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Downregulated GTCPH I/BH4 Pathway and Decreased Function of Circulating Endothelial Progenitor Cells and Their Relationship with Endothelial Dysfunction in Overweight Postmenopausal Women
Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial...
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Published in: | Stem cells international 2018-01, Vol.2018 (2018), p.1-11 |
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container_title | Stem cells international |
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creator | Zeng, Haitao Yan, Quanneng Zhan, Hong Hu, Da-Jun He, Hao Yao, Shun Li, Xiao-Peng Liu, Zhihao Liao, Jinli Huang, Zhenhua Luo, Ying Ren, Zi |
description | Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism. Compared with normal weight or overweight age-matched men, postmenopausal women (overweight or normal weight) had a diminished number of circulating EPCs and impaired vascular endothelial function, as detected by flow-mediated dilatation. Moreover, GTCPH I expression and the nitric oxide level in overweight postmenopausal women and men were significantly decreased. Together, our findings demonstrate that the number or function of circulating EPCs and endothelial function, which is partially regulated by the GTCPH I/BH4 signaling pathway, is not preserved in overweight postmenopausal women. The GTCPH I/BH4 pathway in circulating EPCs may be a potential therapeutic target for endothelial injury in overweight postmenopausal women. |
doi_str_mv | 10.1155/2018/4756263 |
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Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism. Compared with normal weight or overweight age-matched men, postmenopausal women (overweight or normal weight) had a diminished number of circulating EPCs and impaired vascular endothelial function, as detected by flow-mediated dilatation. Moreover, GTCPH I expression and the nitric oxide level in overweight postmenopausal women and men were significantly decreased. Together, our findings demonstrate that the number or function of circulating EPCs and endothelial function, which is partially regulated by the GTCPH I/BH4 signaling pathway, is not preserved in overweight postmenopausal women. The GTCPH I/BH4 pathway in circulating EPCs may be a potential therapeutic target for endothelial injury in overweight postmenopausal women.</description><identifier>ISSN: 1687-966X</identifier><identifier>ISSN: 1687-9678</identifier><identifier>EISSN: 1687-9678</identifier><identifier>DOI: 10.1155/2018/4756263</identifier><identifier>PMID: 30050577</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Body weight ; Cardiovascular disease ; Cells (biology) ; Comparative analysis ; Endothelium ; Health risk assessment ; Low density lipoprotein ; Menopause ; Nitric oxide ; Obesity ; Overweight ; Post-menopause ; Postmenopausal women ; Progenitor cells ; Sapropterin dihydrochloride ; Signal transduction ; Stem cells ; Stretching ; Therapeutic applications</subject><ispartof>Stem cells international, 2018-01, Vol.2018 (2018), p.1-11</ispartof><rights>Copyright © 2018 Ying Luo et al.</rights><rights>COPYRIGHT 2018 John Wiley & Sons, Inc.</rights><rights>Copyright © 2018 Ying Luo et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2018 Ying Luo et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c635t-33d73bb056fccc8779e04136968ff02246635eed0b96ad3af8f9dedf839e18a93</citedby><cites>FETCH-LOGICAL-c635t-33d73bb056fccc8779e04136968ff02246635eed0b96ad3af8f9dedf839e18a93</cites><orcidid>0000-0001-7797-4135 ; 0000-0001-9541-9151 ; 0000-0002-7427-8596</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2070156970/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2070156970?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30050577$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Bihl, Ji C.</contributor><contributor>Ji C Bihl</contributor><creatorcontrib>Zeng, Haitao</creatorcontrib><creatorcontrib>Yan, Quanneng</creatorcontrib><creatorcontrib>Zhan, Hong</creatorcontrib><creatorcontrib>Hu, Da-Jun</creatorcontrib><creatorcontrib>He, Hao</creatorcontrib><creatorcontrib>Yao, Shun</creatorcontrib><creatorcontrib>Li, Xiao-Peng</creatorcontrib><creatorcontrib>Liu, Zhihao</creatorcontrib><creatorcontrib>Liao, Jinli</creatorcontrib><creatorcontrib>Huang, Zhenhua</creatorcontrib><creatorcontrib>Luo, Ying</creatorcontrib><creatorcontrib>Ren, Zi</creatorcontrib><title>Downregulated GTCPH I/BH4 Pathway and Decreased Function of Circulating Endothelial Progenitor Cells and Their Relationship with Endothelial Dysfunction in Overweight Postmenopausal Women</title><title>Stem cells international</title><addtitle>Stem Cells Int</addtitle><description>Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism. Compared with normal weight or overweight age-matched men, postmenopausal women (overweight or normal weight) had a diminished number of circulating EPCs and impaired vascular endothelial function, as detected by flow-mediated dilatation. Moreover, GTCPH I expression and the nitric oxide level in overweight postmenopausal women and men were significantly decreased. Together, our findings demonstrate that the number or function of circulating EPCs and endothelial function, which is partially regulated by the GTCPH I/BH4 signaling pathway, is not preserved in overweight postmenopausal women. The GTCPH I/BH4 pathway in circulating EPCs may be a potential therapeutic target for endothelial injury in overweight postmenopausal women.</description><subject>Body weight</subject><subject>Cardiovascular disease</subject><subject>Cells (biology)</subject><subject>Comparative analysis</subject><subject>Endothelium</subject><subject>Health risk assessment</subject><subject>Low density lipoprotein</subject><subject>Menopause</subject><subject>Nitric oxide</subject><subject>Obesity</subject><subject>Overweight</subject><subject>Post-menopause</subject><subject>Postmenopausal women</subject><subject>Progenitor cells</subject><subject>Sapropterin dihydrochloride</subject><subject>Signal transduction</subject><subject>Stem cells</subject><subject>Stretching</subject><subject>Therapeutic 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C.</au><au>Ji C Bihl</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulated GTCPH I/BH4 Pathway and Decreased Function of Circulating Endothelial Progenitor Cells and Their Relationship with Endothelial Dysfunction in Overweight Postmenopausal Women</atitle><jtitle>Stem cells international</jtitle><addtitle>Stem Cells Int</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><issn>1687-966X</issn><issn>1687-9678</issn><eissn>1687-9678</eissn><abstract>Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism. Compared with normal weight or overweight age-matched men, postmenopausal women (overweight or normal weight) had a diminished number of circulating EPCs and impaired vascular endothelial function, as detected by flow-mediated dilatation. Moreover, GTCPH I expression and the nitric oxide level in overweight postmenopausal women and men were significantly decreased. Together, our findings demonstrate that the number or function of circulating EPCs and endothelial function, which is partially regulated by the GTCPH I/BH4 signaling pathway, is not preserved in overweight postmenopausal women. The GTCPH I/BH4 pathway in circulating EPCs may be a potential therapeutic target for endothelial injury in overweight postmenopausal women.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30050577</pmid><doi>10.1155/2018/4756263</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-7797-4135</orcidid><orcidid>https://orcid.org/0000-0001-9541-9151</orcidid><orcidid>https://orcid.org/0000-0002-7427-8596</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Body weight Cardiovascular disease Cells (biology) Comparative analysis Endothelium Health risk assessment Low density lipoprotein Menopause Nitric oxide Obesity Overweight Post-menopause Postmenopausal women Progenitor cells Sapropterin dihydrochloride Signal transduction Stem cells Stretching Therapeutic applications |
title | Downregulated GTCPH I/BH4 Pathway and Decreased Function of Circulating Endothelial Progenitor Cells and Their Relationship with Endothelial Dysfunction in Overweight Postmenopausal Women |
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