Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways
Estrogen induces endothelial progenitor cells (EPCs) migration and proliferation, which may serve as a potential target for coronary artery disease, but the mechanisms are unclear. We hypothesized that estrogen receptors (ERs) and phosphatidylinositol 3-kinase (PI3K) signaling pathway, which represe...
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| Veröffentlicht in: | Microvascular research 2008, Vol.75 (1), p.45-52 |
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| creator | Zhao, Xiaohui Huang, Lan Yin, Yangguang Fang, Yuqiang Zhao, Jinghong Chen, Jianfei |
| description | Estrogen induces endothelial progenitor cells (EPCs) migration and proliferation, which may serve as a potential target for coronary artery disease, but the mechanisms are unclear. We hypothesized that estrogen receptors (ERs) and phosphatidylinositol 3-kinase (PI3K) signaling pathway, which represent particularly important roles of action for estrogen, may contribute to estrogen-induced EPCs migration and proliferation. Bone marrow mononuclear cells (MNCs) were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with growth factors as previously described. A total of 87.32
±
5.13% of adherent cells showed uptake of acetylated low-density lipoprotein and lectin binding. Immunostaining and fluorescence activated cell sorting confirmed the endothelial progenitor phenotype. RT-PCR, immunocytochemistry staining and Western blot demonstrated expression of ERs. Exposure to 17β-estradiol significantly improved EPCs migration and proliferation. Those effects were blocked by pretreatment with the pharmacological PI3K blockers LY294002 (1 h, 10 umol/L) and ICI-182780 (1 h, 10 umol/L), a specific estrogen receptor antagonist, which show involvement of estrogen receptors and PI3K pathway. These results suggest that estrogen induces EPCs migration and proliferation via ERs and PI3K pathway which provided a novel insight and treatment strategy of vascular biology. |
| doi_str_mv | 10.1016/j.mvr.2007.02.009 |
| format | Article |
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±
5.13% of adherent cells showed uptake of acetylated low-density lipoprotein and lectin binding. Immunostaining and fluorescence activated cell sorting confirmed the endothelial progenitor phenotype. RT-PCR, immunocytochemistry staining and Western blot demonstrated expression of ERs. Exposure to 17β-estradiol significantly improved EPCs migration and proliferation. Those effects were blocked by pretreatment with the pharmacological PI3K blockers LY294002 (1 h, 10 umol/L) and ICI-182780 (1 h, 10 umol/L), a specific estrogen receptor antagonist, which show involvement of estrogen receptors and PI3K pathway. These results suggest that estrogen induces EPCs migration and proliferation via ERs and PI3K pathway which provided a novel insight and treatment strategy of vascular biology.</description><identifier>ISSN: 0026-2862</identifier><identifier>EISSN: 1095-9319</identifier><identifier>DOI: 10.1016/j.mvr.2007.02.009</identifier><identifier>PMID: 17524430</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cells, Cultured ; Chromones - pharmacology ; Endothelial Cells - drug effects ; Endothelial Cells - enzymology ; Endothelial Cells - metabolism ; Endothelial progenitor cells ; Estradiol - analogs & derivatives ; Estradiol - metabolism ; Estradiol - pharmacology ; Estrogen ; Estrogen Antagonists - pharmacology ; Estrogen Receptor alpha - antagonists & inhibitors ; Estrogen Receptor alpha - metabolism ; Estrogen Receptor beta - antagonists & inhibitors ; Estrogen Receptor beta - metabolism ; Estrogen receptors ; Female ; Humans ; Mice ; Mice, Inbred C57BL ; Migration ; Morpholines - pharmacology ; Phenotype ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K pathway ; Proliferation ; Protein Kinase Inhibitors - pharmacology ; Signal Transduction ; Stem Cells - drug effects ; Stem Cells - enzymology ; Stem Cells - metabolism</subject><ispartof>Microvascular research, 2008, Vol.75 (1), p.45-52</ispartof><rights>2007 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0026286207000246$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17524430$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Xiaohui</creatorcontrib><creatorcontrib>Huang, Lan</creatorcontrib><creatorcontrib>Yin, Yangguang</creatorcontrib><creatorcontrib>Fang, Yuqiang</creatorcontrib><creatorcontrib>Zhao, Jinghong</creatorcontrib><creatorcontrib>Chen, Jianfei</creatorcontrib><title>Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways</title><title>Microvascular research</title><addtitle>Microvasc Res</addtitle><description>Estrogen induces endothelial progenitor cells (EPCs) migration and proliferation, which may serve as a potential target for coronary artery disease, but the mechanisms are unclear. We hypothesized that estrogen receptors (ERs) and phosphatidylinositol 3-kinase (PI3K) signaling pathway, which represent particularly important roles of action for estrogen, may contribute to estrogen-induced EPCs migration and proliferation. Bone marrow mononuclear cells (MNCs) were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with growth factors as previously described. A total of 87.32
±
5.13% of adherent cells showed uptake of acetylated low-density lipoprotein and lectin binding. Immunostaining and fluorescence activated cell sorting confirmed the endothelial progenitor phenotype. RT-PCR, immunocytochemistry staining and Western blot demonstrated expression of ERs. Exposure to 17β-estradiol significantly improved EPCs migration and proliferation. Those effects were blocked by pretreatment with the pharmacological PI3K blockers LY294002 (1 h, 10 umol/L) and ICI-182780 (1 h, 10 umol/L), a specific estrogen receptor antagonist, which show involvement of estrogen receptors and PI3K pathway. These results suggest that estrogen induces EPCs migration and proliferation via ERs and PI3K pathway which provided a novel insight and treatment strategy of vascular biology.</description><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Chromones - pharmacology</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - enzymology</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial progenitor cells</subject><subject>Estradiol - analogs & derivatives</subject><subject>Estradiol - metabolism</subject><subject>Estradiol - pharmacology</subject><subject>Estrogen</subject><subject>Estrogen Antagonists - pharmacology</subject><subject>Estrogen Receptor alpha - antagonists & inhibitors</subject><subject>Estrogen Receptor alpha - metabolism</subject><subject>Estrogen Receptor beta - antagonists & inhibitors</subject><subject>Estrogen Receptor beta - metabolism</subject><subject>Estrogen receptors</subject><subject>Female</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Migration</subject><subject>Morpholines - pharmacology</subject><subject>Phenotype</subject><subject>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K pathway</subject><subject>Proliferation</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Signal Transduction</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - enzymology</subject><subject>Stem Cells - metabolism</subject><issn>0026-2862</issn><issn>1095-9319</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kctOwzAQRS0EoqXwAWxQVuwSxs7DtVghVKCiEixgbTn2pHWVF3FaVPHzOH2srPGcubozl5BbChEFmj2so2rbRQyAR8AiAHFGxhREGoqYinMyBmBZyKYZG5Er59YAlKaCXZIR5SlLkhjG5G_m-q5ZYh3Y2mw0ugBr0_QrLK0qg3bfsn3TBRrL0g0fpS2wU71t6kDVJqjs8ljluwBPYh1qbP2Y2zOf8_g9NNh6aaz7oFX96lft3DW5KFTp8Ob4Tsj3y-zr-S1cfLzOn58WIbKM9qE2Kk-TqeaaUsOESTSFBGlRZEZQlfFCJLxI8xgUoADIuMq5LjLNDKYshyKekPuDrnf_s_EeZWXdsI-qsdk4ycGfRcTcg3dHcJNXaGTb2Up1O3k6lwceDwB6u1uLnXTaYq3RWL9xL01jJQU5hCPX0ocjh3AkMOnDif8BpvuE8g</recordid><startdate>2008</startdate><enddate>2008</enddate><creator>Zhao, Xiaohui</creator><creator>Huang, Lan</creator><creator>Yin, Yangguang</creator><creator>Fang, Yuqiang</creator><creator>Zhao, Jinghong</creator><creator>Chen, Jianfei</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>2008</creationdate><title>Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways</title><author>Zhao, Xiaohui ; Huang, Lan ; Yin, Yangguang ; Fang, Yuqiang ; Zhao, Jinghong ; Chen, Jianfei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e261t-cdab548c7c11d29d4c104e1ff6d91a67f947f5b30a0e90067ab7cf6c2de52b0f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Chromones - pharmacology</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - enzymology</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial progenitor cells</topic><topic>Estradiol - analogs & derivatives</topic><topic>Estradiol - metabolism</topic><topic>Estradiol - pharmacology</topic><topic>Estrogen</topic><topic>Estrogen Antagonists - pharmacology</topic><topic>Estrogen Receptor alpha - antagonists & inhibitors</topic><topic>Estrogen Receptor alpha - metabolism</topic><topic>Estrogen Receptor beta - antagonists & inhibitors</topic><topic>Estrogen Receptor beta - metabolism</topic><topic>Estrogen receptors</topic><topic>Female</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Migration</topic><topic>Morpholines - pharmacology</topic><topic>Phenotype</topic><topic>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K pathway</topic><topic>Proliferation</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Signal Transduction</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - enzymology</topic><topic>Stem Cells - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Xiaohui</creatorcontrib><creatorcontrib>Huang, Lan</creatorcontrib><creatorcontrib>Yin, Yangguang</creatorcontrib><creatorcontrib>Fang, Yuqiang</creatorcontrib><creatorcontrib>Zhao, Jinghong</creatorcontrib><creatorcontrib>Chen, Jianfei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Microvascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Xiaohui</au><au>Huang, Lan</au><au>Yin, Yangguang</au><au>Fang, Yuqiang</au><au>Zhao, Jinghong</au><au>Chen, Jianfei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways</atitle><jtitle>Microvascular research</jtitle><addtitle>Microvasc Res</addtitle><date>2008</date><risdate>2008</risdate><volume>75</volume><issue>1</issue><spage>45</spage><epage>52</epage><pages>45-52</pages><issn>0026-2862</issn><eissn>1095-9319</eissn><abstract>Estrogen induces endothelial progenitor cells (EPCs) migration and proliferation, which may serve as a potential target for coronary artery disease, but the mechanisms are unclear. We hypothesized that estrogen receptors (ERs) and phosphatidylinositol 3-kinase (PI3K) signaling pathway, which represent particularly important roles of action for estrogen, may contribute to estrogen-induced EPCs migration and proliferation. Bone marrow mononuclear cells (MNCs) were cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with growth factors as previously described. A total of 87.32
±
5.13% of adherent cells showed uptake of acetylated low-density lipoprotein and lectin binding. Immunostaining and fluorescence activated cell sorting confirmed the endothelial progenitor phenotype. RT-PCR, immunocytochemistry staining and Western blot demonstrated expression of ERs. Exposure to 17β-estradiol significantly improved EPCs migration and proliferation. Those effects were blocked by pretreatment with the pharmacological PI3K blockers LY294002 (1 h, 10 umol/L) and ICI-182780 (1 h, 10 umol/L), a specific estrogen receptor antagonist, which show involvement of estrogen receptors and PI3K pathway. These results suggest that estrogen induces EPCs migration and proliferation via ERs and PI3K pathway which provided a novel insight and treatment strategy of vascular biology.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17524430</pmid><doi>10.1016/j.mvr.2007.02.009</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Cells, Cultured Chromones - pharmacology Endothelial Cells - drug effects Endothelial Cells - enzymology Endothelial Cells - metabolism Endothelial progenitor cells Estradiol - analogs & derivatives Estradiol - metabolism Estradiol - pharmacology Estrogen Estrogen Antagonists - pharmacology Estrogen Receptor alpha - antagonists & inhibitors Estrogen Receptor alpha - metabolism Estrogen Receptor beta - antagonists & inhibitors Estrogen Receptor beta - metabolism Estrogen receptors Female Humans Mice Mice, Inbred C57BL Migration Morpholines - pharmacology Phenotype Phosphatidylinositol 3-Kinases - antagonists & inhibitors Phosphatidylinositol 3-Kinases - metabolism PI3K pathway Proliferation Protein Kinase Inhibitors - pharmacology Signal Transduction Stem Cells - drug effects Stem Cells - enzymology Stem Cells - metabolism |
| title | Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways |
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