Restraint-induced corticotrophin-releasing hormone elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the fas/fasl system
Mechanisms by which psychological stress damages oocytes are largely undetermined. Although a previous study showed that the stress-induced corticotrophin-releasing hormone (CRH) elevation impaired oocyte competence by triggering apoptosis of ovarian cells, how CRH causes apoptosis in ovarian cells...
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| Veröffentlicht in: | Biology of reproduction 2018-10, Vol.99 (4), p.828-837 |
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| creator | Li, Chuan-Yong Li, Zhi-Bin Kong, Qiao-Qiao Han, Xiao Xiao, Bin Li, Xiao Chang, Zhong-Le Tan, Jing-He |
| description | Mechanisms by which psychological stress damages oocytes are largely undetermined. Although a previous study showed that the stress-induced corticotrophin-releasing hormone (CRH) elevation impaired oocyte competence by triggering apoptosis of ovarian cells, how CRH causes apoptosis in ovarian cells and oocytes is unknown. In this study, we have examined the hypothesis that restraint stress (RS)-induced CRH elevation triggers apoptosis of ovarian cells and impairs oocyte competence through activating the Fas/FasL system. The results showed that RS of female mice impaired oocyte competence, enhanced expression of CRH and CRH receptor (CRH-R) in the ovary, and induced apoptosis while activating the Fas/FasL system in mural granulosa cells (MGCs) and oocytes. Injecting mice with CRH-R1 antagonist antalarmin significantly alleviated the adverse effect of RS on oocyte developmental potential. Treatment of cultured MGCs recapitulated the effects of CRH and antalarmin on apoptosis and Fas/FasL expression in MGCs. Silencing FasL gene by RNA interference in cultured MGCs further confirmed the involvement of the Fas/FasL system in the CRH triggered apoptosis of ovarian cells. It is concluded that the RS-induced CRH elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the Fas/FasL system. Summary Sentence Both in vivo and in vitro trials demonstrated that the restraint stress-induced CRH elevation in female mice triggered apoptosis of ovarian cells and impaired oocyte competence via activation of the Fas/FasL system. |
| doi_str_mv | 10.1093/biolre/ioy091 |
| format | Article |
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Although a previous study showed that the stress-induced corticotrophin-releasing hormone (CRH) elevation impaired oocyte competence by triggering apoptosis of ovarian cells, how CRH causes apoptosis in ovarian cells and oocytes is unknown. In this study, we have examined the hypothesis that restraint stress (RS)-induced CRH elevation triggers apoptosis of ovarian cells and impairs oocyte competence through activating the Fas/FasL system. The results showed that RS of female mice impaired oocyte competence, enhanced expression of CRH and CRH receptor (CRH-R) in the ovary, and induced apoptosis while activating the Fas/FasL system in mural granulosa cells (MGCs) and oocytes. Injecting mice with CRH-R1 antagonist antalarmin significantly alleviated the adverse effect of RS on oocyte developmental potential. Treatment of cultured MGCs recapitulated the effects of CRH and antalarmin on apoptosis and Fas/FasL expression in MGCs. Silencing FasL gene by RNA interference in cultured MGCs further confirmed the involvement of the Fas/FasL system in the CRH triggered apoptosis of ovarian cells. It is concluded that the RS-induced CRH elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the Fas/FasL system. Summary Sentence Both in vivo and in vitro trials demonstrated that the restraint stress-induced CRH elevation in female mice triggered apoptosis of ovarian cells and impaired oocyte competence via activation of the Fas/FasL system.</description><identifier>ISSN: 0006-3363</identifier><identifier>EISSN: 1529-7268</identifier><identifier>DOI: 10.1093/biolre/ioy091</identifier><identifier>PMID: 29668880</identifier><language>eng</language><publisher>United States: Society for the Study of Reproduction</publisher><subject>Apoptosis ; CRH ; Fas/FasL ; oocyte competence ; psychological stress</subject><ispartof>Biology of reproduction, 2018-10, Vol.99 (4), p.828-837</ispartof><rights>The Author(s) 2018. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com journals.permissions@oup.com</rights><rights>The Author(s) 2018. Published by Oxford University Press on behalf of Society for the Study of Reproduction. 2018</rights><rights>The Author(s) 2018. Published by Oxford University Press on behalf of Society for the Study of Reproduction.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b523t-b72526e09523e22499c5811d56df2fd439e3bc0c55192c63cd3483d505359b083</citedby><cites>FETCH-LOGICAL-b523t-b72526e09523e22499c5811d56df2fd439e3bc0c55192c63cd3483d505359b083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1584,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29668880$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Chuan-Yong</creatorcontrib><creatorcontrib>Li, Zhi-Bin</creatorcontrib><creatorcontrib>Kong, Qiao-Qiao</creatorcontrib><creatorcontrib>Han, Xiao</creatorcontrib><creatorcontrib>Xiao, Bin</creatorcontrib><creatorcontrib>Li, Xiao</creatorcontrib><creatorcontrib>Chang, Zhong-Le</creatorcontrib><creatorcontrib>Tan, Jing-He</creatorcontrib><title>Restraint-induced corticotrophin-releasing hormone elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the fas/fasl system</title><title>Biology of reproduction</title><addtitle>Biol Reprod</addtitle><description>Mechanisms by which psychological stress damages oocytes are largely undetermined. Although a previous study showed that the stress-induced corticotrophin-releasing hormone (CRH) elevation impaired oocyte competence by triggering apoptosis of ovarian cells, how CRH causes apoptosis in ovarian cells and oocytes is unknown. In this study, we have examined the hypothesis that restraint stress (RS)-induced CRH elevation triggers apoptosis of ovarian cells and impairs oocyte competence through activating the Fas/FasL system. The results showed that RS of female mice impaired oocyte competence, enhanced expression of CRH and CRH receptor (CRH-R) in the ovary, and induced apoptosis while activating the Fas/FasL system in mural granulosa cells (MGCs) and oocytes. Injecting mice with CRH-R1 antagonist antalarmin significantly alleviated the adverse effect of RS on oocyte developmental potential. Treatment of cultured MGCs recapitulated the effects of CRH and antalarmin on apoptosis and Fas/FasL expression in MGCs. Silencing FasL gene by RNA interference in cultured MGCs further confirmed the involvement of the Fas/FasL system in the CRH triggered apoptosis of ovarian cells. It is concluded that the RS-induced CRH elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the Fas/FasL system. Summary Sentence Both in vivo and in vitro trials demonstrated that the restraint stress-induced CRH elevation in female mice triggered apoptosis of ovarian cells and impaired oocyte competence via activation of the Fas/FasL system.</description><subject>Apoptosis</subject><subject>CRH</subject><subject>Fas/FasL</subject><subject>oocyte competence</subject><subject>psychological stress</subject><issn>0006-3363</issn><issn>1529-7268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkcuKFDEUhoM4OO3o0q0E3AhS07lUUslSBm8wMCC6LlKpU90ZqpIySTX0-_igk6ZaBTe9CCEn3_nP5UfoDSW3lGi-7VwYI2xdOBJNn6ENFUxXDZPqOdoQQmTFueTX6GVKj4TQmjP-Al0zLaVSimzQ7--QcjTO58r5frHQYxtidjbkGOa981WEEUxyfof3IU7BAy6Bg8kueJyj2-0gJmzmMOeQXMJhwOFgojMeWxjH8uV77KbZuIKFYI8ZSoVphgzeAj44g43N7ixYsvMe8GDStpwRp2PKML1CV4MZE7w-3zfo5-dPP-6-VvcPX77dfbyvOsF4rrqGCSaB6PICxmqtrVCU9kL2Axv6mmvgnSVWCKqZldz2vFa8F0RwoTui-A16v-rOMfxaymLayaXTFMZDWFLLCGuEkpLTgr77D30MS_Slu5ZRXTe1asgFSglNS_0TVa2UjSGlCEM7RzeZeGwpaU8mt6vJ7Wpy4d-eVZdugv4v_cfVf3OEZb6o9WFFS7h4e4F-AhKlxBM</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Li, Chuan-Yong</creator><creator>Li, Zhi-Bin</creator><creator>Kong, Qiao-Qiao</creator><creator>Han, Xiao</creator><creator>Xiao, Bin</creator><creator>Li, Xiao</creator><creator>Chang, Zhong-Le</creator><creator>Tan, Jing-He</creator><general>Society for the Study of Reproduction</general><general>Oxford University Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20181001</creationdate><title>Restraint-induced corticotrophin-releasing hormone elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the fas/fasl system</title><author>Li, Chuan-Yong ; Li, Zhi-Bin ; Kong, Qiao-Qiao ; Han, Xiao ; Xiao, Bin ; Li, Xiao ; Chang, Zhong-Le ; Tan, Jing-He</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b523t-b72526e09523e22499c5811d56df2fd439e3bc0c55192c63cd3483d505359b083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Apoptosis</topic><topic>CRH</topic><topic>Fas/FasL</topic><topic>oocyte competence</topic><topic>psychological stress</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Chuan-Yong</creatorcontrib><creatorcontrib>Li, Zhi-Bin</creatorcontrib><creatorcontrib>Kong, Qiao-Qiao</creatorcontrib><creatorcontrib>Han, Xiao</creatorcontrib><creatorcontrib>Xiao, Bin</creatorcontrib><creatorcontrib>Li, Xiao</creatorcontrib><creatorcontrib>Chang, Zhong-Le</creatorcontrib><creatorcontrib>Tan, Jing-He</creatorcontrib><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>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</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>Engineering Research Database</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>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biology of reproduction</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Chuan-Yong</au><au>Li, Zhi-Bin</au><au>Kong, Qiao-Qiao</au><au>Han, Xiao</au><au>Xiao, Bin</au><au>Li, Xiao</au><au>Chang, Zhong-Le</au><au>Tan, Jing-He</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Restraint-induced corticotrophin-releasing hormone elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the fas/fasl system</atitle><jtitle>Biology of reproduction</jtitle><addtitle>Biol Reprod</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>99</volume><issue>4</issue><spage>828</spage><epage>837</epage><pages>828-837</pages><issn>0006-3363</issn><eissn>1529-7268</eissn><abstract>Mechanisms by which psychological stress damages oocytes are largely undetermined. Although a previous study showed that the stress-induced corticotrophin-releasing hormone (CRH) elevation impaired oocyte competence by triggering apoptosis of ovarian cells, how CRH causes apoptosis in ovarian cells and oocytes is unknown. In this study, we have examined the hypothesis that restraint stress (RS)-induced CRH elevation triggers apoptosis of ovarian cells and impairs oocyte competence through activating the Fas/FasL system. The results showed that RS of female mice impaired oocyte competence, enhanced expression of CRH and CRH receptor (CRH-R) in the ovary, and induced apoptosis while activating the Fas/FasL system in mural granulosa cells (MGCs) and oocytes. Injecting mice with CRH-R1 antagonist antalarmin significantly alleviated the adverse effect of RS on oocyte developmental potential. Treatment of cultured MGCs recapitulated the effects of CRH and antalarmin on apoptosis and Fas/FasL expression in MGCs. Silencing FasL gene by RNA interference in cultured MGCs further confirmed the involvement of the Fas/FasL system in the CRH triggered apoptosis of ovarian cells. It is concluded that the RS-induced CRH elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the Fas/FasL system. Summary Sentence Both in vivo and in vitro trials demonstrated that the restraint stress-induced CRH elevation in female mice triggered apoptosis of ovarian cells and impaired oocyte competence via activation of the Fas/FasL system.</abstract><cop>United States</cop><pub>Society for the Study of Reproduction</pub><pmid>29668880</pmid><doi>10.1093/biolre/ioy091</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis CRH Fas/FasL oocyte competence psychological stress |
| title | Restraint-induced corticotrophin-releasing hormone elevation triggers apoptosis of ovarian cells and impairs oocyte competence via activation of the fas/fasl system |
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