Inducers of G-protein coupled estrogen receptor (GPER) in endometriosis: potential implications for macrophages and follicle maturation
Abstract Endometriosis is an estrogen dependent chronic inflammation and thus a condition of stress. Though the G-protein coupled estrogen receptor (GPER) has been shown to be up-regulated in ovarian endometriosis, insights involved in inducing this receptor expression are largely elusive. Therefore...
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| Veröffentlicht in: | Journal of reproductive immunology 2013-03, Vol.97 (1), p.95-103 |
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| container_title | Journal of reproductive immunology |
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| creator | Heublein, Sabine Vrekoussis, Thomas Kuhn, Christina Friese, Klaus Makrigiannakis, Antonis Mayr, Doris Lenhard, Miriam Jeschke, Udo |
| description | Abstract Endometriosis is an estrogen dependent chronic inflammation and thus a condition of stress. Though the G-protein coupled estrogen receptor (GPER) has been shown to be up-regulated in ovarian endometriosis, insights involved in inducing this receptor expression are largely elusive. Therefore, this study investigated whether stress-related factors (ACTH, prednisolone) or inflammatory factors (IL-1β, TNFα, and PGE2 ) factors may affect GPER. To further link GPER to endometriosis pathophysiology it was tracked in macrophages and follicles of endometriotic ovaries. This study found GPER expression to be modulated by stress-related hormones as well as inflammation and to be up-regulated in endometriosis-associated macrophages. At the same time, follicles of ovaries affected by endometriosis presented significantly reduced GPER positivity when compared to controls, suggesting a possible way by which endometriosis may affect folliculogenesis. The multiple roles of GPER as presented herein make it a promising future candidate for targeted molecular endometriosis treatment. |
| doi_str_mv | 10.1016/j.jri.2012.10.013 |
| format | Article |
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Though the G-protein coupled estrogen receptor (GPER) has been shown to be up-regulated in ovarian endometriosis, insights involved in inducing this receptor expression are largely elusive. Therefore, this study investigated whether stress-related factors (ACTH, prednisolone) or inflammatory factors (IL-1β, TNFα, and PGE2 ) factors may affect GPER. To further link GPER to endometriosis pathophysiology it was tracked in macrophages and follicles of endometriotic ovaries. This study found GPER expression to be modulated by stress-related hormones as well as inflammation and to be up-regulated in endometriosis-associated macrophages. At the same time, follicles of ovaries affected by endometriosis presented significantly reduced GPER positivity when compared to controls, suggesting a possible way by which endometriosis may affect folliculogenesis. The multiple roles of GPER as presented herein make it a promising future candidate for targeted molecular endometriosis treatment.</description><identifier>ISSN: 0165-0378</identifier><identifier>EISSN: 1872-7603</identifier><identifier>DOI: 10.1016/j.jri.2012.10.013</identifier><identifier>PMID: 23432876</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Adrenocorticotropic Hormone - immunology ; Adrenocorticotropic Hormone - metabolism ; Adult ; Cell Line, Tumor ; Dinoprostone - immunology ; Dinoprostone - metabolism ; Endometriosis ; Endometriosis - drug therapy ; Endometriosis - metabolism ; Endometrium - metabolism ; Endometrium - pathology ; Female ; Gene Expression Regulation - immunology ; GPER ; Humans ; Inflammation ; Inflammation - drug therapy ; Inflammation - metabolism ; Interleukin-1beta - immunology ; Interleukin-1beta - metabolism ; Macrophages ; Middle Aged ; Molecular Targeted Therapy ; Obstetrics and Gynecology ; Prednisolone - immunology ; Prednisolone - metabolism ; Receptors, Estrogen - genetics ; Receptors, Estrogen - metabolism ; Receptors, G-Protein-Coupled - genetics ; Receptors, G-Protein-Coupled - metabolism ; Stress, Psychological - drug therapy ; Stress, Psychological - metabolism ; Tumor Necrosis Factor-alpha - immunology ; Tumor Necrosis Factor-alpha - metabolism ; Young Adult</subject><ispartof>Journal of reproductive immunology, 2013-03, Vol.97 (1), p.95-103</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2013 Elsevier Ireland Ltd</rights><rights>Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-3af1d6bf9e306344133def6c9f4621214c8ea2c5a394d984b6564422990d1b5f3</citedby><cites>FETCH-LOGICAL-c474t-3af1d6bf9e306344133def6c9f4621214c8ea2c5a394d984b6564422990d1b5f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jri.2012.10.013$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23432876$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Heublein, Sabine</creatorcontrib><creatorcontrib>Vrekoussis, Thomas</creatorcontrib><creatorcontrib>Kuhn, Christina</creatorcontrib><creatorcontrib>Friese, Klaus</creatorcontrib><creatorcontrib>Makrigiannakis, Antonis</creatorcontrib><creatorcontrib>Mayr, Doris</creatorcontrib><creatorcontrib>Lenhard, Miriam</creatorcontrib><creatorcontrib>Jeschke, Udo</creatorcontrib><title>Inducers of G-protein coupled estrogen receptor (GPER) in endometriosis: potential implications for macrophages and follicle maturation</title><title>Journal of reproductive immunology</title><addtitle>J Reprod Immunol</addtitle><description>Abstract Endometriosis is an estrogen dependent chronic inflammation and thus a condition of stress. Though the G-protein coupled estrogen receptor (GPER) has been shown to be up-regulated in ovarian endometriosis, insights involved in inducing this receptor expression are largely elusive. Therefore, this study investigated whether stress-related factors (ACTH, prednisolone) or inflammatory factors (IL-1β, TNFα, and PGE2 ) factors may affect GPER. To further link GPER to endometriosis pathophysiology it was tracked in macrophages and follicles of endometriotic ovaries. This study found GPER expression to be modulated by stress-related hormones as well as inflammation and to be up-regulated in endometriosis-associated macrophages. At the same time, follicles of ovaries affected by endometriosis presented significantly reduced GPER positivity when compared to controls, suggesting a possible way by which endometriosis may affect folliculogenesis. The multiple roles of GPER as presented herein make it a promising future candidate for targeted molecular endometriosis treatment.</description><subject>Adrenocorticotropic Hormone - immunology</subject><subject>Adrenocorticotropic Hormone - metabolism</subject><subject>Adult</subject><subject>Cell Line, Tumor</subject><subject>Dinoprostone - immunology</subject><subject>Dinoprostone - metabolism</subject><subject>Endometriosis</subject><subject>Endometriosis - drug therapy</subject><subject>Endometriosis - metabolism</subject><subject>Endometrium - metabolism</subject><subject>Endometrium - pathology</subject><subject>Female</subject><subject>Gene Expression Regulation - immunology</subject><subject>GPER</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>Interleukin-1beta - immunology</subject><subject>Interleukin-1beta - metabolism</subject><subject>Macrophages</subject><subject>Middle Aged</subject><subject>Molecular Targeted Therapy</subject><subject>Obstetrics and Gynecology</subject><subject>Prednisolone - immunology</subject><subject>Prednisolone - metabolism</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Stress, Psychological - drug therapy</subject><subject>Stress, Psychological - metabolism</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Young Adult</subject><issn>0165-0378</issn><issn>1872-7603</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9ks9u1DAQhyMEotvCA3BBPpZDFo_tOBuQkFDVLpUqgfhztrz2pDg4drATpD4Br43DFg4cOFkef7-R57Or6hnQLVCQL4ftkNyWUWBlv6XAH1Qb2LWsbiXlD6tNYZqa8nZ3Up3mPFAKLe3gcXXCuOBs18pN9fM62MVgyiT2ZF9PKc7oAjFxmTxagnlO8RYDSWhwmmMi5_sPlx9fkMJgsHHEObmYXX5FppIMs9OeuHHyzujZxZBJXzKjNilOX_UtZqKDLTVfAI_lYF7Sb_BJ9ajXPuPT-_Ws-nJ1-fniXX3zfn998famNqIVc811D1Ye-g45lVwI4NxiL03XC8mAgTA71Mw0mnfCdjtxkI0UgrGuoxYOTc_PqvNj3zLp96WMp0aXDXqvA8YlK-DApATeNgWFI1oun3PCXk3JjTrdKaBq9a8GVfyr1f9aKv5L5vl9--Uwov2b-CO8AK-PAJYhfzhMKhuHwaB1RfGsbHT_bf_mn7TxLhTX_hveYR7ikkKxp0Blpqj6tH6A9f2BUSpFx_kvQ3KsWg</recordid><startdate>20130301</startdate><enddate>20130301</enddate><creator>Heublein, Sabine</creator><creator>Vrekoussis, Thomas</creator><creator>Kuhn, Christina</creator><creator>Friese, Klaus</creator><creator>Makrigiannakis, Antonis</creator><creator>Mayr, Doris</creator><creator>Lenhard, Miriam</creator><creator>Jeschke, Udo</creator><general>Elsevier Ireland Ltd</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>7X8</scope></search><sort><creationdate>20130301</creationdate><title>Inducers of G-protein coupled estrogen receptor (GPER) in endometriosis: potential implications for macrophages and follicle maturation</title><author>Heublein, Sabine ; Vrekoussis, Thomas ; Kuhn, Christina ; Friese, Klaus ; Makrigiannakis, Antonis ; Mayr, Doris ; Lenhard, Miriam ; Jeschke, Udo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-3af1d6bf9e306344133def6c9f4621214c8ea2c5a394d984b6564422990d1b5f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adrenocorticotropic Hormone - immunology</topic><topic>Adrenocorticotropic Hormone - metabolism</topic><topic>Adult</topic><topic>Cell Line, Tumor</topic><topic>Dinoprostone - immunology</topic><topic>Dinoprostone - metabolism</topic><topic>Endometriosis</topic><topic>Endometriosis - drug therapy</topic><topic>Endometriosis - metabolism</topic><topic>Endometrium - metabolism</topic><topic>Endometrium - pathology</topic><topic>Female</topic><topic>Gene Expression Regulation - immunology</topic><topic>GPER</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - metabolism</topic><topic>Interleukin-1beta - immunology</topic><topic>Interleukin-1beta - metabolism</topic><topic>Macrophages</topic><topic>Middle Aged</topic><topic>Molecular Targeted Therapy</topic><topic>Obstetrics and Gynecology</topic><topic>Prednisolone - immunology</topic><topic>Prednisolone - metabolism</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Receptors, G-Protein-Coupled - genetics</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>Stress, Psychological - drug therapy</topic><topic>Stress, Psychological - metabolism</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Heublein, Sabine</creatorcontrib><creatorcontrib>Vrekoussis, Thomas</creatorcontrib><creatorcontrib>Kuhn, Christina</creatorcontrib><creatorcontrib>Friese, Klaus</creatorcontrib><creatorcontrib>Makrigiannakis, Antonis</creatorcontrib><creatorcontrib>Mayr, Doris</creatorcontrib><creatorcontrib>Lenhard, Miriam</creatorcontrib><creatorcontrib>Jeschke, Udo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of reproductive immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Heublein, Sabine</au><au>Vrekoussis, Thomas</au><au>Kuhn, Christina</au><au>Friese, Klaus</au><au>Makrigiannakis, Antonis</au><au>Mayr, Doris</au><au>Lenhard, Miriam</au><au>Jeschke, Udo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inducers of G-protein coupled estrogen receptor (GPER) in endometriosis: potential implications for macrophages and follicle maturation</atitle><jtitle>Journal of reproductive immunology</jtitle><addtitle>J Reprod Immunol</addtitle><date>2013-03-01</date><risdate>2013</risdate><volume>97</volume><issue>1</issue><spage>95</spage><epage>103</epage><pages>95-103</pages><issn>0165-0378</issn><eissn>1872-7603</eissn><abstract>Abstract Endometriosis is an estrogen dependent chronic inflammation and thus a condition of stress. Though the G-protein coupled estrogen receptor (GPER) has been shown to be up-regulated in ovarian endometriosis, insights involved in inducing this receptor expression are largely elusive. Therefore, this study investigated whether stress-related factors (ACTH, prednisolone) or inflammatory factors (IL-1β, TNFα, and PGE2 ) factors may affect GPER. To further link GPER to endometriosis pathophysiology it was tracked in macrophages and follicles of endometriotic ovaries. This study found GPER expression to be modulated by stress-related hormones as well as inflammation and to be up-regulated in endometriosis-associated macrophages. At the same time, follicles of ovaries affected by endometriosis presented significantly reduced GPER positivity when compared to controls, suggesting a possible way by which endometriosis may affect folliculogenesis. 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| ispartof | Journal of reproductive immunology, 2013-03, Vol.97 (1), p.95-103 |
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| subjects | Adrenocorticotropic Hormone - immunology Adrenocorticotropic Hormone - metabolism Adult Cell Line, Tumor Dinoprostone - immunology Dinoprostone - metabolism Endometriosis Endometriosis - drug therapy Endometriosis - metabolism Endometrium - metabolism Endometrium - pathology Female Gene Expression Regulation - immunology GPER Humans Inflammation Inflammation - drug therapy Inflammation - metabolism Interleukin-1beta - immunology Interleukin-1beta - metabolism Macrophages Middle Aged Molecular Targeted Therapy Obstetrics and Gynecology Prednisolone - immunology Prednisolone - metabolism Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Receptors, G-Protein-Coupled - genetics Receptors, G-Protein-Coupled - metabolism Stress, Psychological - drug therapy Stress, Psychological - metabolism Tumor Necrosis Factor-alpha - immunology Tumor Necrosis Factor-alpha - metabolism Young Adult |
| title | Inducers of G-protein coupled estrogen receptor (GPER) in endometriosis: potential implications for macrophages and follicle maturation |
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