Advantages in Wound Healing Process in Female Mice Require Upregulation A2A-Mediated Angiogenesis under the Stimulation of 17β-Estradiol
Estrogenic steroids and adenosine A2A receptors promote the wound healing and angiogenesis processes. However, so far, it is unclear whether estrogen may regulate the expression and pro-angiogenic activity of A2A receptors. Using in vivo analyses, we showed that female wild type (WT) mice have a mor...
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Veröffentlicht in: | International journal of molecular sciences 2020-09, Vol.21 (19), p.7145 |
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creator | Troncoso, Felipe Herlitz, Kurt Acurio, Jesenia Aguayo, Claudio Guevara, Katherine Castro, Fidel Ovidio Godoy, Alejandro S. San Martin, Sebastian Escudero, Carlos |
description | Estrogenic steroids and adenosine A2A receptors promote the wound healing and angiogenesis processes. However, so far, it is unclear whether estrogen may regulate the expression and pro-angiogenic activity of A2A receptors. Using in vivo analyses, we showed that female wild type (WT) mice have a more rapid wound healing process than female or male A2A-deficient mice (A2AKO) mice. We also found that pulmonary endothelial cells (mPEC) isolated from female WT mice showed higher expression of A2A receptor than mPEC from male WT mice. mPEC from female WT mice were more sensitive to A2A-mediated pro-angiogenic response, suggesting an ER and A2A crosstalk, which was confirmed using cells isolated from A2AKO. In those female cells, 17β-estradiol potentiated A2A-mediated cell proliferation, an effect that was inhibited by selective antagonists of estrogen receptors (ER), ERα, and ERβ. Therefore, estrogen regulates the expression and/or pro-angiogenic activity of A2A adenosine receptors, likely involving activation of ERα and ERβ receptors. Sexual dimorphism in wound healing observed in the A2AKO mice process reinforces the functional crosstalk between ER and A2A receptors. |
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However, so far, it is unclear whether estrogen may regulate the expression and pro-angiogenic activity of A2A receptors. Using in vivo analyses, we showed that female wild type (WT) mice have a more rapid wound healing process than female or male A2A-deficient mice (A2AKO) mice. We also found that pulmonary endothelial cells (mPEC) isolated from female WT mice showed higher expression of A2A receptor than mPEC from male WT mice. mPEC from female WT mice were more sensitive to A2A-mediated pro-angiogenic response, suggesting an ER and A2A crosstalk, which was confirmed using cells isolated from A2AKO. In those female cells, 17β-estradiol potentiated A2A-mediated cell proliferation, an effect that was inhibited by selective antagonists of estrogen receptors (ER), ERα, and ERβ. Therefore, estrogen regulates the expression and/or pro-angiogenic activity of A2A adenosine receptors, likely involving activation of ERα and ERβ receptors. Sexual dimorphism in wound healing observed in the A2AKO mice process reinforces the functional crosstalk between ER and A2A receptors.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms21197145</identifier><identifier>PMID: 32998232</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>17β-Estradiol ; Adenosine ; Adenosine A2A receptors ; Angiogenesis ; Cell growth ; Cell proliferation ; Crosstalk ; Endothelial cells ; Estrogen receptors ; Estrogens ; Rodents ; Sexual dimorphism ; Steroid hormones ; Vascular endothelial growth factor ; Wound healing ; Xenoestrogens</subject><ispartof>International journal of molecular sciences, 2020-09, Vol.21 (19), p.7145</ispartof><rights>2020 by the authors. Licensee MDPI, Basel, Switzerland. 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However, so far, it is unclear whether estrogen may regulate the expression and pro-angiogenic activity of A2A receptors. Using in vivo analyses, we showed that female wild type (WT) mice have a more rapid wound healing process than female or male A2A-deficient mice (A2AKO) mice. We also found that pulmonary endothelial cells (mPEC) isolated from female WT mice showed higher expression of A2A receptor than mPEC from male WT mice. mPEC from female WT mice were more sensitive to A2A-mediated pro-angiogenic response, suggesting an ER and A2A crosstalk, which was confirmed using cells isolated from A2AKO. In those female cells, 17β-estradiol potentiated A2A-mediated cell proliferation, an effect that was inhibited by selective antagonists of estrogen receptors (ER), ERα, and ERβ. Therefore, estrogen regulates the expression and/or pro-angiogenic activity of A2A adenosine receptors, likely involving activation of ERα and ERβ receptors. Sexual dimorphism in wound healing observed in the A2AKO mice process reinforces the functional crosstalk between ER and A2A receptors.</description><subject>17β-Estradiol</subject><subject>Adenosine</subject><subject>Adenosine A2A receptors</subject><subject>Angiogenesis</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Crosstalk</subject><subject>Endothelial cells</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Rodents</subject><subject>Sexual dimorphism</subject><subject>Steroid hormones</subject><subject>Vascular endothelial growth factor</subject><subject>Wound healing</subject><subject>Xenoestrogens</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1qFzEUxYMo9kN3PkDAjYuO5jszG2EorRVaFLW4DGlyZ5o_M8m_yUzBR_B1fJA-k6mtUru693J_HM7hIPSKkrecd-Rd2MyFUdppKuQTtEsFYw0hSj99sO-gvVI2hDDOZPcc7XDWdW09dtHP3l_buNgRCg4Rf09r9PgE7BTiiD_n5KD8eRzDbCfAZ8EB_gJXa8iAz7cZxnWyS0gR96xvzsAHu4DHfRxDGiFCCQVXRch4uQT8dQnzXz4NmOqbX81RWbL1IU0v0LPBTgVe3s99dH589O3wpDn99OHjYX_aOE6EbFwnOi-dZGSo8WtCafWF5K3zAOBYS5WtK5PaKsYHpYFILZVzWrlBUA98H72_092uFzN4B7EamMw2h9nmHybZYP7_xHBpxnRttGy5VrwKvLkXyOlqhbKYORQH02QjpLUYJoRuBZWsq-jrR-gmrTnWeIZJ0SqlNWsrdXBHuZxKyTD8M0OJue3YPOyY_wYcM5rd</recordid><startdate>20200928</startdate><enddate>20200928</enddate><creator>Troncoso, Felipe</creator><creator>Herlitz, Kurt</creator><creator>Acurio, Jesenia</creator><creator>Aguayo, Claudio</creator><creator>Guevara, Katherine</creator><creator>Castro, Fidel Ovidio</creator><creator>Godoy, Alejandro S.</creator><creator>San Martin, Sebastian</creator><creator>Escudero, Carlos</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8828-1449</orcidid><orcidid>https://orcid.org/0000-0003-4565-9602</orcidid><orcidid>https://orcid.org/0000-0001-7688-4621</orcidid></search><sort><creationdate>20200928</creationdate><title>Advantages in Wound Healing Process in Female Mice Require Upregulation A2A-Mediated Angiogenesis under the Stimulation of 17β-Estradiol</title><author>Troncoso, Felipe ; 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However, so far, it is unclear whether estrogen may regulate the expression and pro-angiogenic activity of A2A receptors. Using in vivo analyses, we showed that female wild type (WT) mice have a more rapid wound healing process than female or male A2A-deficient mice (A2AKO) mice. We also found that pulmonary endothelial cells (mPEC) isolated from female WT mice showed higher expression of A2A receptor than mPEC from male WT mice. mPEC from female WT mice were more sensitive to A2A-mediated pro-angiogenic response, suggesting an ER and A2A crosstalk, which was confirmed using cells isolated from A2AKO. In those female cells, 17β-estradiol potentiated A2A-mediated cell proliferation, an effect that was inhibited by selective antagonists of estrogen receptors (ER), ERα, and ERβ. Therefore, estrogen regulates the expression and/or pro-angiogenic activity of A2A adenosine receptors, likely involving activation of ERα and ERβ receptors. Sexual dimorphism in wound healing observed in the A2AKO mice process reinforces the functional crosstalk between ER and A2A receptors.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>32998232</pmid><doi>10.3390/ijms21197145</doi><orcidid>https://orcid.org/0000-0001-8828-1449</orcidid><orcidid>https://orcid.org/0000-0003-4565-9602</orcidid><orcidid>https://orcid.org/0000-0001-7688-4621</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 17β-Estradiol Adenosine Adenosine A2A receptors Angiogenesis Cell growth Cell proliferation Crosstalk Endothelial cells Estrogen receptors Estrogens Rodents Sexual dimorphism Steroid hormones Vascular endothelial growth factor Wound healing Xenoestrogens |
title | Advantages in Wound Healing Process in Female Mice Require Upregulation A2A-Mediated Angiogenesis under the Stimulation of 17β-Estradiol |
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