The Effects of Adiponectin and Leptin on Human Endothelial Cell Proliferation: A Live-Cell Study
The effect of adiponectin and leptin on the proliferation of the human microvascular endothelial cell line (HMEC-1) was studied in the absence or presence of fetal bovine serum (FBS). The participation of extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt (PI-3K/Akt) p...
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creator | Álvarez, Granada Visitación Bartolomé, M. Miana, María Jurado-López, Raquel Martín, Ruben Zuluaga, Pilar Martinez-Martinez, Ernesto Nieto, M. Luisa Alvarez-Sala, Luis A. Millán, Jesús Lahera, Vicente Cachofeiro, Victoria |
description | The effect of adiponectin and leptin on the proliferation of the human microvascular endothelial cell line (HMEC-1) was studied in the absence or presence of fetal bovine serum (FBS). The participation of extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt (PI-3K/Akt) pathways in this effect were evaluated. We studied the effect of both adipokines on the motility, mitosis, proliferation and cell death processes of HMEC-1 cells using live-cell imaging techniques. Adiponectin but not leptin further increased the proliferative effect induced by FBS on HMEC-1. This effect seems to be the consequence of an increase in the mitotic index in adiponectin-treated cells when compared to untreated ones. The presence of either the mitogen-activated protein kinase (MAPK) inhibitor (PD98059), or PI-3K inhibitor (LY294002), reduced the effect of adiponectin in a dose-dependent manner. Neither adipokine was able to affect HMEC-1 proliferation in FBS-free conditions. Duration of mitosis, cell motility and the cell death process were similar in all conditions. These data suggest that adiponectin and leptin exert different effects on endothelial cell function. Adiponectin was able to potentiate proliferation of HMEC-1. This effect involves the activation of both PI3-K/Akt and ERK/MAPK pathways. However, it seems to exert minimal effects on HMEC-1 function in the case of leptin. |
doi_str_mv | 10.1159/000332332 |
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Luisa ; Alvarez-Sala, Luis A. ; Millán, Jesús ; Lahera, Vicente ; Cachofeiro, Victoria</creator><creatorcontrib>Álvarez, Granada ; Visitación Bartolomé, M. ; Miana, María ; Jurado-López, Raquel ; Martín, Ruben ; Zuluaga, Pilar ; Martinez-Martinez, Ernesto ; Nieto, M. Luisa ; Alvarez-Sala, Luis A. ; Millán, Jesús ; Lahera, Vicente ; Cachofeiro, Victoria</creatorcontrib><description>The effect of adiponectin and leptin on the proliferation of the human microvascular endothelial cell line (HMEC-1) was studied in the absence or presence of fetal bovine serum (FBS). The participation of extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt (PI-3K/Akt) pathways in this effect were evaluated. We studied the effect of both adipokines on the motility, mitosis, proliferation and cell death processes of HMEC-1 cells using live-cell imaging techniques. Adiponectin but not leptin further increased the proliferative effect induced by FBS on HMEC-1. This effect seems to be the consequence of an increase in the mitotic index in adiponectin-treated cells when compared to untreated ones. The presence of either the mitogen-activated protein kinase (MAPK) inhibitor (PD98059), or PI-3K inhibitor (LY294002), reduced the effect of adiponectin in a dose-dependent manner. Neither adipokine was able to affect HMEC-1 proliferation in FBS-free conditions. Duration of mitosis, cell motility and the cell death process were similar in all conditions. These data suggest that adiponectin and leptin exert different effects on endothelial cell function. Adiponectin was able to potentiate proliferation of HMEC-1. This effect involves the activation of both PI3-K/Akt and ERK/MAPK pathways. However, it seems to exert minimal effects on HMEC-1 function in the case of leptin.</description><identifier>ISSN: 1018-1172</identifier><identifier>EISSN: 1423-0135</identifier><identifier>DOI: 10.1159/000332332</identifier><identifier>PMID: 22249107</identifier><identifier>CODEN: JVREE9</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Adiponectin - pharmacology ; Biological and medical sciences ; Cell Line ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Chromones - pharmacology ; Endothelium, Vascular - cytology ; Extracellular Signal-Regulated MAP Kinases - drug effects ; Flavonoids - pharmacology ; Fundamental and applied biological sciences. Psychology ; Humans ; Leptin - pharmacology ; Microcirculation ; Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors ; Morpholines - pharmacology ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Research Paper ; Vertebrates: cardiovascular system</subject><ispartof>Journal of vascular research, 2012-01, Vol.49 (2), p.111-122</ispartof><rights>2012 S. Karger AG, Basel</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 S. Karger AG, Basel.</rights><rights>Copyright (c) 2012 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-d32c956e781b5c1c918ad032685adae1985b54e994c5849d4a8034016536ad043</citedby><cites>FETCH-LOGICAL-c398t-d32c956e781b5c1c918ad032685adae1985b54e994c5849d4a8034016536ad043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25784511$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22249107$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Álvarez, Granada</creatorcontrib><creatorcontrib>Visitación Bartolomé, M.</creatorcontrib><creatorcontrib>Miana, María</creatorcontrib><creatorcontrib>Jurado-López, Raquel</creatorcontrib><creatorcontrib>Martín, Ruben</creatorcontrib><creatorcontrib>Zuluaga, Pilar</creatorcontrib><creatorcontrib>Martinez-Martinez, Ernesto</creatorcontrib><creatorcontrib>Nieto, M. 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Adiponectin but not leptin further increased the proliferative effect induced by FBS on HMEC-1. This effect seems to be the consequence of an increase in the mitotic index in adiponectin-treated cells when compared to untreated ones. The presence of either the mitogen-activated protein kinase (MAPK) inhibitor (PD98059), or PI-3K inhibitor (LY294002), reduced the effect of adiponectin in a dose-dependent manner. Neither adipokine was able to affect HMEC-1 proliferation in FBS-free conditions. Duration of mitosis, cell motility and the cell death process were similar in all conditions. These data suggest that adiponectin and leptin exert different effects on endothelial cell function. Adiponectin was able to potentiate proliferation of HMEC-1. This effect involves the activation of both PI3-K/Akt and ERK/MAPK pathways. However, it seems to exert minimal effects on HMEC-1 function in the case of leptin.</description><subject>Adiponectin - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Chromones - pharmacology</subject><subject>Endothelium, Vascular - cytology</subject><subject>Extracellular Signal-Regulated MAP Kinases - drug effects</subject><subject>Flavonoids - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Leptin - pharmacology</subject><subject>Microcirculation</subject><subject>Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors</subject><subject>Morpholines - pharmacology</subject><subject>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</subject><subject>Research Paper</subject><subject>Vertebrates: cardiovascular system</subject><issn>1018-1172</issn><issn>1423-0135</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</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><recordid>eNpd0N9LWzEUB_AgG1adD76PERgyfLiakx-3yd5KqVMoKKw-X9Mkd0Zvky65d-B_b7S1wiCQE_LhnMMXoRMg5wBCXRBCGKPl7KED4JRVBJj4VGoCsgIY0xE6zPmREOBK1vtoRCnlCsj4AN0vHhyeta0zfcaxxRPr1zGUlw9YB4vnbv1axoCvhpUOeBZs7B9c53WHp67r8G2KnW9d0r2P4See4Ln_56q3r9_9YJ-_oM-t7rI73t5H6O5ytpheVfObX9fTybwyTMm-sowaJWo3lrAUBowCqS1htJZCW-1ASbEU3CnFjZBcWa4lYZxALVhdIGdH6Mem7zrFv4PLfbPy2ZQ1dHBxyI2qJRAqalrk9__kYxxSKMs1RVBag-SyqLONMinmnFzbrJNf6fRcUPOaerNLvdhv247DcuXsTr7HXMDpFuhsdNcmHYzPH06MJRcAxX3duCed_ri0A9s5L1NRjuY</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Álvarez, Granada</creator><creator>Visitación Bartolomé, M.</creator><creator>Miana, María</creator><creator>Jurado-López, Raquel</creator><creator>Martín, Ruben</creator><creator>Zuluaga, Pilar</creator><creator>Martinez-Martinez, Ernesto</creator><creator>Nieto, M. 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Luisa</au><au>Alvarez-Sala, Luis A.</au><au>Millán, Jesús</au><au>Lahera, Vicente</au><au>Cachofeiro, Victoria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Effects of Adiponectin and Leptin on Human Endothelial Cell Proliferation: A Live-Cell Study</atitle><jtitle>Journal of vascular research</jtitle><addtitle>J Vasc Res</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>49</volume><issue>2</issue><spage>111</spage><epage>122</epage><pages>111-122</pages><issn>1018-1172</issn><eissn>1423-0135</eissn><coden>JVREE9</coden><abstract>The effect of adiponectin and leptin on the proliferation of the human microvascular endothelial cell line (HMEC-1) was studied in the absence or presence of fetal bovine serum (FBS). The participation of extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt (PI-3K/Akt) pathways in this effect were evaluated. We studied the effect of both adipokines on the motility, mitosis, proliferation and cell death processes of HMEC-1 cells using live-cell imaging techniques. Adiponectin but not leptin further increased the proliferative effect induced by FBS on HMEC-1. This effect seems to be the consequence of an increase in the mitotic index in adiponectin-treated cells when compared to untreated ones. The presence of either the mitogen-activated protein kinase (MAPK) inhibitor (PD98059), or PI-3K inhibitor (LY294002), reduced the effect of adiponectin in a dose-dependent manner. Neither adipokine was able to affect HMEC-1 proliferation in FBS-free conditions. Duration of mitosis, cell motility and the cell death process were similar in all conditions. These data suggest that adiponectin and leptin exert different effects on endothelial cell function. Adiponectin was able to potentiate proliferation of HMEC-1. This effect involves the activation of both PI3-K/Akt and ERK/MAPK pathways. However, it seems to exert minimal effects on HMEC-1 function in the case of leptin.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>22249107</pmid><doi>10.1159/000332332</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adiponectin - pharmacology Biological and medical sciences Cell Line Cell Movement - drug effects Cell Proliferation - drug effects Chromones - pharmacology Endothelium, Vascular - cytology Extracellular Signal-Regulated MAP Kinases - drug effects Flavonoids - pharmacology Fundamental and applied biological sciences. Psychology Humans Leptin - pharmacology Microcirculation Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors Morpholines - pharmacology Phosphatidylinositol 3-Kinases - antagonists & inhibitors Research Paper Vertebrates: cardiovascular system |
title | The Effects of Adiponectin and Leptin on Human Endothelial Cell Proliferation: A Live-Cell Study |
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