Circulating Endothelial Progenitor Cells During Normal Pregnancy and Pre-Eclampsia

Problem Endothelial progenitor cell (EPC), which mediates neovascularization of uterine endometrium may be involved in the neovascularization in the utero‐placental circulation. We evaluated whether EPC proliferation in pre‐eclampsia (PE) differed from that in normal pregnancy. Method of study EPC n...

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Veröffentlicht in:American journal of reproductive immunology (1989) 2006-08, Vol.56 (2), p.79-85
Hauptverfasser: Matsubara, Keiichi, Abe, Emiko, Matsubara, Yuko, Kameda, Kenji, Ito, Masaharu
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container_end_page 85
container_issue 2
container_start_page 79
container_title American journal of reproductive immunology (1989)
container_volume 56
creator Matsubara, Keiichi
Abe, Emiko
Matsubara, Yuko
Kameda, Kenji
Ito, Masaharu
description Problem Endothelial progenitor cell (EPC), which mediates neovascularization of uterine endometrium may be involved in the neovascularization in the utero‐placental circulation. We evaluated whether EPC proliferation in pre‐eclampsia (PE) differed from that in normal pregnancy. Method of study EPC number in peripheral blood (20 non‐pregnancy, 36 normal pregnancy, 10 PE) was measured using flow cytometry. Peripheral blood mononuclear cell was cultured for 7 days and EPC proliferation was assessed based on detection of the uptake of acetylated low‐density lipoprotein and lectin. Furthermore, the proliferative activity induced by angiotensin II (Ang II) and tumor necrosis factor‐α (TNF‐α) was measured by BrdU assay. Results EPC number in peripheral blood did not differ significantly between PE and normal pregnancy; however, EPC proliferation was significantly increased in PE. Furthermore, Ang II and TNF‐α induced the proliferation of EPC derived from patients with PE. Conclusions In PE, some factors including Ang II and TNF‐α stimulated EPC proliferation; however, the impairment of EPC mobilization into systemic circulation by serum factors may contribute to insufficient regeneration of EC in disturbed utero‐placental circulation of PE.
doi_str_mv 10.1111/j.1600-0897.2006.00387.x
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We evaluated whether EPC proliferation in pre‐eclampsia (PE) differed from that in normal pregnancy. Method of study EPC number in peripheral blood (20 non‐pregnancy, 36 normal pregnancy, 10 PE) was measured using flow cytometry. Peripheral blood mononuclear cell was cultured for 7 days and EPC proliferation was assessed based on detection of the uptake of acetylated low‐density lipoprotein and lectin. Furthermore, the proliferative activity induced by angiotensin II (Ang II) and tumor necrosis factor‐α (TNF‐α) was measured by BrdU assay. Results EPC number in peripheral blood did not differ significantly between PE and normal pregnancy; however, EPC proliferation was significantly increased in PE. Furthermore, Ang II and TNF‐α induced the proliferation of EPC derived from patients with PE. Conclusions In PE, some factors including Ang II and TNF‐α stimulated EPC proliferation; however, the impairment of EPC mobilization into systemic circulation by serum factors may contribute to insufficient regeneration of EC in disturbed utero‐placental circulation of PE.</description><identifier>ISSN: 1046-7408</identifier><identifier>EISSN: 1600-0897</identifier><identifier>DOI: 10.1111/j.1600-0897.2006.00387.x</identifier><identifier>PMID: 16836609</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Angiotensin II ; Cell Proliferation ; Cells, Cultured ; Endothelial Cells - cytology ; Endothelial Cells - immunology ; endothelial progenitor cell ; Female ; Humans ; Leukocytes, Mononuclear - cytology ; Leukocytes, Mononuclear - immunology ; pre-eclampsia ; Pre-Eclampsia - blood ; Pre-Eclampsia - immunology ; Pregnancy - blood ; Stem Cells - cytology ; Stem Cells - immunology ; tumor necrosis factor-α</subject><ispartof>American journal of reproductive immunology (1989), 2006-08, Vol.56 (2), p.79-85</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5567-1434837e31a77503c719448d15a212dbc308521e652000ac258b7584027885fb3</citedby><cites>FETCH-LOGICAL-c5567-1434837e31a77503c719448d15a212dbc308521e652000ac258b7584027885fb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1600-0897.2006.00387.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-0897.2006.00387.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16836609$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsubara, Keiichi</creatorcontrib><creatorcontrib>Abe, Emiko</creatorcontrib><creatorcontrib>Matsubara, Yuko</creatorcontrib><creatorcontrib>Kameda, Kenji</creatorcontrib><creatorcontrib>Ito, Masaharu</creatorcontrib><title>Circulating Endothelial Progenitor Cells During Normal Pregnancy and Pre-Eclampsia</title><title>American journal of reproductive immunology (1989)</title><addtitle>Am J Reprod Immunol</addtitle><description>Problem Endothelial progenitor cell (EPC), which mediates neovascularization of uterine endometrium may be involved in the neovascularization in the utero‐placental circulation. We evaluated whether EPC proliferation in pre‐eclampsia (PE) differed from that in normal pregnancy. Method of study EPC number in peripheral blood (20 non‐pregnancy, 36 normal pregnancy, 10 PE) was measured using flow cytometry. Peripheral blood mononuclear cell was cultured for 7 days and EPC proliferation was assessed based on detection of the uptake of acetylated low‐density lipoprotein and lectin. Furthermore, the proliferative activity induced by angiotensin II (Ang II) and tumor necrosis factor‐α (TNF‐α) was measured by BrdU assay. Results EPC number in peripheral blood did not differ significantly between PE and normal pregnancy; however, EPC proliferation was significantly increased in PE. Furthermore, Ang II and TNF‐α induced the proliferation of EPC derived from patients with PE. Conclusions In PE, some factors including Ang II and TNF‐α stimulated EPC proliferation; however, the impairment of EPC mobilization into systemic circulation by serum factors may contribute to insufficient regeneration of EC in disturbed utero‐placental circulation of PE.</description><subject>Adult</subject><subject>Angiotensin II</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - immunology</subject><subject>endothelial progenitor cell</subject><subject>Female</subject><subject>Humans</subject><subject>Leukocytes, Mononuclear - cytology</subject><subject>Leukocytes, Mononuclear - immunology</subject><subject>pre-eclampsia</subject><subject>Pre-Eclampsia - blood</subject><subject>Pre-Eclampsia - immunology</subject><subject>Pregnancy - blood</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - immunology</subject><subject>tumor necrosis factor-α</subject><issn>1046-7408</issn><issn>1600-0897</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEtP4zAURi0E4tHhL6Cs2CVcx_EjEhsUSgeoOgjNaJaW67jFJY9iJ5r23-PQCpaMN37c813bB6EIQ4LDuFolmAHEIHKepAAsASCCJ5sDdPpZOAxryFjMMxAn6Mz7FUA4J_wYnWAmCGOQn6LnwjrdV6qzzTIaN2XbvZjKqip6cu3SNLZrXVSYqvLRbe8GZta6-qNslo1q9DZSTTns4rGuVL32Vv1ARwtVeXO-n0foz934d_Eznv6a3Bc301hTyniMM5IJwg3BinMKRHOcZ5koMVUpTsu5JiBoig2j4YegdErFnFORQcqFoIs5GaHLXd-1a9964ztZW6_DW1Vj2t5LJhgRgrNvQZyTlPGcBlDsQO1a751ZyLWztXJbiUEO4uVKDn7l4FcO4uWHeLkJ0Yv9Hf28NuVXcG86ANc74J-tzPa_G8ubh_uwCPF4F7e-M5vPuHKvknHCqfw7m8iCEn77OHuQKXkHV5yd_Q</recordid><startdate>200608</startdate><enddate>200608</enddate><creator>Matsubara, Keiichi</creator><creator>Abe, Emiko</creator><creator>Matsubara, Yuko</creator><creator>Kameda, Kenji</creator><creator>Ito, Masaharu</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200608</creationdate><title>Circulating Endothelial Progenitor Cells During Normal Pregnancy and Pre-Eclampsia</title><author>Matsubara, Keiichi ; Abe, Emiko ; Matsubara, Yuko ; Kameda, Kenji ; Ito, Masaharu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5567-1434837e31a77503c719448d15a212dbc308521e652000ac258b7584027885fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Angiotensin II</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - immunology</topic><topic>endothelial progenitor cell</topic><topic>Female</topic><topic>Humans</topic><topic>Leukocytes, Mononuclear - cytology</topic><topic>Leukocytes, Mononuclear - immunology</topic><topic>pre-eclampsia</topic><topic>Pre-Eclampsia - blood</topic><topic>Pre-Eclampsia - immunology</topic><topic>Pregnancy - blood</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - immunology</topic><topic>tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsubara, Keiichi</creatorcontrib><creatorcontrib>Abe, Emiko</creatorcontrib><creatorcontrib>Matsubara, Yuko</creatorcontrib><creatorcontrib>Kameda, Kenji</creatorcontrib><creatorcontrib>Ito, Masaharu</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of reproductive immunology (1989)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsubara, Keiichi</au><au>Abe, Emiko</au><au>Matsubara, Yuko</au><au>Kameda, Kenji</au><au>Ito, Masaharu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Circulating Endothelial Progenitor Cells During Normal Pregnancy and Pre-Eclampsia</atitle><jtitle>American journal of reproductive immunology (1989)</jtitle><addtitle>Am J Reprod Immunol</addtitle><date>2006-08</date><risdate>2006</risdate><volume>56</volume><issue>2</issue><spage>79</spage><epage>85</epage><pages>79-85</pages><issn>1046-7408</issn><eissn>1600-0897</eissn><abstract>Problem Endothelial progenitor cell (EPC), which mediates neovascularization of uterine endometrium may be involved in the neovascularization in the utero‐placental circulation. We evaluated whether EPC proliferation in pre‐eclampsia (PE) differed from that in normal pregnancy. Method of study EPC number in peripheral blood (20 non‐pregnancy, 36 normal pregnancy, 10 PE) was measured using flow cytometry. Peripheral blood mononuclear cell was cultured for 7 days and EPC proliferation was assessed based on detection of the uptake of acetylated low‐density lipoprotein and lectin. Furthermore, the proliferative activity induced by angiotensin II (Ang II) and tumor necrosis factor‐α (TNF‐α) was measured by BrdU assay. Results EPC number in peripheral blood did not differ significantly between PE and normal pregnancy; however, EPC proliferation was significantly increased in PE. Furthermore, Ang II and TNF‐α induced the proliferation of EPC derived from patients with PE. Conclusions In PE, some factors including Ang II and TNF‐α stimulated EPC proliferation; however, the impairment of EPC mobilization into systemic circulation by serum factors may contribute to insufficient regeneration of EC in disturbed utero‐placental circulation of PE.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16836609</pmid><doi>10.1111/j.1600-0897.2006.00387.x</doi><tpages>7</tpages></addata></record>
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source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Adult
Angiotensin II
Cell Proliferation
Cells, Cultured
Endothelial Cells - cytology
Endothelial Cells - immunology
endothelial progenitor cell
Female
Humans
Leukocytes, Mononuclear - cytology
Leukocytes, Mononuclear - immunology
pre-eclampsia
Pre-Eclampsia - blood
Pre-Eclampsia - immunology
Pregnancy - blood
Stem Cells - cytology
Stem Cells - immunology
tumor necrosis factor-α
title Circulating Endothelial Progenitor Cells During Normal Pregnancy and Pre-Eclampsia
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