Journal of Cellular Physiology最新文献

{"title":"Serinc5 Regulates Sequential Chondrocyte Differentiation by Inhibiting Sox9 Function in Pre-Hypertrophic Chondrocytes","authors":"Kenji Hata,&nbsp;Kanta Wakamori,&nbsp;Akane Hirakawa-Yamamura,&nbsp;Sachi Ichiyama-Kobayashi,&nbsp;Masaya Yamaguchi,&nbsp;Daisuke Okuzaki,&nbsp;Yoshifumi Takahata,&nbsp;Tomohiko Murakami,&nbsp;Narikazu Uzawa,&nbsp;Takashi Yamashiro,&nbsp;Riko Nishimura","doi":"10.1002/jcp.31490","DOIUrl":"10.1002/jcp.31490","url":null,"abstract":"<p>The growth plate is the primary site of longitudinal bone growth with chondrocytes playing a pivotal role in endochondral bone development. Chondrocytes undergo a series of differentiation steps, resulting in the formation of a unique hierarchical columnar structure comprising round, proliferating, pre-hypertrophic, and hypertrophic chondrocytes. Pre-hypertrophic chondrocytes, which exist in the transitional stage between proliferating and hypertrophic stages, are a critical cell population in the growth plate. However, the molecular basis of pre-hypertrophic chondrocytes remains largely undefined. Here, we employed scRNA-seq analysis on fluorescently labeled growth plate chondrocytes for their molecular characterization. Serine incorporator 5 (<i>Serinc5</i>) was identified as a marker gene for pre-hypertrophic chondrocytes. Histological analysis revealed that Serinc5 is specifically expressed in pre-hypertrophic chondrocytes, overlapping with Indian hedgehog (Ihh). Serinc5 represses cell proliferation and <i>Col2a1</i> and <i>Acan</i> expression by inhibiting the transcriptional activity of Sox9 in primary chondrocytes. Chromatin profiling using ChIP-seq and ATAC-seq revealed an active enhancer of <i>Serinc5</i> located in intron 1, with its chromatin status progressively activated during chondrocyte differentiation. Collectively, our findings suggest that Serinc5 regulates sequential chondrocyte differentiation from proliferation to hypertrophy by inhibiting Sox9 function in pre-hypertrophic chondrocytes, providing novel insights into the mechanisms underlying chondrocyte differentiation in growth plates.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11747958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681883","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":"RETRACTION: Reduction of Nuclear Y654-p-β-Catenin Expression Through SH3GL2-Meditated Downregulation of EGFR in Chemotolerance TNBC: Clinical and Prognostic Importance","authors":"","doi":"10.1002/jcp.31485","DOIUrl":"10.1002/jcp.31485","url":null,"abstract":"<p><b>RETRACTION:</b> S. Islam, H. Dasgupta, M. Basu, A. Roy, N. Alam, S. Roychoudhury, C. K. Panda, “Reduction of Nuclear Y654-p-β-Catenin Expression Through SH3GL2-Meditated Downregulation of EGFR in Chemotolerance TNBC: Clinical and Prognostic Importance,” <i>Journal of Cellular Physiology</i> 235, no. 11 (2020): 8114-8128. https://doi.org/10.1002/jcp.29466.</p><p>The above article, published online on 20 January 2020, in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The journal received notice of concerns from a third party regarding duplications and rotation of images between Figures 2 C and 2 G in this article as well as concerns that Figures 2 F and 3 C had been re-used in a different article by some of the same authors (Islam, et al. 2020 [https://doi.org/10.1007/s13402-020-00525-5]). Additional investigation by the publisher also confirmed image duplications within Figure 4 F and between Supplementary Figures 1 C and 1 F in this article. In response to an inquiry by the publisher, the authors stated that the duplication between figures 2 C and 2 G was due to the fact that serial sections of tissue were analyzed. The authors acknowledged that the same samples had been used between this article and the article published in a different journal, but reported that they had mislabeled the samples in the other article. Lastly, the authors stated that the duplications in Figure 4 F and between Supplementary Figures 1 C and 1 F were caused by a mistake during figure preparation. The parties agree that the explanation does not account for the multiple duplications and rotations of images both within this article and between this article and the article published in another journal. The parties also agree that the original data as provided does not adequately support the authors’ explanation. The retraction has been agreed to because the evidence of image duplication and manipulation fundamentally compromises the conclusions presented in the article. The authors disagree with the retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31485","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681879","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":"WHAMM Inhibits Type II Alveolar Epithelial Cell EMT by Mediating Autophagic Degradation of TGF-β1 in Bronchopulmonary Dysplasia","authors":"Shaodong Hua,&nbsp;Jinghan Chi,&nbsp;Ning Zhang,&nbsp;Xiao Yang,&nbsp;Pan Zhang,&nbsp;Chenyang Jiang,&nbsp;Yao Feng,&nbsp;Xiaoyang Hong,&nbsp;Zhichun Feng,&nbsp;Yurou Yan","doi":"10.1002/jcp.31486","DOIUrl":"10.1002/jcp.31486","url":null,"abstract":"<div>\u0000 \u0000 <p>Bronchopulmonary dysplasia (BPD) is one of the most prevalent complication in preterm infants, primarily characterized by arrested alveolar growth. The involvement of epithelial–mesenchymal transition (EMT) of AECII cells is proposed to have a crucial role in the pathogenesis of BPD; however, the underlying mechanism remains unclear. The present study reveals a significant reduction of WHAMM (WASP homolog associated with actin, membranes, and microtubules) in hyperoxia-induced BPD mice, highlighting its crucial role in suppressing the progression of BPD through the inhibition of EMT in AECIIs. We demonstrated that hyperoxia-induced downregulation of WHAMM leads to the accumulation of TGF-β1 primarily through its mediation of the autophagic degradation pathway. Mechanistically, WHAMM enhanced the autophagosomal localization of TGF-β1 and concurrently promoted the process of autophagy, thereby comprehensively facilitating the autophagic degradation of TGF-β1. These findings reveal the important role of WHAMM in the development of BPD, and the proposed WHAMM/autophagy/TGF-β1/EMT pathway may represent a potential therapeutic strategy for BPD treatment.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675850","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":"Cholesterol Depletion Activate Hepatic Stellate Cells Mediated Through SREBP-2 Signaling","authors":"Nivya Vijayan,&nbsp;Madan Kumar Perumal","doi":"10.1002/jcp.31476","DOIUrl":"10.1002/jcp.31476","url":null,"abstract":"<div>\u0000 \u0000 <p>Liver fibrosis is one of the leading cause of death worldwide. In liver, hepatic stellate cells are the primary cell type that gets activated during fibrosis. LX-2 cells are human-derived hepatic stellate cell lines typically employed for studying liver fibrosis mechanisms and screening anti-fibrotic lead molecules. Although LX-2 cells are partially activated in culture conditions, numerous stimuli including TGF-β, H₂O₂, hypoxia, LPS were reported to activate LX-2 cells. In this study, for the first time, the effect of cholesterol depletion on LX-2 cells was studied. Under cholesterol-depleted conditions, the mRNA and protein expression of HSC activation markers (α-SMA, GFAP) were significantly increased. Also, the expression of SREBP-2, HMGCR were significantly upregulated in response to cholesterol depletion. Treatment with fatostatin, a reported SREBP inhibitor abolished nuclear SREBP-1 and SREBP-2 expression and regulated the SREBP signaling. Transmission electron microscopic imaging showed distinct ultrastructural changes in response to cholesterol depletion. Furthermore, cholesterol depletion did not affect the cell-cycle profile of LX-2 cells compared with untreated while fatostatin treatment induced G2 cell-cycle arrest. Overall, cholesterol depletion activated LX-2 cells mediated by SREBP-2 signaling and therefore could be further employed as stimuli for LX-2 activation and screening lead molecules targeting SREBPs.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620615","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":"Estrogen Regulates Mitochondrial Activity Through Inducing Brain-Derived Neurotrophic Factor Expression in Skeletal Muscle","authors":"Margaret Chui Ling Tse,&nbsp;Brian Pak Shing Pang,&nbsp;Xinyi Bi,&nbsp;Teresa Xinci Ooi,&nbsp;Wing Suen Chan,&nbsp;Jiangwen Zhang,&nbsp;Chi Bun Chan","doi":"10.1002/jcp.31483","DOIUrl":"10.1002/jcp.31483","url":null,"abstract":"<div>\u0000 \u0000 <p>Estrogen is an essential hormone for the development and functional activities of reproductive organs. Recent studies showed that estrogen signaling is also an important regulator of lipid and glucose metabolism in a number of tissues, but the molecular mechanism is not fully understood. We report here that estrogen is a stimulator of brain-derived neurotrophic factor (BDNF) synthesis in the skeletal muscle. Estradiol (E2), but not testosterone, induces a dose- and time-dependent BDNF production in cultured myotubes. Estrogen depletion in ovariectomized mice significantly reduced <i>Bdnf</i> expression in the glycolytic myofibers, which could be rescued after E2 administration. Mechanistically, E2 stimulation triggered the tethering of estrogen receptor (ER) α, but not ERβ, to the estrogen-responsive element on promoter VI of the <i>Bdnf</i> gene in skeletal muscle. When <i>Bdnf</i> production was inhibited by shRNA in C2C12 myotubes, E2-induced mitochondria activation and pyruvate dehydrogenase kinase 4 expressions were jeopardized. Collectively, our results demonstrate that BDNF is an underrecognized effector of estrogen in regulating mitochondrial activity and fuel metabolism in the skeletal muscle.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620626","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":"Glucose Upregulates ChREBP via Phosphorylation of AKT and AMPK to Modulate MALT1 and WISP1 Expression","authors":"Syue-Ting Chen,&nbsp;Kang-Shuo Chang,&nbsp;Yu-Hsiang Lin,&nbsp;Chen-Pang Hou,&nbsp;Wei-Yin Lin,&nbsp;Shu-Yuan Hsu,&nbsp;Hsin-Ching Sung,&nbsp;Tsui-Hsia Feng,&nbsp;Ke-Hung Tsui,&nbsp;Horng-Heng Juang","doi":"10.1002/jcp.31478","DOIUrl":"10.1002/jcp.31478","url":null,"abstract":"<div>\u0000 \u0000 <p>Glucose can activate the carbohydrate response element binding protein (ChREBP) transcription factor to control gene expressions in the metabolic pathways. The way of ChREBP involvement in human prostate cancer development remains undetermined. This study examined the interactions between prostate fibroblasts and cancer cells under the influences of ChREBP. Results showed that high glucose (30 mM) increased the phosphorylation of AKT at S473 and AMP-activated protein kinase (AMPK) at S485 in human prostate fibroblast (HPrF) cells and prostate cancer PC-3 cells. High glucose enhanced the expression of ChREBP, which increased the expressions of fibronectin, alpha-smooth muscle actin (α-SMA), and WNT1 inducible signaling pathway protein 1 (WISP1), magnifying the cell growth and contraction in HPrF cells in vitro. The cell proliferation, invasion, and tumor growth in prostate cancer PC-3 cells were enhanced by inducing the expressions of ChREBP, mucosa-associated lymphoid tissue 1 (MALT1), and epithelial-mesenchymal transition markers with high glucose treatment. Moreover, ectopic ChREBP overexpression induced NF-κB signaling activities via upregulating MALT1 expression in PC-3 cells. Our findings illustrated that ChREBP is an oncogene in the human prostate. High glucose condition induces a glucose/ChREBP/MALT1/NF-κB axis which links the glucose metabolism to the NF-κB activation in prostate cancer cells, and a glucose/ChREBP/WISP1 axis mediating autocrine and paracrine signaling between fibroblasts and cancer cells to promote cell migration, contraction, growth, and invasion of the human prostate.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620596","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":"Cover Image, Volume 239, Number 11, November 2024","authors":"Laventa M. Obare,&nbsp;Stephen Priest,&nbsp;Anas Ismail,&nbsp;Mona Mashayekhi,&nbsp;Xiuqi Zhang,&nbsp;Lindsey K. Stolze,&nbsp;Quanhu Sheng,&nbsp;Kisyua Nthenge,&nbsp;Zer Vue,&nbsp;Kit Neikirk,&nbsp;Heather K. Beasley,&nbsp;Curtis Gabriel,&nbsp;Tecla Temu,&nbsp;Sara Gianella,&nbsp;Simon A. Mallal,&nbsp;John R. Koethe,&nbsp;Antentor Hinton Jr.,&nbsp;Samuel S. Bailin,&nbsp;Celestine N. Wanjalla","doi":"10.1002/jcp.31493","DOIUrl":"https://doi.org/10.1002/jcp.31493","url":null,"abstract":"<p><b>Front Cover Caption:</b> The cover image is based on the article <i>Cytokine and chemokine receptor profiles in adipose tissue vasculature unravel endothelial cell responses in HIV</i> by Laventa M. Obare et al., https://doi.org/10.1002/jcp.31415.\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":"239 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31493","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142665884","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":"Dynamic mRNA Stability Buffer Transcriptional Activation During Neuronal Differentiation and Is Regulated by SAMD4A","authors":"Yuan Zhou,&nbsp;Sherif Rashad,&nbsp;Daisuke Ando,&nbsp;Yuki Kobayashi,&nbsp;Teiji Tominaga,&nbsp;Kuniyasu Niizuma","doi":"10.1002/jcp.31477","DOIUrl":"10.1002/jcp.31477","url":null,"abstract":"<p>Neurons are exceptionally sensitive to oxidative stress, which is the basis for many neurodegenerative disease pathophysiologies. The posttranscriptional basis for neuronal differentiation and behavior is not well characterized. The steady-state levels of mRNA are outcomes of an interplay between RNA transcription and decay. However, the correlation between mRNA transcription, translation, and stability remains elusive. We utilized a SH-SY5Y-based neural differentiation model that is widely used to study neurodegenerative diseases. After neuronal differentiation, we observed enhanced sensitivity of mature neurons to mitochondrial stresses and ferroptosis induction. We employed a newly developed simplified mRNA stability profiling technique to explore the role of mRNA stability in SH-SY5Y neuronal differentiation model. Transcriptome-wide mRNA stability analysis revealed neural-specific RNA stability kinetics. Our analysis revealed that mRNA stability could either exert the buffering effect on gene products or change in the same direction as transcription. Importantly, we observed that changes in mRNA stability corrected over or under transcription of mRNAs to maintain mRNA translation dynamics. Furthermore, we conducted integrative analysis of our mRNA stability data set, and a published CRISPR-i screen focused on neuronal oxidative stress responses. Our analysis unveiled novel neuronal stress response genes that were not evident at the transcriptional or translational levels. SEPHS2 emerged as an important neuronal stress regulator based on this integrative analysis. Motif analysis unveiled SAMD4A as a major regulator of the dynamic changes in mRNA stability observed during differentiation. Knockdown of SAMD4A impaired neuronal differentiation and influenced the response to oxidative stress. Mechanistically, SAMD4A was found to alter the stability of several mRNAs. The novel insights into the interplay between mRNA stability and cellular behaviors provide a foundation for understanding neurodevelopmental processes and neurodegenerative disorders and highlight dynamic mRNA stability as an important layer of gene expression.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11747957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603522","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":"RETRACTION: Downregulation of miRNA-30a Enhanced Autophagy in Osthole-Alleviated Myocardium Ischemia/Reperfusion Injury","authors":"","doi":"10.1002/jcp.31479","DOIUrl":"10.1002/jcp.31479","url":null,"abstract":"<p><b>RETRACTION:</b> S. Liu, Y. He, J. Shi, L. Liu, H. Ma, L. He, and Y. Guo, “Downregulation of miRNAmiRNA-30a-30a Enhanced Autophagy in Osthole-Alleviated Myocardium Ischemia/Reperfusion Injury,” <i>Journal of Cellular Biochemistry</i> (Early View): https://doi.org/10.1002/jcp.28556.</p><p>The above article, published online on 24 April 2019 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 major unattributed overlap with a previously published article from the same group of authors.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31479","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603670","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":"Shear stress effects on epididymal epithelial cell via primary cilia mechanosensory signaling","authors":"Sepideh Fakhari,&nbsp;Gabriel Campolina-Silva,&nbsp;Farnaz Asayesh,&nbsp;Laura Girardet,&nbsp;Marie-Pier Scott-Boyer,&nbsp;Arnaud Droit,&nbsp;Denis Soulet,&nbsp;Jesse Greener,&nbsp;Clémence Belleannée","doi":"10.1002/jcp.31475","DOIUrl":"10.1002/jcp.31475","url":null,"abstract":"<p>Shear stress, resulting from fluid flow, is a fundamental mechanical stimulus affecting various cellular functions. The epididymis, essential for sperm maturation, offers a compelling model to study the effects of shear stress on cellular behavior. This organ undergoes extensive proliferation and differentiation until puberty, achieving full functionality as spermatozoa commence their post-testicular maturation. Although the mechanical tension exerted by testicular fluid is hypothesized to drive epithelial proliferation and differentiation, the precise mechanisms remain unclear. Here we assessed whether the responsiveness of the epididymal cells to shear stress depends on functional primary cilia by combining microfluidic strategies on immortalized epididymal cells, calcium signaling assays, and high-throughput gene expression analysis. We identified 97 genes overexpressed in response to shear stress, including early growth response (Egr) 2/3, cellular communication network factor (Ccn) 1/2, and Fos proto-oncogene (Fos). While shear stress triggered a rapid increase of intracellular Ca²⁺, this response was abrogated following the impairment of primary ciliogenesis through pharmacological and siRNA approaches. Overall, our findings provide valuable insights into how mechanical forces influence the development of the male reproductive system, a requisite to sperm maturation.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603694","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}