases with age in murine bone in vivo and negatively correlates with that of Runx2, osteocalcin and alkaline phosphatase. Moreover, age-dependent overexpression of Cav-1 and caveolae disruption is associated with alterations in PTHrP-dependent bone gene expression in ex vivo cultured bones. FRAP analysis revealed that Cav1 causes PTH1R temporary retention at Cav1 microdomains upon receptor activation, delaying PTH1R internalization. We conclude that PTH1R signaling and PTHrP actions in bone cells are regulated by Cav1 and that Cav1 overexpression with age conditions PTH1R responses in bone.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 7","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144635420","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}