microRNA-126 inhibits tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway
It's critical for tube formation and angiogenesis to repair ischemic myocardium or stroke. This study aimed to investigate role of microRNA-126 (miR-126) in tube formation in human umbilical vein endothelial cells (HUVECs) and associated mechanisms. Primary neural stem cells (NSCs) and HUVECs w...
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| Veröffentlicht in: | Biomedicine & pharmacotherapy 2019-08, Vol.116, p.109007-109007, Article 109007 |
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| creator | Li, Qiang Cheng, Kai Wang, Ai-Yue Xu, Qiong-Guang Fu, Zhou-Feng He, Shao-Yu Xu, Peng-Xiang |
| description | It's critical for tube formation and angiogenesis to repair ischemic myocardium or stroke. This study aimed to investigate role of microRNA-126 (miR-126) in tube formation in human umbilical vein endothelial cells (HUVECs) and associated mechanisms. Primary neural stem cells (NSCs) and HUVECs were cultured and transfected with microRNA-126 mimics and miR-126 inhibitor. Cell counting kit-8 (CCK-8) and cell cycle assay were conducted for evaluating NSCs viability. Transwell assay was conducted to observe invasive ability of HUVECs. Quantitative real-time PCR (qRT-PCR) assay was used to examine epidermal growth factor like domain 7 (EGFL7) and miR-126 mRNA both in vitro and animal models. Tube forming capability was evaluated in HUVECs. Dual luciferase assay was performed to evaluate interaction between miR-126 and EGFL7 gene. Western blot assay was used to determine phosphoinositide-3-kinase/protein kinase-B (PI3K/AKT) signaling molecules and EGFL7. The results indicated that miR-126 significantly decreased cell viability, inhibited invasive ability and modulated cell cycle of NSCs compared to miR-NC group (p |
| doi_str_mv | 10.1016/j.biopha.2019.109007 |
| format | Article |
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This study aimed to investigate role of microRNA-126 (miR-126) in tube formation in human umbilical vein endothelial cells (HUVECs) and associated mechanisms. Primary neural stem cells (NSCs) and HUVECs were cultured and transfected with microRNA-126 mimics and miR-126 inhibitor. Cell counting kit-8 (CCK-8) and cell cycle assay were conducted for evaluating NSCs viability. Transwell assay was conducted to observe invasive ability of HUVECs. Quantitative real-time PCR (qRT-PCR) assay was used to examine epidermal growth factor like domain 7 (EGFL7) and miR-126 mRNA both in vitro and animal models. Tube forming capability was evaluated in HUVECs. Dual luciferase assay was performed to evaluate interaction between miR-126 and EGFL7 gene. Western blot assay was used to determine phosphoinositide-3-kinase/protein kinase-B (PI3K/AKT) signaling molecules and EGFL7. The results indicated that miR-126 significantly decreased cell viability, inhibited invasive ability and modulated cell cycle of NSCs compared to miR-NC group (p < 0.05). miR-126 significantly inhibited tube formation of HUVECs compared to miR-NC group (p < 0.05). miR-126 significantly down-regulated EGFL7 mRNA and protein expression compared to miR-NC (p < 0.05). Atorvastatin significantly increased CD34 and enhanced EGFL7 expression in traumatic brain injury (TBI) rats brain tissues compared to Model group (p < 0.05). miR-126 significantly down-regulated and atorvastatin up-regulated PI3K/AKT signaling pathway (p < 0.05). Atorvastatin significantly increased EGFL7 and down-regulated miR-126 expression in TBI rats brain tissues compared to Model group (p < 0.05). miR-126 interacted with and negatively correlated with EGFL7 gene both in vitro and in TBI models. In conclusion, microRNA-126 inhibited tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway.]]></description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2019.109007</identifier><identifier>PMID: 31170663</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Animals ; Antigens, CD34 - metabolism ; Atorvastatin - administration & dosage ; Atorvastatin - pharmacology ; Base Sequence ; Brain Injuries, Traumatic - genetics ; Brain Injuries, Traumatic - pathology ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - metabolism ; Cell Cycle - drug effects ; Cell Cycle - genetics ; Cell Survival - drug effects ; Cell Survival - genetics ; Down-Regulation - drug effects ; Down-Regulation - genetics ; EGF Family of Proteins - genetics ; EGF Family of Proteins - metabolism ; EGFL7 ; Endothelial Growth Factors - metabolism ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; microRNA-126 ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Neovascularization, Physiologic - drug effects ; Neovascularization, Physiologic - genetics ; Neural Stem Cells - drug effects ; Neural Stem Cells - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K/AKT signaling pathway ; Proto-Oncogene Proteins c-akt - metabolism ; Rats, Sprague-Dawley ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal Transduction ; Tube formation ; Up-Regulation - drug effects ; Up-Regulation - genetics</subject><ispartof>Biomedicine & pharmacotherapy, 2019-08, Vol.116, p.109007-109007, Article 109007</ispartof><rights>2019 The Authors</rights><rights>Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-3f4509c337a8a1277fa5b94ec8e9370a7b91391d1cc5f2e3959ea161f87904bb3</citedby><cites>FETCH-LOGICAL-c408t-3f4509c337a8a1277fa5b94ec8e9370a7b91391d1cc5f2e3959ea161f87904bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0753332219311680$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31170663$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Qiang</creatorcontrib><creatorcontrib>Cheng, Kai</creatorcontrib><creatorcontrib>Wang, Ai-Yue</creatorcontrib><creatorcontrib>Xu, Qiong-Guang</creatorcontrib><creatorcontrib>Fu, Zhou-Feng</creatorcontrib><creatorcontrib>He, Shao-Yu</creatorcontrib><creatorcontrib>Xu, Peng-Xiang</creatorcontrib><title>microRNA-126 inhibits tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description><![CDATA[It's critical for tube formation and angiogenesis to repair ischemic myocardium or stroke. This study aimed to investigate role of microRNA-126 (miR-126) in tube formation in human umbilical vein endothelial cells (HUVECs) and associated mechanisms. Primary neural stem cells (NSCs) and HUVECs were cultured and transfected with microRNA-126 mimics and miR-126 inhibitor. Cell counting kit-8 (CCK-8) and cell cycle assay were conducted for evaluating NSCs viability. Transwell assay was conducted to observe invasive ability of HUVECs. Quantitative real-time PCR (qRT-PCR) assay was used to examine epidermal growth factor like domain 7 (EGFL7) and miR-126 mRNA both in vitro and animal models. Tube forming capability was evaluated in HUVECs. Dual luciferase assay was performed to evaluate interaction between miR-126 and EGFL7 gene. Western blot assay was used to determine phosphoinositide-3-kinase/protein kinase-B (PI3K/AKT) signaling molecules and EGFL7. The results indicated that miR-126 significantly decreased cell viability, inhibited invasive ability and modulated cell cycle of NSCs compared to miR-NC group (p < 0.05). miR-126 significantly inhibited tube formation of HUVECs compared to miR-NC group (p < 0.05). miR-126 significantly down-regulated EGFL7 mRNA and protein expression compared to miR-NC (p < 0.05). Atorvastatin significantly increased CD34 and enhanced EGFL7 expression in traumatic brain injury (TBI) rats brain tissues compared to Model group (p < 0.05). miR-126 significantly down-regulated and atorvastatin up-regulated PI3K/AKT signaling pathway (p < 0.05). Atorvastatin significantly increased EGFL7 and down-regulated miR-126 expression in TBI rats brain tissues compared to Model group (p < 0.05). miR-126 interacted with and negatively correlated with EGFL7 gene both in vitro and in TBI models. In conclusion, microRNA-126 inhibited tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway.]]></description><subject>Animals</subject><subject>Antigens, CD34 - metabolism</subject><subject>Atorvastatin - administration & dosage</subject><subject>Atorvastatin - pharmacology</subject><subject>Base Sequence</subject><subject>Brain Injuries, Traumatic - genetics</subject><subject>Brain Injuries, Traumatic - pathology</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Cycle - genetics</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - genetics</subject><subject>Down-Regulation - drug effects</subject><subject>Down-Regulation - genetics</subject><subject>EGF Family of Proteins - genetics</subject><subject>EGF Family of Proteins - metabolism</subject><subject>EGFL7</subject><subject>Endothelial Growth Factors - metabolism</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>microRNA-126</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Neovascularization, Physiologic - genetics</subject><subject>Neural Stem Cells - drug effects</subject><subject>Neural Stem Cells - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K/AKT signaling pathway</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction</subject><subject>Tube formation</subject><subject>Up-Regulation - drug effects</subject><subject>Up-Regulation - genetics</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P4zAQQK0VCLos_2CFfOSSYsdJHF9WqqryISpACPZq2c6kdZXEXduh6r_flABHTjOaeTOjeQj9pmRKCS2uNlNt3XatpimhYigJQvgPNKEiJ0kx5EdoQnjOEsbS9BT9DGFDCMkLVp6gU0YpJ0XBJmjXWuPd88MsoWmBbbe22saAY68B1863KlrXYVfj29e_i3nAej9AEbwy0XYrvLNxjRc310uOVVfhyu26xMOqb9R7--mO3V_N7l9wsKtONYfSVsX1Tu1_oeNaNQHOP-IZer1evMxvk-Xjzd18tkxMRsqYsDrLiTCMcVUqmnJeq1yLDEwJgnGiuBaUCVpRY_I6BSZyAYoWtC65IJnW7Axdjnu33v3rIUTZ2mCgaVQHrg8yTTOWlQWn5YBmIzoICcFDLbfetsrvJSXyoFxu5KhcHpTLUfkwdvFxodctVF9Dn44H4M8IwPDnmwUvg7HQGaisBxNl5ez3F_4DLleSZQ</recordid><startdate>201908</startdate><enddate>201908</enddate><creator>Li, Qiang</creator><creator>Cheng, Kai</creator><creator>Wang, Ai-Yue</creator><creator>Xu, Qiong-Guang</creator><creator>Fu, Zhou-Feng</creator><creator>He, Shao-Yu</creator><creator>Xu, Peng-Xiang</creator><general>Elsevier Masson SAS</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope></search><sort><creationdate>201908</creationdate><title>microRNA-126 inhibits tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway</title><author>Li, Qiang ; Cheng, Kai ; Wang, Ai-Yue ; Xu, Qiong-Guang ; Fu, Zhou-Feng ; He, Shao-Yu ; Xu, Peng-Xiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-3f4509c337a8a1277fa5b94ec8e9370a7b91391d1cc5f2e3959ea161f87904bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Antigens, CD34 - metabolism</topic><topic>Atorvastatin - administration & dosage</topic><topic>Atorvastatin - pharmacology</topic><topic>Base Sequence</topic><topic>Brain Injuries, Traumatic - genetics</topic><topic>Brain Injuries, Traumatic - pathology</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Cycle - genetics</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - genetics</topic><topic>Down-Regulation - drug effects</topic><topic>Down-Regulation - genetics</topic><topic>EGF Family of Proteins - genetics</topic><topic>EGF Family of Proteins - metabolism</topic><topic>EGFL7</topic><topic>Endothelial Growth Factors - metabolism</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>microRNA-126</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Neovascularization, Physiologic - genetics</topic><topic>Neural Stem Cells - drug effects</topic><topic>Neural Stem Cells - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K/AKT signaling pathway</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction</topic><topic>Tube formation</topic><topic>Up-Regulation - drug effects</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Qiang</creatorcontrib><creatorcontrib>Cheng, Kai</creatorcontrib><creatorcontrib>Wang, Ai-Yue</creatorcontrib><creatorcontrib>Xu, Qiong-Guang</creatorcontrib><creatorcontrib>Fu, Zhou-Feng</creatorcontrib><creatorcontrib>He, Shao-Yu</creatorcontrib><creatorcontrib>Xu, Peng-Xiang</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biomedicine & pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Qiang</au><au>Cheng, Kai</au><au>Wang, Ai-Yue</au><au>Xu, Qiong-Guang</au><au>Fu, Zhou-Feng</au><au>He, Shao-Yu</au><au>Xu, Peng-Xiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>microRNA-126 inhibits tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2019-08</date><risdate>2019</risdate><volume>116</volume><spage>109007</spage><epage>109007</epage><pages>109007-109007</pages><artnum>109007</artnum><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract><![CDATA[It's critical for tube formation and angiogenesis to repair ischemic myocardium or stroke. This study aimed to investigate role of microRNA-126 (miR-126) in tube formation in human umbilical vein endothelial cells (HUVECs) and associated mechanisms. Primary neural stem cells (NSCs) and HUVECs were cultured and transfected with microRNA-126 mimics and miR-126 inhibitor. Cell counting kit-8 (CCK-8) and cell cycle assay were conducted for evaluating NSCs viability. Transwell assay was conducted to observe invasive ability of HUVECs. Quantitative real-time PCR (qRT-PCR) assay was used to examine epidermal growth factor like domain 7 (EGFL7) and miR-126 mRNA both in vitro and animal models. Tube forming capability was evaluated in HUVECs. Dual luciferase assay was performed to evaluate interaction between miR-126 and EGFL7 gene. Western blot assay was used to determine phosphoinositide-3-kinase/protein kinase-B (PI3K/AKT) signaling molecules and EGFL7. The results indicated that miR-126 significantly decreased cell viability, inhibited invasive ability and modulated cell cycle of NSCs compared to miR-NC group (p < 0.05). miR-126 significantly inhibited tube formation of HUVECs compared to miR-NC group (p < 0.05). miR-126 significantly down-regulated EGFL7 mRNA and protein expression compared to miR-NC (p < 0.05). Atorvastatin significantly increased CD34 and enhanced EGFL7 expression in traumatic brain injury (TBI) rats brain tissues compared to Model group (p < 0.05). miR-126 significantly down-regulated and atorvastatin up-regulated PI3K/AKT signaling pathway (p < 0.05). Atorvastatin significantly increased EGFL7 and down-regulated miR-126 expression in TBI rats brain tissues compared to Model group (p < 0.05). miR-126 interacted with and negatively correlated with EGFL7 gene both in vitro and in TBI models. In conclusion, microRNA-126 inhibited tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway.]]></abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>31170663</pmid><doi>10.1016/j.biopha.2019.109007</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antigens, CD34 - metabolism Atorvastatin - administration & dosage Atorvastatin - pharmacology Base Sequence Brain Injuries, Traumatic - genetics Brain Injuries, Traumatic - pathology Calcium-Binding Proteins - genetics Calcium-Binding Proteins - metabolism Cell Cycle - drug effects Cell Cycle - genetics Cell Survival - drug effects Cell Survival - genetics Down-Regulation - drug effects Down-Regulation - genetics EGF Family of Proteins - genetics EGF Family of Proteins - metabolism EGFL7 Endothelial Growth Factors - metabolism Human Umbilical Vein Endothelial Cells - metabolism Humans microRNA-126 MicroRNAs - genetics MicroRNAs - metabolism Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - genetics Neural Stem Cells - drug effects Neural Stem Cells - metabolism Phosphatidylinositol 3-Kinases - metabolism PI3K/AKT signaling pathway Proto-Oncogene Proteins c-akt - metabolism Rats, Sprague-Dawley RNA, Messenger - genetics RNA, Messenger - metabolism Signal Transduction Tube formation Up-Regulation - drug effects Up-Regulation - genetics |
| title | microRNA-126 inhibits tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway |
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