Regulation of the PI3K/Akt pathway during decidualization of endometrial stromal cells
Infertility is constantly increasing in Canada, where 16% of Canadian couples are experiencing difficulty conceiving. It is thought that infertility can emanate from the dysregulated communication between the embryo and the maternal endometrium. In order to allow for this window of implantation to b...
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| creator | Fabi, François Grenier, Kathy Parent, Sophie Adam, Pascal Tardif, Laurence Leblanc, Valérie Asselin, Eric |
| description | Infertility is constantly increasing in Canada, where 16% of Canadian couples are experiencing difficulty conceiving. It is thought that infertility can emanate from the dysregulated communication between the embryo and the maternal endometrium. In order to allow for this window of implantation to be open at the right moment, endometrial stromal cells proliferate and differentiate by a mechanism called decidualization. Intracellular and molecular mechanisms involved in the regulation of apoptosis and cell proliferation during decidualization of the endometrium are yet to be fully understood. It has been well demonstrated previously that Akt is importantly involved in cell survival and glycogen synthesis. Akt1, Akt2 and Akt3 isoforms have distinct physiological roles; this could also be the case during decidualization and pregnancy. The aim of this study is to investigate the regulation of PI3K/Akt pathway during the decidualization process of endometrial stromal cells. Expression of Akt isoforms, Akt activity (phospho-Akt), pIκB and substrates of Akt during decidualization were measured. To our knowledge, these results are the first to suggest a decrease in levels of Akt isoforms as well as a downregulation of Akt activity in the process of decidualization of human endometrial stromal cells. We also uncovered that decidualization induced nuclear localization of p65 through the phosphorylation of IκB, its inhibitory subunit; however, Par-4, a recently uncovered regulator of cell differentiation, was displaced from the nucleus upon decidualization. Our results also suggest that HIESC cells exhibit decreased motility during decidualization and that PI3K pathway inhibition could be involved in this process. Finally, we demonstrate that specific Akt isoforms present unique effects on the successful induction of decidualization. Further analyses will involve investigations to understand the precise signaling mechanisms by which this pathway is regulated. |
| doi_str_mv | 10.1371/journal.pone.0177387 |
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It is thought that infertility can emanate from the dysregulated communication between the embryo and the maternal endometrium. In order to allow for this window of implantation to be open at the right moment, endometrial stromal cells proliferate and differentiate by a mechanism called decidualization. Intracellular and molecular mechanisms involved in the regulation of apoptosis and cell proliferation during decidualization of the endometrium are yet to be fully understood. It has been well demonstrated previously that Akt is importantly involved in cell survival and glycogen synthesis. Akt1, Akt2 and Akt3 isoforms have distinct physiological roles; this could also be the case during decidualization and pregnancy. The aim of this study is to investigate the regulation of PI3K/Akt pathway during the decidualization process of endometrial stromal cells. Expression of Akt isoforms, Akt activity (phospho-Akt), pIκB and substrates of Akt during decidualization were measured. To our knowledge, these results are the first to suggest a decrease in levels of Akt isoforms as well as a downregulation of Akt activity in the process of decidualization of human endometrial stromal cells. We also uncovered that decidualization induced nuclear localization of p65 through the phosphorylation of IκB, its inhibitory subunit; however, Par-4, a recently uncovered regulator of cell differentiation, was displaced from the nucleus upon decidualization. Our results also suggest that HIESC cells exhibit decreased motility during decidualization and that PI3K pathway inhibition could be involved in this process. Finally, we demonstrate that specific Akt isoforms present unique effects on the successful induction of decidualization. Further analyses will involve investigations to understand the precise signaling mechanisms by which this pathway is regulated.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0177387</identifier><identifier>PMID: 28475617</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Phosphatidylinositol 3-kinase ; Actin ; Activation ; ADAM protein ; Adenosine monophosphate ; AKT protein ; AKT1 protein ; AKT2 protein ; Amino acids ; AMP ; Analogs ; Angiogenesis ; Apoptosis ; Biochemical characteristics ; Biochemistry ; Biology ; Biology and Life Sciences ; Brain ; c-Met protein ; C-Terminus ; Cancer ; Catalytic converters ; Cell cycle ; Cell differentiation ; Cell growth ; Cell Line ; Cell proliferation ; Cell Survival - physiology ; Cellular signal transduction ; Compensation ; Diabetes mellitus ; Differentiation (biology) ; Embryos ; Endometrium ; Endometrium - cytology ; Endometrium - metabolism ; Female ; Glucose ; Growth factors ; Homology ; Humans ; Immune system ; Infertility ; Inflammation ; Insulin ; Isoforms ; Kinases ; Lipids ; Mammary gland ; Markers ; Medical research ; Medicine and Health Sciences ; Menstrual cycle ; Metabolism ; Mice ; Morphology ; Motility ; Mutation ; pH effects ; Pharmacology ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Placenta ; Pregnancy ; Prolactin - metabolism ; Proteasome Endopeptidase Complex - metabolism ; Protein-serine/threonine kinase ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Reproductive cycle ; Secretions ; Signal Transduction - physiology ; Stromal Cells - cytology ; Stromal Cells - metabolism ; Survival</subject><ispartof>PloS one, 2017-05, Vol.12 (5), p.e0177387-e0177387</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Fabi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Fabi et al 2017 Fabi et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-aa4ae50f43ac29edc9e860e9ba687f72e0acdd89b2a66cafcaf5943db61592d83</citedby><cites>FETCH-LOGICAL-c758t-aa4ae50f43ac29edc9e860e9ba687f72e0acdd89b2a66cafcaf5943db61592d83</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/PMC5419658/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5419658/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28475617$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Yang, Zeng-Ming</contributor><creatorcontrib>Fabi, François</creatorcontrib><creatorcontrib>Grenier, Kathy</creatorcontrib><creatorcontrib>Parent, Sophie</creatorcontrib><creatorcontrib>Adam, Pascal</creatorcontrib><creatorcontrib>Tardif, Laurence</creatorcontrib><creatorcontrib>Leblanc, Valérie</creatorcontrib><creatorcontrib>Asselin, Eric</creatorcontrib><title>Regulation of the PI3K/Akt pathway during decidualization of endometrial stromal cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Infertility is constantly increasing in Canada, where 16% of Canadian couples are experiencing difficulty conceiving. It is thought that infertility can emanate from the dysregulated communication between the embryo and the maternal endometrium. In order to allow for this window of implantation to be open at the right moment, endometrial stromal cells proliferate and differentiate by a mechanism called decidualization. Intracellular and molecular mechanisms involved in the regulation of apoptosis and cell proliferation during decidualization of the endometrium are yet to be fully understood. It has been well demonstrated previously that Akt is importantly involved in cell survival and glycogen synthesis. Akt1, Akt2 and Akt3 isoforms have distinct physiological roles; this could also be the case during decidualization and pregnancy. The aim of this study is to investigate the regulation of PI3K/Akt pathway during the decidualization process of endometrial stromal cells. Expression of Akt isoforms, Akt activity (phospho-Akt), pIκB and substrates of Akt during decidualization were measured. To our knowledge, these results are the first to suggest a decrease in levels of Akt isoforms as well as a downregulation of Akt activity in the process of decidualization of human endometrial stromal cells. We also uncovered that decidualization induced nuclear localization of p65 through the phosphorylation of IκB, its inhibitory subunit; however, Par-4, a recently uncovered regulator of cell differentiation, was displaced from the nucleus upon decidualization. Our results also suggest that HIESC cells exhibit decreased motility during decidualization and that PI3K pathway inhibition could be involved in this process. Finally, we demonstrate that specific Akt isoforms present unique effects on the successful induction of decidualization. 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physiology</subject><subject>Cellular signal transduction</subject><subject>Compensation</subject><subject>Diabetes mellitus</subject><subject>Differentiation (biology)</subject><subject>Embryos</subject><subject>Endometrium</subject><subject>Endometrium - cytology</subject><subject>Endometrium - metabolism</subject><subject>Female</subject><subject>Glucose</subject><subject>Growth factors</subject><subject>Homology</subject><subject>Humans</subject><subject>Immune system</subject><subject>Infertility</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Isoforms</subject><subject>Kinases</subject><subject>Lipids</subject><subject>Mammary gland</subject><subject>Markers</subject><subject>Medical research</subject><subject>Medicine and Health Sciences</subject><subject>Menstrual cycle</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Morphology</subject><subject>Motility</subject><subject>Mutation</subject><subject>pH effects</subject><subject>Pharmacology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Placenta</subject><subject>Pregnancy</subject><subject>Prolactin - metabolism</subject><subject>Proteasome Endopeptidase Complex - metabolism</subject><subject>Protein-serine/threonine kinase</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Reproductive cycle</subject><subject>Secretions</subject><subject>Signal Transduction - physiology</subject><subject>Stromal Cells - cytology</subject><subject>Stromal Cells - metabolism</subject><subject>Survival</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1v0zAUhiMEYmPwDxBEQkJw0c6O4zi-QaomPiomDQ3YrXXqOKmLE3e2A4xfj7NmVYN2gWzJlv2c9xwfv0nyHKM5JgyfbmzvOjDzre3UHGHGSMkeJMeYk2xWZIg8PNgfJU-83yBESVkUj5OjrMwZLTA7Tq4uVdMbCNp2qa3TsFbplyX5fLr4EdIthPUvuEmr3umuSSslddWD0X_2uOoq26rgNJjUB2fbuEpljH-aPKrBePVsXE-S7x_efzv7NDu_-Lg8W5zPJKNlmAHkoCiqcwIy46qSXJUFUnwFRclqlikEsqpKvsqgKCTUcVKek2pVYMqzqiQnycud7tZYL8aWeIFLTguGKMojsdwRlYWN2DrdgrsRFrS4PbCuEeCClkYJxFHJMCCKpcpJpjiXkGeAFAVJVpBFrXdjtn7VxmpVFxyYiej0ptNr0difguaYF3Qo980o4Ox1r3wQrfZDw6BTtr-tu0CEs4xG9NU_6P2vG6kG4gN0V9uYVw6iYpFzjBmmjEdqfg8VR6VaLaN_ah3PJwFvJwGRCep3aKD3Xiy_Xv4_e3E1ZV8fsGsFJqy9Nf3gJz8F8x0onfXeqXrfZIzEYP-7bojB_mK0fwx7cfhB-6A7v5O_ONsAqA</recordid><startdate>20170505</startdate><enddate>20170505</enddate><creator>Fabi, François</creator><creator>Grenier, Kathy</creator><creator>Parent, Sophie</creator><creator>Adam, Pascal</creator><creator>Tardif, Laurence</creator><creator>Leblanc, Valérie</creator><creator>Asselin, Eric</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20170505</creationdate><title>Regulation of the PI3K/Akt pathway during decidualization of endometrial stromal cells</title><author>Fabi, François ; Grenier, Kathy ; Parent, Sophie ; Adam, Pascal ; Tardif, Laurence ; Leblanc, Valérie ; Asselin, Eric</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-aa4ae50f43ac29edc9e860e9ba687f72e0acdd89b2a66cafcaf5943db61592d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Actin</topic><topic>Activation</topic><topic>ADAM protein</topic><topic>Adenosine monophosphate</topic><topic>AKT protein</topic><topic>AKT1 protein</topic><topic>AKT2 protein</topic><topic>Amino acids</topic><topic>AMP</topic><topic>Analogs</topic><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Biochemical characteristics</topic><topic>Biochemistry</topic><topic>Biology</topic><topic>Biology and Life Sciences</topic><topic>Brain</topic><topic>c-Met protein</topic><topic>C-Terminus</topic><topic>Cancer</topic><topic>Catalytic converters</topic><topic>Cell cycle</topic><topic>Cell differentiation</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cell proliferation</topic><topic>Cell Survival - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fabi, François</au><au>Grenier, Kathy</au><au>Parent, Sophie</au><au>Adam, Pascal</au><au>Tardif, Laurence</au><au>Leblanc, Valérie</au><au>Asselin, Eric</au><au>Yang, Zeng-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of the PI3K/Akt pathway during decidualization of endometrial stromal cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-05-05</date><risdate>2017</risdate><volume>12</volume><issue>5</issue><spage>e0177387</spage><epage>e0177387</epage><pages>e0177387-e0177387</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Infertility is constantly increasing in Canada, where 16% of Canadian couples are experiencing difficulty conceiving. It is thought that infertility can emanate from the dysregulated communication between the embryo and the maternal endometrium. In order to allow for this window of implantation to be open at the right moment, endometrial stromal cells proliferate and differentiate by a mechanism called decidualization. Intracellular and molecular mechanisms involved in the regulation of apoptosis and cell proliferation during decidualization of the endometrium are yet to be fully understood. It has been well demonstrated previously that Akt is importantly involved in cell survival and glycogen synthesis. Akt1, Akt2 and Akt3 isoforms have distinct physiological roles; this could also be the case during decidualization and pregnancy. The aim of this study is to investigate the regulation of PI3K/Akt pathway during the decidualization process of endometrial stromal cells. Expression of Akt isoforms, Akt activity (phospho-Akt), pIκB and substrates of Akt during decidualization were measured. To our knowledge, these results are the first to suggest a decrease in levels of Akt isoforms as well as a downregulation of Akt activity in the process of decidualization of human endometrial stromal cells. We also uncovered that decidualization induced nuclear localization of p65 through the phosphorylation of IκB, its inhibitory subunit; however, Par-4, a recently uncovered regulator of cell differentiation, was displaced from the nucleus upon decidualization. Our results also suggest that HIESC cells exhibit decreased motility during decidualization and that PI3K pathway inhibition could be involved in this process. Finally, we demonstrate that specific Akt isoforms present unique effects on the successful induction of decidualization. Further analyses will involve investigations to understand the precise signaling mechanisms by which this pathway is regulated.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28475617</pmid><doi>10.1371/journal.pone.0177387</doi><tpages>e0177387</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2017-05, Vol.12 (5), p.e0177387-e0177387 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1895670504 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science website; Free E-Journal (出版社公開部分のみ）; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 1-Phosphatidylinositol 3-kinase Actin Activation ADAM protein Adenosine monophosphate AKT protein AKT1 protein AKT2 protein Amino acids AMP Analogs Angiogenesis Apoptosis Biochemical characteristics Biochemistry Biology Biology and Life Sciences Brain c-Met protein C-Terminus Cancer Catalytic converters Cell cycle Cell differentiation Cell growth Cell Line Cell proliferation Cell Survival - physiology Cellular signal transduction Compensation Diabetes mellitus Differentiation (biology) Embryos Endometrium Endometrium - cytology Endometrium - metabolism Female Glucose Growth factors Homology Humans Immune system Infertility Inflammation Insulin Isoforms Kinases Lipids Mammary gland Markers Medical research Medicine and Health Sciences Menstrual cycle Metabolism Mice Morphology Motility Mutation pH effects Pharmacology Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Placenta Pregnancy Prolactin - metabolism Proteasome Endopeptidase Complex - metabolism Protein-serine/threonine kinase Proteins Proto-Oncogene Proteins c-akt - metabolism Reproductive cycle Secretions Signal Transduction - physiology Stromal Cells - cytology Stromal Cells - metabolism Survival |
| title | Regulation of the PI3K/Akt pathway during decidualization of endometrial stromal cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T06%3A00%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Regulation%20of%20the%20PI3K/Akt%20pathway%20during%20decidualization%20of%20endometrial%20stromal%20cells&rft.jtitle=PloS%20one&rft.au=Fabi,%20Fran%C3%A7ois&rft.date=2017-05-05&rft.volume=12&rft.issue=5&rft.spage=e0177387&rft.epage=e0177387&rft.pages=e0177387-e0177387&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0177387&rft_dat=%3Cgale_plos_%3EA491171579%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1895670504&rft_id=info:pmid/28475617&rft_galeid=A491171579&rft_doaj_id=oai_doaj_org_article_090871a051ce432e99ca42a0e5ac3ba2&rfr_iscdi=true |