AQP1 modulates tendon stem/progenitor cells senescence during tendon aging
The link between tendon stem/progenitor cells (TSPCs) senescence and tendon aging has been well recognized. However, the cellular and molecular mechanisms of TSPCs senescence are still not fully understood. In present study, we investigated the role of Aquaporin 1 (AQP1) in TSPCs senescence. We show...
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| Veröffentlicht in: | Cell death & disease 2020-03, Vol.11 (3), p.193-193, Article 193 |
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| creator | Chen, Minhao Li, Yingjuan Xiao, Longfei Dai, Guangchun Lu, Panpan Wang, Youhua Rui, Yunfeng |
| description | The link between tendon stem/progenitor cells (TSPCs) senescence and tendon aging has been well recognized. However, the cellular and molecular mechanisms of TSPCs senescence are still not fully understood. In present study, we investigated the role of Aquaporin 1 (AQP1) in TSPCs senescence. We showed that AQP1 expression declines with age during tendon aging. In aged TSPCs, overexpression of AQP1 significantly attenuated TSPCs senescence. In addition, AQP1 overexpression also restored the age-related dysfunction of self-renewal, migration and tenogenic differentiation. Furthermore, we demonstrated that the JAK-STAT signaling pathway is activated in aged TSPCs, and AQP1 overexpression inhibited the JAK-STAT signaling pathway activation which indicated that AQP1 attenuates senescence and age-related dysfunction of TSPCs through the repression of JAK−STAT signaling pathway. Taken together, our findings demonstrated the critical role of AQP1 in the regulation of TSPCs senescence and provided a novel target for antagonizing tendon aging. |
| doi_str_mv | 10.1038/s41419-020-2386-3 |
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However, the cellular and molecular mechanisms of TSPCs senescence are still not fully understood. In present study, we investigated the role of Aquaporin 1 (AQP1) in TSPCs senescence. We showed that AQP1 expression declines with age during tendon aging. In aged TSPCs, overexpression of AQP1 significantly attenuated TSPCs senescence. In addition, AQP1 overexpression also restored the age-related dysfunction of self-renewal, migration and tenogenic differentiation. Furthermore, we demonstrated that the JAK-STAT signaling pathway is activated in aged TSPCs, and AQP1 overexpression inhibited the JAK-STAT signaling pathway activation which indicated that AQP1 attenuates senescence and age-related dysfunction of TSPCs through the repression of JAK−STAT signaling pathway. Taken together, our findings demonstrated the critical role of AQP1 in the regulation of TSPCs senescence and provided a novel target for antagonizing tendon aging.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-2386-3</identifier><identifier>PMID: 32188840</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/100 ; 13/31 ; 38/109 ; 38/39 ; 38/61 ; 38/89 ; 38/91 ; 631/532/7 ; 631/80/509 ; 96/95 ; Aging ; Aging - physiology ; Animals ; Antibodies ; Aquaporin 1 ; Aquaporin 1 - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; Cell Differentiation - physiology ; Cell self-renewal ; Cellular Senescence - physiology ; Immunology ; Kinases ; Life Sciences ; Male ; Molecular modelling ; Progenitor cells ; Rats ; Rats, Sprague-Dawley ; Senescence ; Signal transduction ; Stem cells ; Stem Cells - cytology ; Stem Cells - metabolism ; Tendons - cytology ; Tendons - metabolism</subject><ispartof>Cell death & disease, 2020-03, Vol.11 (3), p.193-193, Article 193</ispartof><rights>The Author(s) 2020</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-e6e51ab8ef7b70eda96f64cfca7c22920a162d9cf5ab88a9f2a7e5f6cf2e6e5f3</citedby><cites>FETCH-LOGICAL-c470t-e6e51ab8ef7b70eda96f64cfca7c22920a162d9cf5ab88a9f2a7e5f6cf2e6e5f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7080760/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7080760/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32188840$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Minhao</creatorcontrib><creatorcontrib>Li, Yingjuan</creatorcontrib><creatorcontrib>Xiao, Longfei</creatorcontrib><creatorcontrib>Dai, Guangchun</creatorcontrib><creatorcontrib>Lu, Panpan</creatorcontrib><creatorcontrib>Wang, Youhua</creatorcontrib><creatorcontrib>Rui, Yunfeng</creatorcontrib><title>AQP1 modulates tendon stem/progenitor cells senescence during tendon aging</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>The link between tendon stem/progenitor cells (TSPCs) senescence and tendon aging has been well recognized. However, the cellular and molecular mechanisms of TSPCs senescence are still not fully understood. In present study, we investigated the role of Aquaporin 1 (AQP1) in TSPCs senescence. We showed that AQP1 expression declines with age during tendon aging. In aged TSPCs, overexpression of AQP1 significantly attenuated TSPCs senescence. In addition, AQP1 overexpression also restored the age-related dysfunction of self-renewal, migration and tenogenic differentiation. Furthermore, we demonstrated that the JAK-STAT signaling pathway is activated in aged TSPCs, and AQP1 overexpression inhibited the JAK-STAT signaling pathway activation which indicated that AQP1 attenuates senescence and age-related dysfunction of TSPCs through the repression of JAK−STAT signaling pathway. Taken together, our findings demonstrated the critical role of AQP1 in the regulation of TSPCs senescence and provided a novel target for antagonizing tendon aging.</description><subject>13/100</subject><subject>13/31</subject><subject>38/109</subject><subject>38/39</subject><subject>38/61</subject><subject>38/89</subject><subject>38/91</subject><subject>631/532/7</subject><subject>631/80/509</subject><subject>96/95</subject><subject>Aging</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Aquaporin 1</subject><subject>Aquaporin 1 - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Differentiation - physiology</subject><subject>Cell self-renewal</subject><subject>Cellular Senescence - physiology</subject><subject>Immunology</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Molecular modelling</subject><subject>Progenitor cells</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Senescence</subject><subject>Signal transduction</subject><subject>Stem cells</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - metabolism</subject><subject>Tendons - cytology</subject><subject>Tendons - metabolism</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kUtLxDAUhYMojuj8ADdScOOmTl7TpBtBxCeCCroOmfRm7NAmY9IK_ntTxhkfYDZJyHfPvScHoUOCTwlmchI54aTMMcU5ZbLI2Rbao5iTnEtZbv84j9A4xgVOizFMp8UuGjFKpJQc76G786dHkrW-6hvdQcw6cJV3WeygnSyDn4OrOx8yA00TswgOogFnIKv6ULv5GtfzdDlAO1Y3EcZf-z56ubp8vrjJ7x-uby_O73PDBe5yKGBK9EyCFTOBodJlYQturNHCUFpSrElBq9LYaYKkLi3VAqa2MJYOpZbto7OV7rKftVClebqgG7UMdavDh_K6Vr9fXP2q5v5dCSyxKHASOPkSCP6th9ipto6DQ-3A91FRJkpMBeciocd_0IXvg0v2BkpKWnIiE0VWlAk-xgB2MwzBaghLrcJSKSw1hKVYqjn66WJTsY4mAXQFxOXw1RC-W_-v-gmqs6EF</recordid><startdate>20200318</startdate><enddate>20200318</enddate><creator>Chen, Minhao</creator><creator>Li, Yingjuan</creator><creator>Xiao, Longfei</creator><creator>Dai, Guangchun</creator><creator>Lu, Panpan</creator><creator>Wang, Youhua</creator><creator>Rui, Yunfeng</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><scope>C6C</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200318</creationdate><title>AQP1 modulates tendon stem/progenitor cells senescence during tendon aging</title><author>Chen, Minhao ; Li, Yingjuan ; Xiao, Longfei ; Dai, Guangchun ; Lu, Panpan ; Wang, Youhua ; Rui, Yunfeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-e6e51ab8ef7b70eda96f64cfca7c22920a162d9cf5ab88a9f2a7e5f6cf2e6e5f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13/100</topic><topic>13/31</topic><topic>38/109</topic><topic>38/39</topic><topic>38/61</topic><topic>38/89</topic><topic>38/91</topic><topic>631/532/7</topic><topic>631/80/509</topic><topic>96/95</topic><topic>Aging</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Aquaporin 1</topic><topic>Aquaporin 1 - metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Cell Differentiation - physiology</topic><topic>Cell self-renewal</topic><topic>Cellular Senescence - physiology</topic><topic>Immunology</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Molecular modelling</topic><topic>Progenitor cells</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Senescence</topic><topic>Signal transduction</topic><topic>Stem cells</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - metabolism</topic><topic>Tendons - cytology</topic><topic>Tendons - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Minhao</creatorcontrib><creatorcontrib>Li, Yingjuan</creatorcontrib><creatorcontrib>Xiao, Longfei</creatorcontrib><creatorcontrib>Dai, Guangchun</creatorcontrib><creatorcontrib>Lu, Panpan</creatorcontrib><creatorcontrib>Wang, Youhua</creatorcontrib><creatorcontrib>Rui, Yunfeng</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Minhao</au><au>Li, Yingjuan</au><au>Xiao, Longfei</au><au>Dai, Guangchun</au><au>Lu, Panpan</au><au>Wang, Youhua</au><au>Rui, Yunfeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AQP1 modulates tendon stem/progenitor cells senescence during tendon aging</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-03-18</date><risdate>2020</risdate><volume>11</volume><issue>3</issue><spage>193</spage><epage>193</epage><pages>193-193</pages><artnum>193</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>The link between tendon stem/progenitor cells (TSPCs) senescence and tendon aging has been well recognized. However, the cellular and molecular mechanisms of TSPCs senescence are still not fully understood. In present study, we investigated the role of Aquaporin 1 (AQP1) in TSPCs senescence. We showed that AQP1 expression declines with age during tendon aging. In aged TSPCs, overexpression of AQP1 significantly attenuated TSPCs senescence. In addition, AQP1 overexpression also restored the age-related dysfunction of self-renewal, migration and tenogenic differentiation. Furthermore, we demonstrated that the JAK-STAT signaling pathway is activated in aged TSPCs, and AQP1 overexpression inhibited the JAK-STAT signaling pathway activation which indicated that AQP1 attenuates senescence and age-related dysfunction of TSPCs through the repression of JAK−STAT signaling pathway. Taken together, our findings demonstrated the critical role of AQP1 in the regulation of TSPCs senescence and provided a novel target for antagonizing tendon aging.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32188840</pmid><doi>10.1038/s41419-020-2386-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/100 13/31 38/109 38/39 38/61 38/89 38/91 631/532/7 631/80/509 96/95 Aging Aging - physiology Animals Antibodies Aquaporin 1 Aquaporin 1 - metabolism Biochemistry Biomedical and Life Sciences Cell Biology Cell Culture Cell Differentiation - physiology Cell self-renewal Cellular Senescence - physiology Immunology Kinases Life Sciences Male Molecular modelling Progenitor cells Rats Rats, Sprague-Dawley Senescence Signal transduction Stem cells Stem Cells - cytology Stem Cells - metabolism Tendons - cytology Tendons - metabolism |
| title | AQP1 modulates tendon stem/progenitor cells senescence during tendon aging |
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