Connective Tissue Research最新文献

{"title":"Axin2-lineage cells contribute to neonatal tendon regeneration.","authors":"B Walia,&nbsp;T M Li,&nbsp;G Crosio,&nbsp;A M Montero,&nbsp;A H Huang","doi":"10.1080/03008207.2022.2036732","DOIUrl":"https://doi.org/10.1080/03008207.2022.2036732","url":null,"abstract":"<p><strong>Purpose: </strong>Tendon injuries are a challenging clinical problem with few treatment options. Identifying the molecular regulators of tendon is required for the development of new therapies. While the Wnt pathway is critical for the maintenance and differentiation of many tissues, the role of Wnt signaling in tendon cell biology remains largely unexplored.</p><p><strong>Methods: </strong>The effects of Wnt activation were tested <i>in vitro</i> using neonatal tendon-derived cells cultured in 2D and 3D conditions. The inducible Axin2CreERT2 was then used to label Axin2+ cells <i>in vivo</i> and cells were traced during neonatal tendon regeneration.</p><p><strong>Results: </strong>We showed that activation of Wnt signaling results in proliferation of neonatal tendon cells. While tendon marker expression was inhibited by Wnt activation under 2D conditions, <i>Scx</i> expression was not affected under 3D uniaxial tension, suggesting that the microenvironment contextualizes tendon cell response to Wnt signaling. Using an <i>in vivo</i> model of neonatal tendon regeneration, we further showed that Wnt signaling cells comprise a subpopulation of tenocyte and epitenon cells that proliferate after injury and are recruited during regeneration.</p><p><strong>Discussion: </strong>Collectively, these studies suggest that Wnt signaling may play a role in tendon cell proliferation, differentiation, and regeneration.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 5","pages":"530-543"},"PeriodicalIF":2.9,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9491382/pdf/nihms-1835287.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10134216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C5a complement receptor modulates odontogenic dental pulp stem cell differentiation under hypoxia.","authors":"Ryan Pasiewicz,&nbsp;Yessenia Valverde,&nbsp;Raghuvaran Narayanan,&nbsp;Ji-Hyun Kim,&nbsp;Muhammad Irfan,&nbsp;Nam-Seob Lee,&nbsp;Anne George,&nbsp;Lyndon F Cooper,&nbsp;Satish B Alapati,&nbsp;Seung Chung","doi":"10.1080/03008207.2021.1924696","DOIUrl":"https://doi.org/10.1080/03008207.2021.1924696","url":null,"abstract":"<p><strong>Aim: </strong>Alterations in the microenvironment change the phenotypes of dental pulp stem cells (DPSCs). The role of complement component C5a in the differentiation of DPSCs is unknown, especially under oxygen-deprived conditions. The aim of this study was to determine the effect of C5a on the odontogenic differentiation of DPSCs under normoxia and hypoxia.</p><p><strong>Material and methods: </strong>Human DPSCs were subjected to odontogenic differentiation in osteogenic media and treated with the C5a receptor antagonist-W54011 under normal and hypoxic conditions (2% oxygen). Immunochemistry, western blot, and PCR analysis for the various odontogenic differentiation genes/proteins were performed.</p><p><strong>Results: </strong>Our results demonstrated that C5a plays a positive role in the odontogenic differentiation of DPSCs. C5a receptor inhibition resulted in a significant decrease in odontogenic differentiation genes, such as DMP1, ON, RUNX2, DSPP compared with the control. This observation was further supported by the Western blot data for DSPP and DMP1 and immunohistochemical analysis. The hypoxic condition reversed this effect.</p><p><strong>Conclusions: </strong>Our results demonstrate that C5a regulates the odontogenic DPSC differentiation under normoxia. Under hypoxia, C5a exerts a reversed function for DPSC differentiation. Taken together, we identified that C5a and oxygen levels are key initial signals during pulp inflammation to control the odontogenic differentiation of DPSCs, thereby, providing a mechanism for potential therapeutic interventions for dentin repair and vital tooth preservation.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 4","pages":"339-348"},"PeriodicalIF":2.9,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/03008207.2021.1924696","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9727007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles from human umbilical cord mesenchymal stem cells reduce lipopolysaccharide-induced spinal cord injury neuronal apoptosis by mediating miR-29b-3p/PTEN","authors":"Xiao Xiao, Weiwei Li, Zhenchao Xu, Zhicheng Sun, Hongru Ye, Yunqi Wu, Yilu Zhang, L. Xie, Dingyu Jiang, Runze Jia, Xiyang Wang","doi":"10.1080/03008207.2022.2060826","DOIUrl":"https://doi.org/10.1080/03008207.2022.2060826","url":null,"abstract":"ABSTRACT Objective This study investigated the molecular mechanism of whether hUC-MSCs-EVs repressed PTEN expression and activated the PI3K/AKT pathway through miR-29b-3p, thus inhibiting LPS-induced neuronal injury. Methods hUC-MSCs were cultured and then identified. Cell morphology was observed. Alizarin red, oil red O, and alcian blue staining were used for inducing osteogenesis, adipogenesis, and chondrogenesis. EVs were extracted from hUC-MSCs and identified by transmission electron microscope observation and Western blot. SCI neuron model was established by 24h lipopolysaccharide (LPS) induction. After the cells were cultured with EVs without any treatment, uptake of EVs by SCI neurons, miR-29b-3p expression, cell viability, apoptosis, caspase-3, cleaved caspase-3, caspase 9, Bcl-2, PTEN, PI3K, AKT, and p-Akt protein levels, caspase 3 and caspase 9 activities, and inflammatory factors IL-6 and IL-1β levels were detected by immunofluorescence labeling, RT-qPCR, MTT, flow cytometry, Western blot, caspase 3 and caspase 9 activity detection kits, and ELISA. The binding sites between PTEN and miR-29b-3p were predicted by the database and verified by dual-luciferase assay. Results LPS-induced SCI cell model was successfully established, and hUC-MSCs-EVs inhibited LPS-induced apoptosis of injured spinal cord neurons. EVs transferred miR-29b-3p into LPS-induced injured neurons. miR-29b-3p silencing reversed EV effects on reducing LPS-induced neuronal apoptosis. miR-29b-3p reduced LPS-induced neuronal apoptosis by targeting PTEN. After EVs-miR-inhi and si-PTEN treatment, inhibition of the PI3K/AKT pathway reversed hUC-MSCs-EVs effects on reducing LPS-induced neuronal apoptosis. Conclusion hUC-MSCs-EVs activated the PI3K/AKT pathway by carrying miR-29b-3p into SCI neurons and silencing PTEN, thus reducing neuronal apoptosis.","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 1","pages":"634 - 649"},"PeriodicalIF":2.9,"publicationDate":"2022-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49123930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implantable biosensors for musculoskeletal health.","authors":"Kylie E Nash,&nbsp;Keat Ghee Ong,&nbsp;Robert E Guldberg","doi":"10.1080/03008207.2022.2041002","DOIUrl":"https://doi.org/10.1080/03008207.2022.2041002","url":null,"abstract":"<p><strong>Purpose: </strong>A healthy musculoskeletal system requires complex functional integration of bone, muscle, cartilage, and connective tissues responsible for bodily support, motion, and the protection of vital organs. Conditions or injuries to musculoskeeltal tissues can devastate an individual's quality of life. Some conditions that are particularly disabling include severe bone and muscle injuries to the extremities and amputations resulting from unmanageable musculoskeletal conditions or injuries. Monitoring and managing musculoskeletal health is intricate because of the complex mechanobiology of these interconnected tissues.</p><p><strong>Methods: </strong>For this article, we reviewed literature on implantable biosensors related to clinical data of the musculoskeletal system, therapeutics for complex bone injuries, and osseointegrated prosthetics as example applications.</p><p><strong>Results: </strong>As a result, a brief summary of biosensors technologies is provided along with review of noteworthy biosensors and future developments needed to fully realize the translational benefit of biosensors for musculoskeletal health.</p><p><strong>Conclusions: </strong>Novel implantable biosensors capable of tracking biophysical parameters in vivo are highly relevant to musculoskeletal health because of their ability to collect clinical data relevant to medical decisions, complex trauma treatment, and the performance of osseointegrated prostheses.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 3","pages":"228-242"},"PeriodicalIF":2.9,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8977250/pdf/nihms-1780342.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9378247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Collagen misfolding mutations: the contribution of the unfolded protein response to the molecular pathology.","authors":"John F Bateman,&nbsp;Matthew D Shoulders,&nbsp;Shireen R Lamandé","doi":"10.1080/03008207.2022.2036735","DOIUrl":"https://doi.org/10.1080/03008207.2022.2036735","url":null,"abstract":"<p><p>Mutations in collagen genes cause a broad range of connective tissue pathologies. Structural mutations that impact procollagen assembly or triple helix formation and stability are a common and important mutation class. How misfolded procollagens engage with the cellular proteostasis machinery and whether they can elicit a cytotoxic unfolded protein response (UPR) is a topic of considerable research interest. Such interest is well justified since modulating the UPR could offer a new approach to treat collagenopathies for which there are no current disease mechanism-targeting therapies. This review scrutinizes the evidence underpinning the view that endoplasmic reticulum stress and chronic UPR activation contributes significantly to the pathophysiology of the collagenopathies. While there is strong evidence that the UPR contributes to the pathology for collagen X misfolding mutations, the evidence that misfolding mutations in other collagen types induce a canonical, cytotoxic UPR is incomplete. To gain a more comprehensive understanding about how the UPR amplifies to pathology, and thus what types of manipulations of the UPR might have therapeutic relevance, much more information is needed about how specific misfolding mutation types engage differentially with the UPR and downstream signaling responses. Most importantly, since the capacity of the proteostasis machinery to respond to collagen misfolding is likely to vary between cell types, reflecting their functional roles in collagen and extracellular matrix biosynthesis, detailed studies on the UPR should focus as much as possible on the actual target cells involved in the collagen pathologies.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 3","pages":"210-227"},"PeriodicalIF":2.9,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8977234/pdf/nihms-1776496.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From the editor: Connective Tissue Research is in its 50th year","authors":"G. Balian","doi":"10.1080/03008207.2022.2055098","DOIUrl":"https://doi.org/10.1080/03008207.2022.2055098","url":null,"abstract":"","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 1","pages":"199 - 199"},"PeriodicalIF":2.9,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48767890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal changes in the muscle extracellular matrix due to volumetric muscle loss injury.","authors":"Daniel B Hoffman,&nbsp;Christiana J Raymond-Pope,&nbsp;Jacob R Sorensen,&nbsp;Benjamin T Corona,&nbsp;Sarah M Greising","doi":"10.1080/03008207.2021.1886285","DOIUrl":"https://doi.org/10.1080/03008207.2021.1886285","url":null,"abstract":"<p><strong>Purpose/aim: </strong>Volumetric muscle loss (VML) is a devastating orthopedic injury resulting in chronic persistent functional deficits, loss of joint range of motion, pathologic fibrotic deposition and lifelong disability. However, there is only limited mechanistic understanding of VML-induced fibrosis. Herein we examined the temporal changes in the fibrotic deposition at 3, 7, 14, 28, and 48 days post-VML injury.</p><p><strong>Materials and methods: </strong>Adult male Lewis rats (n = 39) underwent a full thickness ~20% (~85 mg) VML injury to the tibialis anterior (TA) muscle unilaterally, the contralateral TA muscle served as the control group. All TA muscles were harvested for biochemical and histologic evaluation.</p><p><strong>Results: </strong>The ratio of collagen I/III was decreased at 3, 7, and 14 days post-VML, but significantly increased at 48 days. Decorin content followed an opposite trend, significantly increasing by day 3 before dropping to below control levels by 48 days. Histological evaluation of the defect area indicates a shift from loosely packed collagen at early time points post-VML, to a densely packed fibrotic scar by 48 days.</p><p><strong>Conclusions: </strong>The shift from early wound healing efforts to a fibrotic scar with densely packed collagen within the skeletal muscle occurs around 21 days after VML injury through dogmatic synchronous reduction of collagen III and increase in collagen I. Thus, there appears to be an early window for therapeutic intervention to prevent pathologic fibrous tissue formation, potentially by targeting CCN2/CTGF or using decorin as a therapeutic.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 2","pages":"124-137"},"PeriodicalIF":2.9,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/03008207.2021.1886285","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10797675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Raloxifene and tibial loading on bone mass and mechanics in male and female mice.","authors":"Alycia G Berman,&nbsp;John G Damrath,&nbsp;Jennifer Hatch,&nbsp;Alexis N Pulliam,&nbsp;Katherine M Powell,&nbsp;Madicyn Hinton,&nbsp;Joseph M Wallace","doi":"10.1080/03008207.2020.1865938","DOIUrl":"https://doi.org/10.1080/03008207.2020.1865938","url":null,"abstract":"<p><p><b>Purpose:</b> Raloxifene (RAL) is a selective estrogen receptor modulator (SERM) that has previously been shown to cause acellular benefits to bone tissue. Due to these improvements, RAL was combined with targeted tibial loading to assess if RAL treatment during periods of active bone formation would allow for further mechanical enhancements.<b>Methods:</b> Structural, mechanical, and microstructural effects were assessed in bone from C57BL/6 mice that were treated with RAL (0.5 mg/kg), tibial loading, or both for 6 weeks, beginning at 10 weeks of age.<b>Results:</b><i>Ex vivo</i> microcomputed tomography (CT) images indicated RAL and loading work together to improve bone mass and architecture, especially within the cancellous region of males. Increases in cancellous bone volume fraction were heavily driven by increases in trabecular thickness, though there were some effects on trabecular spacing and number. In the cortical regions, RAL and loading both increased cross-sectional area, cortical area, and cortical thickness. Whole-bone mechanical testing primarily indicated the effects of loading. Further characterization through Raman spectroscopy and nanoindentation showed load-based changes in mineralization and micromechanics, while both loading and RAL caused changes in the secondary collagen structure. In contrast to males, in females, there were large load-based effects in the cancellous and cortical regions, resulting in increased whole-bone mechanical properties. RAL had less of an effect on cancellous and cortical architecture, though some effects were still present.<b>Conclusion:</b> RAL and loading work together to impact bone architecture and mechanical integrity, leading to greater improvements than either treatment individually.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 1","pages":"3-15"},"PeriodicalIF":2.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/03008207.2020.1865938","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10447326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of osteogenic ambulatory mechanical stimulation on early stages of BMP-2 mediated bone repair.","authors":"Brett S Klosterhoff,&nbsp;Casey E Vantucci,&nbsp;Jarred Kaiser,&nbsp;Keat Ghee Ong,&nbsp;Levi B Wood,&nbsp;Jeffrey A Weiss,&nbsp;Robert E Guldberg,&nbsp;Nick J Willett","doi":"10.1080/03008207.2021.1897582","DOIUrl":"https://doi.org/10.1080/03008207.2021.1897582","url":null,"abstract":"<p><p><b>Purpose</b>: Mechanical loading of bone defects through rehabilitation is a promising approach to stimulate repair and reduce nonunion risk; however, little is known about how therapeutic mechanical stimuli modulate early-stage repair before mineralized bone formation. The objective of this study was to investigate the early effects of osteogenic loading on cytokine expression and angiogenesis during the first 3 weeks of BMP-2 mediated segmental bone defect repair.<b>Materials and Methods</b>: A rat model of BMP-2 mediated bone defect repair was subjected to an osteogenic mechanical loading protocol using ambulatory rehabilitation and a compliant, load-sharing fixator with an integrated implantable strain sensor. The effect of fixator load-sharing on local tissue strain, angiogenesis, and cytokine expression was evaluated.<b>Results</b>: Using sensor readings for local measurements of boundary conditions, finite element simulations showed strain became amplified in remaining soft tissue regions between 1 and 3 weeks (Week 3: load-sharing: -1.89 ± 0.35% and load-shielded: -1.38 ± 0.35% vs. Week 1: load-sharing: -1.54 ± 0.17%; load-shielded: -0.76 ± 0.06%). Multivariate analysis of cytokine arrays revealed that load-sharing significantly altered expression profiles in the defect tissue at 2 weeks compared to load-shielded defects. Specifically, loading reduced VEGF (p = 0.052) and increased CXCL5 (LIX) levels. Subsequently, vascular volume in loaded defects was reduced relative to load-shielded defects but similar to intact bone at 3 weeks. Endochondral bone repair was also observed histologically in loaded defects at 3 weeks.<b>Conclusions</b>: Together, these results demonstrate that moderate ambulatory strains previously shown to stimulate bone regeneration significantly alter early angiogenic and cytokine signaling and may promote endochondral ossification.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 1","pages":"16-27"},"PeriodicalIF":2.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/03008207.2021.1897582","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10822686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of chondrocyte biosynthetic activity by dynamic hydrostatic pressure: the role of TRP channels.","authors":"Alireza Savadipour,&nbsp;Robert J Nims,&nbsp;Dakota B Katz,&nbsp;Farshid Guilak","doi":"10.1080/03008207.2020.1871475","DOIUrl":"https://doi.org/10.1080/03008207.2020.1871475","url":null,"abstract":"<p><strong>Introduction: </strong>Chondrocytes perceive and respond to mechanical loading as signals that regulate their metabolism. Joint loading exposes chondrocytes to multiple modes of mechanical stress, including hydrostatic pressure; however, the mechanisms by which chondrocytes sense physiologically relevant levels of hydrostatic pressure are not well understood. We hypothesized that hydrostatic pressure is transduced to an intracellular signal through mechanosensitive membrane ion channels of chondrocytes. The goals of this study were to examine the effect of hydrostatic loading on the development of engineered cartilage tissue and the contribution of mechanosensitive ion channels on these hydrostatic loading effects.</p><p><strong>Methods: </strong>Using a 3D model of porcine chondrocytes in agarose, we applied specific chemical inhibitors to determine the role of transient receptor potential (TRP) ion channels TRPV1, TRPV4, TRPC3, and TRPC1 in transducing hydrostatic pressure.</p><p><strong>Results: </strong>Hydrostatic loading caused a frequency and magnitude-dependent decrease in sulfated glycosaminoglycans (S-GAG), without changes in DNA content. Inhibiting TRPC3 and TRPV4 decreased S-GAG content; however, only the inhibition of TRPV1 partially attenuated the hydrostatic loading-induced reduction in S-GAG content.</p><p><strong>Conclusions: </strong>Our findings indicate that TRPV1 may serve as a transducer of hydrostatic pressure in chondrocytes, and provide further support for the role of TRPV4 in regulating chondrocyte anabolism, as well as initial evidence implicating TRPC3 in chondrogenesis. These findings add to our further understanding of the chondrocyte \"channelome\" and suggest that a range of ion channels mediate the transduction of different biophysical stimuli such as hydrostatic pressure, membrane stretch, or osmotic stress.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":"63 1","pages":"69-81"},"PeriodicalIF":2.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/03008207.2020.1871475","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9590805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}