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Shear stress regulates endothelial cell function through SRB1‐eNOS signaling pathway
Summary Aim The aim of this study was to explore whether transmembrane flow shear stress could regulate eNOS expression and mediate endothelial cell function via SR‐B1 signaling transduction. Methods Parallel‐plate flow chamber was used to impose laminar shear stress and evaluate the effect of shear...
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| Published in: | Cardiovascular therapeutics 2016-10, Vol.34 (5), p.308-313 |
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| Main Authors: | , , , , , , , , , , |
| Format: | Article |
| Language: | English |
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| container_end_page | 313 |
| container_issue | 5 |
| container_start_page | 308 |
| container_title | Cardiovascular therapeutics |
| container_volume | 34 |
| creator | Zhang, Ying Liao, Bin Li, Miaoling Cheng, Min Fu, Yong Liu, Qing Chen, Qi Liu, Hongduan Fang, Yibing Zhang, Gen Yu, Fengxu |
| description | Summary
Aim
The aim of this study was to explore whether transmembrane flow shear stress could regulate eNOS expression and mediate endothelial cell function via SR‐B1 signaling transduction.
Methods
Parallel‐plate flow chamber was used to impose laminar shear stress and evaluate the effect of shear stress upon human umbilical vein endothelial cells (HUVECs). The expression of SR‐B1 and eNOS at both RNA and protein levels was detected under different dynamic conditions. RNA interference and gene transfection were performed to overexpress and knock down the SRB1 to confirm the role of SR‐B1‐eNOS signaling pathway.
Results
The expression levels of SR‐B1 and eNOS were downregulated when HUVECs were treated with 4.2 dyne/cm2 shear stress compared with those of the control group. However, the expression of SR‐B1 and eNOS was upregulated as HUVECs exposed to 8.4 and 15 dyne/cm2 shear stress. When exposed to 8.4 dyne/cm2, SR‐B1 and eNOS expression was significantly higher compared with those of the other groups. When SR‐B1 was knocked down through RNAi technique, the expression of eNOS was significantly downregulated than those of the other groups. While overexpression of SR‐B1 could upregulate eNOS significantly.
Conclusion
Shear stress regulates endothelial cell function through SR‐B1‐eNOS signaling pathway. SR‐B1 may play a pivotal role in the process of anti‐atherosclerosis. |
| doi_str_mv | 10.1111/1755-5922.12199 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_24P</sourceid><recordid>TN_cdi_proquest_miscellaneous_1825218513</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1825218513</sourcerecordid><originalsourceid>FETCH-LOGICAL-j3929-140eed5fcd4756dd892348102b9feb428020cb23d3cf068d72a912aad9f6a3cd3</originalsourceid><addsrcrecordid>eNpdkctOwzAQRS0EolBYs0OW2LBJscdxGi-hPKWKSi2wtZzYeVRpUuxEVXd8At_Il5C0pQtmM1czR6OrOwhdUDKgbd3QIeceFwADClSIA3SynxzuNfV76NS5OSEBEQE9Rj0YAnAe8hP0McuMstjV1jiHrUmbQtXGYVPqqs5MkasCx6YocNKUcZ1XJa4zWzVphmfTO_rz9W1eJzPs8rRURV6meKnqbKXWZ-goUYUz57veR--PD2-jZ288eXoZ3Y69ORMgPOoTYzRPYu0PeaB1KID5ISUQicREPoQESBwB0yxOSBDqIShBQSktkkCxWLM-ut7eXdrqszGulovcdX5VaarGSRoCBxpyylr06h86rxrb2t5QPhHgU2ipyx3VRAuj5dLmC2XX8i-xFuBbYJUXZr3fUyK7h8guctnFLzcPkaP76UawXzzhfOQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1824092412</pqid></control><display><type>article</type><title>Shear stress regulates endothelial cell function through SRB1‐eNOS signaling pathway</title><source>Wiley Online Library</source><creator>Zhang, Ying ; Liao, Bin ; Li, Miaoling ; Cheng, Min ; Fu, Yong ; Liu, Qing ; Chen, Qi ; Liu, Hongduan ; Fang, Yibing ; Zhang, Gen ; Yu, Fengxu</creator><creatorcontrib>Zhang, Ying ; Liao, Bin ; Li, Miaoling ; Cheng, Min ; Fu, Yong ; Liu, Qing ; Chen, Qi ; Liu, Hongduan ; Fang, Yibing ; Zhang, Gen ; Yu, Fengxu</creatorcontrib><description>Summary
Aim
The aim of this study was to explore whether transmembrane flow shear stress could regulate eNOS expression and mediate endothelial cell function via SR‐B1 signaling transduction.
Methods
Parallel‐plate flow chamber was used to impose laminar shear stress and evaluate the effect of shear stress upon human umbilical vein endothelial cells (HUVECs). The expression of SR‐B1 and eNOS at both RNA and protein levels was detected under different dynamic conditions. RNA interference and gene transfection were performed to overexpress and knock down the SRB1 to confirm the role of SR‐B1‐eNOS signaling pathway.
Results
The expression levels of SR‐B1 and eNOS were downregulated when HUVECs were treated with 4.2 dyne/cm2 shear stress compared with those of the control group. However, the expression of SR‐B1 and eNOS was upregulated as HUVECs exposed to 8.4 and 15 dyne/cm2 shear stress. When exposed to 8.4 dyne/cm2, SR‐B1 and eNOS expression was significantly higher compared with those of the other groups. When SR‐B1 was knocked down through RNAi technique, the expression of eNOS was significantly downregulated than those of the other groups. While overexpression of SR‐B1 could upregulate eNOS significantly.
Conclusion
Shear stress regulates endothelial cell function through SR‐B1‐eNOS signaling pathway. SR‐B1 may play a pivotal role in the process of anti‐atherosclerosis.</description><identifier>ISSN: 1755-5914</identifier><identifier>EISSN: 1755-5922</identifier><identifier>DOI: 10.1111/1755-5922.12199</identifier><identifier>PMID: 27225585</identifier><language>eng</language><publisher>England: Hindawi Limited</publisher><subject>Cells, Cultured ; endothelial cell ; eNOS ; Gene Expression Regulation, Enzymologic ; Human Umbilical Vein Endothelial Cells ; Humans ; mechanosensor ; Mechanotransduction, Cellular ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; RNA Interference ; Scavenger Receptors, Class B - genetics ; Scavenger Receptors, Class B - metabolism ; shear stress ; SR‐B1 ; Stress, Mechanical ; Time Factors ; Transfection</subject><ispartof>Cardiovascular therapeutics, 2016-10, Vol.34 (5), p.308-313</ispartof><rights>2016 John Wiley & Sons Ltd</rights><rights>2016 John Wiley & Sons Ltd.</rights><rights>Copyright © 2016 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1755-5922.12199$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1755-5922.12199$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,11560,27922,27923,46050,46474</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2F1755-5922.12199$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27225585$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Ying</creatorcontrib><creatorcontrib>Liao, Bin</creatorcontrib><creatorcontrib>Li, Miaoling</creatorcontrib><creatorcontrib>Cheng, Min</creatorcontrib><creatorcontrib>Fu, Yong</creatorcontrib><creatorcontrib>Liu, Qing</creatorcontrib><creatorcontrib>Chen, Qi</creatorcontrib><creatorcontrib>Liu, Hongduan</creatorcontrib><creatorcontrib>Fang, Yibing</creatorcontrib><creatorcontrib>Zhang, Gen</creatorcontrib><creatorcontrib>Yu, Fengxu</creatorcontrib><title>Shear stress regulates endothelial cell function through SRB1‐eNOS signaling pathway</title><title>Cardiovascular therapeutics</title><addtitle>Cardiovasc Ther</addtitle><description>Summary
Aim
The aim of this study was to explore whether transmembrane flow shear stress could regulate eNOS expression and mediate endothelial cell function via SR‐B1 signaling transduction.
Methods
Parallel‐plate flow chamber was used to impose laminar shear stress and evaluate the effect of shear stress upon human umbilical vein endothelial cells (HUVECs). The expression of SR‐B1 and eNOS at both RNA and protein levels was detected under different dynamic conditions. RNA interference and gene transfection were performed to overexpress and knock down the SRB1 to confirm the role of SR‐B1‐eNOS signaling pathway.
Results
The expression levels of SR‐B1 and eNOS were downregulated when HUVECs were treated with 4.2 dyne/cm2 shear stress compared with those of the control group. However, the expression of SR‐B1 and eNOS was upregulated as HUVECs exposed to 8.4 and 15 dyne/cm2 shear stress. When exposed to 8.4 dyne/cm2, SR‐B1 and eNOS expression was significantly higher compared with those of the other groups. When SR‐B1 was knocked down through RNAi technique, the expression of eNOS was significantly downregulated than those of the other groups. While overexpression of SR‐B1 could upregulate eNOS significantly.
Conclusion
Shear stress regulates endothelial cell function through SR‐B1‐eNOS signaling pathway. SR‐B1 may play a pivotal role in the process of anti‐atherosclerosis.</description><subject>Cells, Cultured</subject><subject>endothelial cell</subject><subject>eNOS</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>mechanosensor</subject><subject>Mechanotransduction, Cellular</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>RNA Interference</subject><subject>Scavenger Receptors, Class B - genetics</subject><subject>Scavenger Receptors, Class B - metabolism</subject><subject>shear stress</subject><subject>SR‐B1</subject><subject>Stress, Mechanical</subject><subject>Time Factors</subject><subject>Transfection</subject><issn>1755-5914</issn><issn>1755-5922</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNpdkctOwzAQRS0EolBYs0OW2LBJscdxGi-hPKWKSi2wtZzYeVRpUuxEVXd8At_Il5C0pQtmM1czR6OrOwhdUDKgbd3QIeceFwADClSIA3SynxzuNfV76NS5OSEBEQE9Rj0YAnAe8hP0McuMstjV1jiHrUmbQtXGYVPqqs5MkasCx6YocNKUcZ1XJa4zWzVphmfTO_rz9W1eJzPs8rRURV6meKnqbKXWZ-goUYUz57veR--PD2-jZ288eXoZ3Y69ORMgPOoTYzRPYu0PeaB1KID5ISUQicREPoQESBwB0yxOSBDqIShBQSktkkCxWLM-ut7eXdrqszGulovcdX5VaarGSRoCBxpyylr06h86rxrb2t5QPhHgU2ipyx3VRAuj5dLmC2XX8i-xFuBbYJUXZr3fUyK7h8guctnFLzcPkaP76UawXzzhfOQ</recordid><startdate>201610</startdate><enddate>201610</enddate><creator>Zhang, Ying</creator><creator>Liao, Bin</creator><creator>Li, Miaoling</creator><creator>Cheng, Min</creator><creator>Fu, Yong</creator><creator>Liu, Qing</creator><creator>Chen, Qi</creator><creator>Liu, Hongduan</creator><creator>Fang, Yibing</creator><creator>Zhang, Gen</creator><creator>Yu, Fengxu</creator><general>Hindawi Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201610</creationdate><title>Shear stress regulates endothelial cell function through SRB1‐eNOS signaling pathway</title><author>Zhang, Ying ; Liao, Bin ; Li, Miaoling ; Cheng, Min ; Fu, Yong ; Liu, Qing ; Chen, Qi ; Liu, Hongduan ; Fang, Yibing ; Zhang, Gen ; Yu, Fengxu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j3929-140eed5fcd4756dd892348102b9feb428020cb23d3cf068d72a912aad9f6a3cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Cells, Cultured</topic><topic>endothelial cell</topic><topic>eNOS</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Human Umbilical Vein Endothelial Cells</topic><topic>Humans</topic><topic>mechanosensor</topic><topic>Mechanotransduction, Cellular</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>RNA Interference</topic><topic>Scavenger Receptors, Class B - genetics</topic><topic>Scavenger Receptors, Class B - metabolism</topic><topic>shear stress</topic><topic>SR‐B1</topic><topic>Stress, Mechanical</topic><topic>Time Factors</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Ying</creatorcontrib><creatorcontrib>Liao, Bin</creatorcontrib><creatorcontrib>Li, Miaoling</creatorcontrib><creatorcontrib>Cheng, Min</creatorcontrib><creatorcontrib>Fu, Yong</creatorcontrib><creatorcontrib>Liu, Qing</creatorcontrib><creatorcontrib>Chen, Qi</creatorcontrib><creatorcontrib>Liu, Hongduan</creatorcontrib><creatorcontrib>Fang, Yibing</creatorcontrib><creatorcontrib>Zhang, Gen</creatorcontrib><creatorcontrib>Yu, Fengxu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Zhang, Ying</au><au>Liao, Bin</au><au>Li, Miaoling</au><au>Cheng, Min</au><au>Fu, Yong</au><au>Liu, Qing</au><au>Chen, Qi</au><au>Liu, Hongduan</au><au>Fang, Yibing</au><au>Zhang, Gen</au><au>Yu, Fengxu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Shear stress regulates endothelial cell function through SRB1‐eNOS signaling pathway</atitle><jtitle>Cardiovascular therapeutics</jtitle><addtitle>Cardiovasc Ther</addtitle><date>2016-10</date><risdate>2016</risdate><volume>34</volume><issue>5</issue><spage>308</spage><epage>313</epage><pages>308-313</pages><issn>1755-5914</issn><eissn>1755-5922</eissn><abstract>Summary
Aim
The aim of this study was to explore whether transmembrane flow shear stress could regulate eNOS expression and mediate endothelial cell function via SR‐B1 signaling transduction.
Methods
Parallel‐plate flow chamber was used to impose laminar shear stress and evaluate the effect of shear stress upon human umbilical vein endothelial cells (HUVECs). The expression of SR‐B1 and eNOS at both RNA and protein levels was detected under different dynamic conditions. RNA interference and gene transfection were performed to overexpress and knock down the SRB1 to confirm the role of SR‐B1‐eNOS signaling pathway.
Results
The expression levels of SR‐B1 and eNOS were downregulated when HUVECs were treated with 4.2 dyne/cm2 shear stress compared with those of the control group. However, the expression of SR‐B1 and eNOS was upregulated as HUVECs exposed to 8.4 and 15 dyne/cm2 shear stress. When exposed to 8.4 dyne/cm2, SR‐B1 and eNOS expression was significantly higher compared with those of the other groups. When SR‐B1 was knocked down through RNAi technique, the expression of eNOS was significantly downregulated than those of the other groups. While overexpression of SR‐B1 could upregulate eNOS significantly.
Conclusion
Shear stress regulates endothelial cell function through SR‐B1‐eNOS signaling pathway. SR‐B1 may play a pivotal role in the process of anti‐atherosclerosis.</abstract><cop>England</cop><pub>Hindawi Limited</pub><pmid>27225585</pmid><doi>10.1111/1755-5922.12199</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cardiovascular therapeutics, 2016-10, Vol.34 (5), p.308-313 |
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| subjects | Cells, Cultured endothelial cell eNOS Gene Expression Regulation, Enzymologic Human Umbilical Vein Endothelial Cells Humans mechanosensor Mechanotransduction, Cellular Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - metabolism RNA Interference Scavenger Receptors, Class B - genetics Scavenger Receptors, Class B - metabolism shear stress SR‐B1 Stress, Mechanical Time Factors Transfection |
| title | Shear stress regulates endothelial cell function through SRB1‐eNOS signaling pathway |
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