Leptin accelerates the pathogenesis of heterotopic ossification in rat tendon tissues via mTORC1 signaling
Leptin, an adipocyte‐derived cytokine associated with bone metabolism, is believed to play a critical role in the pathogenesis of heterotopic ossification (HO). The effect and underlying action mechanism of leptin were investigated on osteogenic differentiation of tendon‐derived stem cells (TDSCs) i...
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| Veröffentlicht in: | Journal of cellular physiology 2018-02, Vol.233 (2), p.1017-1028 |
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| creator | Jiang, Huaji Chen, Yuhui Chen, Guorong Tian, Xinggui Tang, Jiajun Luo, Lei Huang, Minjun Yan, Bin Ao, Xiang Zhou, Wen Wang, Liping Bai, Xiaochun Zhang, Zhongmin Wang, Liang Xian, Cory J. |
| description | Leptin, an adipocyte‐derived cytokine associated with bone metabolism, is believed to play a critical role in the pathogenesis of heterotopic ossification (HO). The effect and underlying action mechanism of leptin were investigated on osteogenic differentiation of tendon‐derived stem cells (TDSCs) in vitro and the HO formation in rat tendons. Isolated rat TDSCs were treated with various concentrations of leptin in the presence or absence of mTORC1 signaling specific inhibitor rapamycin in vitro. A rat model with Achilles tenotomy was employed to evaluate the effect of leptin on HO formation together with or without rapamycin treatment. In vitro studies with TDSCs showed that leptin increased the expression of osteogenic biomarkers (alkaline phosphatase, runt‐related transcription factor 2, osterix, osteocalcin) and enhanced mineralization of TDSCs via activating the mTORC1 signal pathway (as indicated by phosphorylation of p70 ribosomal S6 kinase 1 and p70 ribosomal S6). However, mTORC1 signaling blockade with rapamycin treatment suppressed leptin‐induced osteogenic differentiation and mineralization. In vivo studies showed that leptin promoted HO formation in the Achilles tendon after tenotomy, and rapamycin treatment blocked leptin‐induced HO formation. In conclusion, leptin can promote TDSC osteogenic differentiation and heterotopic bone formation via mTORC1 signaling in both vitro and vivo model, which provides a new potential therapeutic target for HO prevention.
Leptin promotes the osteogenic differentiation of tendon‐derived stem cells (TDSCs) in heterotopic ossification (HO). mTORC1 signaling favors differentiation of TDSCs into osteoblasts and promotes expression of Runx2 and OSX in HO of Achilles tendon. |
| doi_str_mv | 10.1002/jcp.25955 |
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Leptin promotes the osteogenic differentiation of tendon‐derived stem cells (TDSCs) in heterotopic ossification (HO). mTORC1 signaling favors differentiation of TDSCs into osteoblasts and promotes expression of Runx2 and OSX in HO of Achilles tendon.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.25955</identifier><identifier>PMID: 28407241</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Achilles tendon ; Alkaline phosphatase ; Animals ; Biocompatibility ; Biomarkers ; Biomedical materials ; Bone growth ; Bone turnover ; Cell Differentiation - drug effects ; Cells, Cultured ; Core Binding Factor Alpha 1 Subunit - metabolism ; Differentiation ; Disease Models, Animal ; Dose-Response Relationship, Drug ; In vivo methods and tests ; Leptin ; Leptin - toxicity ; Male ; Mechanistic Target of Rapamycin Complex 1 - metabolism ; Metabolism ; Mineralization ; Ossification (ectopic) ; Ossification, Heterotopic - chemically induced ; Ossification, Heterotopic - enzymology ; Ossification, Heterotopic - pathology ; Osteoblasts - drug effects ; Osteoblasts - enzymology ; Osteoblasts - pathology ; Osteocalcin ; Osteogenesis ; Osteogenesis - drug effects ; osteogenic differentiation ; Pathogenesis ; Phenotype ; Phosphorylation ; Rapamycin ; Rats, Sprague-Dawley ; Receptors, Leptin - metabolism ; Ribosomal protein S6 kinase ; Rodents ; Signal Transduction - drug effects ; Signaling ; Stem cell transplantation ; Stem cells ; Stem Cells - drug effects ; Stem Cells - enzymology ; Stem Cells - pathology ; Tendons ; Tendons - drug effects ; Tendons - enzymology ; Tendons - pathology ; tendon‐derived stem cells ; Transcription Factors - metabolism</subject><ispartof>Journal of cellular physiology, 2018-02, Vol.233 (2), p.1017-1028</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4545-c6b0c33d238a8229e7774bf77cac1f3ddc503aa05c58614390bb9703125b2b963</citedby><cites>FETCH-LOGICAL-c4545-c6b0c33d238a8229e7774bf77cac1f3ddc503aa05c58614390bb9703125b2b963</cites><orcidid>0000-0001-9355-1167 ; 0000-0002-8467-2845</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.25955$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.25955$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27926,27927,45576,45577</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28407241$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Huaji</creatorcontrib><creatorcontrib>Chen, Yuhui</creatorcontrib><creatorcontrib>Chen, Guorong</creatorcontrib><creatorcontrib>Tian, Xinggui</creatorcontrib><creatorcontrib>Tang, Jiajun</creatorcontrib><creatorcontrib>Luo, Lei</creatorcontrib><creatorcontrib>Huang, Minjun</creatorcontrib><creatorcontrib>Yan, Bin</creatorcontrib><creatorcontrib>Ao, Xiang</creatorcontrib><creatorcontrib>Zhou, Wen</creatorcontrib><creatorcontrib>Wang, Liping</creatorcontrib><creatorcontrib>Bai, Xiaochun</creatorcontrib><creatorcontrib>Zhang, Zhongmin</creatorcontrib><creatorcontrib>Wang, Liang</creatorcontrib><creatorcontrib>Xian, Cory J.</creatorcontrib><title>Leptin accelerates the pathogenesis of heterotopic ossification in rat tendon tissues via mTORC1 signaling</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Leptin, an adipocyte‐derived cytokine associated with bone metabolism, is believed to play a critical role in the pathogenesis of heterotopic ossification (HO). The effect and underlying action mechanism of leptin were investigated on osteogenic differentiation of tendon‐derived stem cells (TDSCs) in vitro and the HO formation in rat tendons. Isolated rat TDSCs were treated with various concentrations of leptin in the presence or absence of mTORC1 signaling specific inhibitor rapamycin in vitro. A rat model with Achilles tenotomy was employed to evaluate the effect of leptin on HO formation together with or without rapamycin treatment. In vitro studies with TDSCs showed that leptin increased the expression of osteogenic biomarkers (alkaline phosphatase, runt‐related transcription factor 2, osterix, osteocalcin) and enhanced mineralization of TDSCs via activating the mTORC1 signal pathway (as indicated by phosphorylation of p70 ribosomal S6 kinase 1 and p70 ribosomal S6). However, mTORC1 signaling blockade with rapamycin treatment suppressed leptin‐induced osteogenic differentiation and mineralization. In vivo studies showed that leptin promoted HO formation in the Achilles tendon after tenotomy, and rapamycin treatment blocked leptin‐induced HO formation. In conclusion, leptin can promote TDSC osteogenic differentiation and heterotopic bone formation via mTORC1 signaling in both vitro and vivo model, which provides a new potential therapeutic target for HO prevention.
Leptin promotes the osteogenic differentiation of tendon‐derived stem cells (TDSCs) in heterotopic ossification (HO). mTORC1 signaling favors differentiation of TDSCs into osteoblasts and promotes expression of Runx2 and OSX in HO of Achilles tendon.</description><subject>Achilles tendon</subject><subject>Alkaline phosphatase</subject><subject>Animals</subject><subject>Biocompatibility</subject><subject>Biomarkers</subject><subject>Biomedical materials</subject><subject>Bone growth</subject><subject>Bone turnover</subject><subject>Cell Differentiation - drug effects</subject><subject>Cells, Cultured</subject><subject>Core Binding Factor Alpha 1 Subunit - metabolism</subject><subject>Differentiation</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>In vivo methods and tests</subject><subject>Leptin</subject><subject>Leptin - toxicity</subject><subject>Male</subject><subject>Mechanistic Target of Rapamycin Complex 1 - metabolism</subject><subject>Metabolism</subject><subject>Mineralization</subject><subject>Ossification (ectopic)</subject><subject>Ossification, Heterotopic - chemically induced</subject><subject>Ossification, Heterotopic - enzymology</subject><subject>Ossification, Heterotopic - pathology</subject><subject>Osteoblasts - drug effects</subject><subject>Osteoblasts - enzymology</subject><subject>Osteoblasts - pathology</subject><subject>Osteocalcin</subject><subject>Osteogenesis</subject><subject>Osteogenesis - drug effects</subject><subject>osteogenic differentiation</subject><subject>Pathogenesis</subject><subject>Phenotype</subject><subject>Phosphorylation</subject><subject>Rapamycin</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Leptin - metabolism</subject><subject>Ribosomal protein S6 kinase</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - enzymology</subject><subject>Stem Cells - pathology</subject><subject>Tendons</subject><subject>Tendons - drug effects</subject><subject>Tendons - enzymology</subject><subject>Tendons - pathology</subject><subject>tendon‐derived stem cells</subject><subject>Transcription Factors - metabolism</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtOwzAQRS0EoqWw4AeQJVYs0vqZxEtU8VSlIlTWluM4raM0CbYL6t9jSGHHajSaM0czF4BLjKYYITKrdT8lXHB-BMYYiSxhKSfHYBxnOBGc4RE4875GCAlB6SkYkZyhjDA8BvXC9MG2UGltGuNUMB6GjYG9CptubVrjrYddBTcmGNeFrrcadt7bymoVbNfCuBu3YDBtGbtgvd9FxYdVcLtavs4x9Hbdqsa263NwUqnGm4tDnYC3-7vV_DFZLB-e5reLRDPOeKLTAmlKS0JzlRMiTJZlrKiyTCuNK1qWmiOqFOKa5ylmVKCiEBmimPCCFCKlE3A9eHvXvcdjgqy7nYs3eIlFilguKMsjdTNQ2sV_nKlk7-xWub3ESH6nKmOq8ifVyF4djLtia8o_8jfGCMwG4NM2Zv-_ST7PXwblF-4hgXM</recordid><startdate>201802</startdate><enddate>201802</enddate><creator>Jiang, Huaji</creator><creator>Chen, Yuhui</creator><creator>Chen, Guorong</creator><creator>Tian, Xinggui</creator><creator>Tang, Jiajun</creator><creator>Luo, Lei</creator><creator>Huang, Minjun</creator><creator>Yan, Bin</creator><creator>Ao, Xiang</creator><creator>Zhou, Wen</creator><creator>Wang, Liping</creator><creator>Bai, Xiaochun</creator><creator>Zhang, Zhongmin</creator><creator>Wang, Liang</creator><creator>Xian, Cory J.</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><orcidid>https://orcid.org/0000-0001-9355-1167</orcidid><orcidid>https://orcid.org/0000-0002-8467-2845</orcidid></search><sort><creationdate>201802</creationdate><title>Leptin accelerates the pathogenesis of heterotopic ossification in rat tendon tissues via mTORC1 signaling</title><author>Jiang, Huaji ; Chen, Yuhui ; Chen, Guorong ; Tian, Xinggui ; Tang, Jiajun ; Luo, Lei ; Huang, Minjun ; Yan, Bin ; Ao, Xiang ; Zhou, Wen ; Wang, Liping ; Bai, Xiaochun ; Zhang, Zhongmin ; Wang, Liang ; Xian, Cory J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4545-c6b0c33d238a8229e7774bf77cac1f3ddc503aa05c58614390bb9703125b2b963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Achilles tendon</topic><topic>Alkaline phosphatase</topic><topic>Animals</topic><topic>Biocompatibility</topic><topic>Biomarkers</topic><topic>Biomedical materials</topic><topic>Bone growth</topic><topic>Bone turnover</topic><topic>Cell Differentiation - drug effects</topic><topic>Cells, Cultured</topic><topic>Core Binding Factor Alpha 1 Subunit - metabolism</topic><topic>Differentiation</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>In vivo methods and tests</topic><topic>Leptin</topic><topic>Leptin - toxicity</topic><topic>Male</topic><topic>Mechanistic Target of Rapamycin Complex 1 - metabolism</topic><topic>Metabolism</topic><topic>Mineralization</topic><topic>Ossification (ectopic)</topic><topic>Ossification, Heterotopic - chemically induced</topic><topic>Ossification, Heterotopic - enzymology</topic><topic>Ossification, Heterotopic - pathology</topic><topic>Osteoblasts - drug effects</topic><topic>Osteoblasts - enzymology</topic><topic>Osteoblasts - pathology</topic><topic>Osteocalcin</topic><topic>Osteogenesis</topic><topic>Osteogenesis - drug effects</topic><topic>osteogenic differentiation</topic><topic>Pathogenesis</topic><topic>Phenotype</topic><topic>Phosphorylation</topic><topic>Rapamycin</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Leptin - metabolism</topic><topic>Ribosomal protein S6 kinase</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - enzymology</topic><topic>Stem Cells - pathology</topic><topic>Tendons</topic><topic>Tendons - drug effects</topic><topic>Tendons - enzymology</topic><topic>Tendons - pathology</topic><topic>tendon‐derived stem cells</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Huaji</creatorcontrib><creatorcontrib>Chen, Yuhui</creatorcontrib><creatorcontrib>Chen, Guorong</creatorcontrib><creatorcontrib>Tian, Xinggui</creatorcontrib><creatorcontrib>Tang, Jiajun</creatorcontrib><creatorcontrib>Luo, Lei</creatorcontrib><creatorcontrib>Huang, Minjun</creatorcontrib><creatorcontrib>Yan, Bin</creatorcontrib><creatorcontrib>Ao, Xiang</creatorcontrib><creatorcontrib>Zhou, Wen</creatorcontrib><creatorcontrib>Wang, Liping</creatorcontrib><creatorcontrib>Bai, Xiaochun</creatorcontrib><creatorcontrib>Zhang, Zhongmin</creatorcontrib><creatorcontrib>Wang, Liang</creatorcontrib><creatorcontrib>Xian, Cory J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Huaji</au><au>Chen, Yuhui</au><au>Chen, Guorong</au><au>Tian, Xinggui</au><au>Tang, Jiajun</au><au>Luo, Lei</au><au>Huang, Minjun</au><au>Yan, Bin</au><au>Ao, Xiang</au><au>Zhou, Wen</au><au>Wang, Liping</au><au>Bai, Xiaochun</au><au>Zhang, Zhongmin</au><au>Wang, Liang</au><au>Xian, Cory J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leptin accelerates the pathogenesis of heterotopic ossification in rat tendon tissues via mTORC1 signaling</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2018-02</date><risdate>2018</risdate><volume>233</volume><issue>2</issue><spage>1017</spage><epage>1028</epage><pages>1017-1028</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Leptin, an adipocyte‐derived cytokine associated with bone metabolism, is believed to play a critical role in the pathogenesis of heterotopic ossification (HO). The effect and underlying action mechanism of leptin were investigated on osteogenic differentiation of tendon‐derived stem cells (TDSCs) in vitro and the HO formation in rat tendons. Isolated rat TDSCs were treated with various concentrations of leptin in the presence or absence of mTORC1 signaling specific inhibitor rapamycin in vitro. A rat model with Achilles tenotomy was employed to evaluate the effect of leptin on HO formation together with or without rapamycin treatment. In vitro studies with TDSCs showed that leptin increased the expression of osteogenic biomarkers (alkaline phosphatase, runt‐related transcription factor 2, osterix, osteocalcin) and enhanced mineralization of TDSCs via activating the mTORC1 signal pathway (as indicated by phosphorylation of p70 ribosomal S6 kinase 1 and p70 ribosomal S6). However, mTORC1 signaling blockade with rapamycin treatment suppressed leptin‐induced osteogenic differentiation and mineralization. In vivo studies showed that leptin promoted HO formation in the Achilles tendon after tenotomy, and rapamycin treatment blocked leptin‐induced HO formation. In conclusion, leptin can promote TDSC osteogenic differentiation and heterotopic bone formation via mTORC1 signaling in both vitro and vivo model, which provides a new potential therapeutic target for HO prevention.
Leptin promotes the osteogenic differentiation of tendon‐derived stem cells (TDSCs) in heterotopic ossification (HO). mTORC1 signaling favors differentiation of TDSCs into osteoblasts and promotes expression of Runx2 and OSX in HO of Achilles tendon.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28407241</pmid><doi>10.1002/jcp.25955</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-9355-1167</orcidid><orcidid>https://orcid.org/0000-0002-8467-2845</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Achilles tendon Alkaline phosphatase Animals Biocompatibility Biomarkers Biomedical materials Bone growth Bone turnover Cell Differentiation - drug effects Cells, Cultured Core Binding Factor Alpha 1 Subunit - metabolism Differentiation Disease Models, Animal Dose-Response Relationship, Drug In vivo methods and tests Leptin Leptin - toxicity Male Mechanistic Target of Rapamycin Complex 1 - metabolism Metabolism Mineralization Ossification (ectopic) Ossification, Heterotopic - chemically induced Ossification, Heterotopic - enzymology Ossification, Heterotopic - pathology Osteoblasts - drug effects Osteoblasts - enzymology Osteoblasts - pathology Osteocalcin Osteogenesis Osteogenesis - drug effects osteogenic differentiation Pathogenesis Phenotype Phosphorylation Rapamycin Rats, Sprague-Dawley Receptors, Leptin - metabolism Ribosomal protein S6 kinase Rodents Signal Transduction - drug effects Signaling Stem cell transplantation Stem cells Stem Cells - drug effects Stem Cells - enzymology Stem Cells - pathology Tendons Tendons - drug effects Tendons - enzymology Tendons - pathology tendon‐derived stem cells Transcription Factors - metabolism |
| title | Leptin accelerates the pathogenesis of heterotopic ossification in rat tendon tissues via mTORC1 signaling |
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