GPR68 Senses Flow and Is Essential for Vascular Physiology
Mechanotransduction plays a crucial role in vascular biology. One example of this is the local regulation of vascular resistance via flow-mediated dilation (FMD). Impairment of this process is a hallmark of endothelial dysfunction and a precursor to a wide array of vascular diseases, such as hyperte...
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| Veröffentlicht in: | Cell 2018-04, Vol.173 (3), p.762-775.e16 |
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| creator | Xu, Jie Mathur, Jayanti Vessières, Emilie Hammack, Scott Nonomura, Keiko Favre, Julie Grimaud, Linda Petrus, Matt Francisco, Allain Li, Jingyuan Lee, Van Xiang, Fu-li Mainquist, James K. Cahalan, Stuart M. Orth, Anthony P. Walker, John R. Ma, Shang Lukacs, Viktor Bordone, Laura Bandell, Michael Laffitte, Bryan Xu, Yan Chien, Shu Henrion, Daniel Patapoutian, Ardem |
| description | Mechanotransduction plays a crucial role in vascular biology. One example of this is the local regulation of vascular resistance via flow-mediated dilation (FMD). Impairment of this process is a hallmark of endothelial dysfunction and a precursor to a wide array of vascular diseases, such as hypertension and atherosclerosis. Yet the molecules responsible for sensing flow (shear stress) within endothelial cells remain largely unknown. We designed a 384-well screening system that applies shear stress on cultured cells. We identified a mechanosensitive cell line that exhibits shear stress-activated calcium transients, screened a focused RNAi library, and identified GPR68 as necessary and sufficient for shear stress responses. GPR68 is expressed in endothelial cells of small-diameter (resistance) arteries. Importantly, Gpr68-deficient mice display markedly impaired acute FMD and chronic flow-mediated outward remodeling in mesenteric arterioles. Therefore, GPR68 is an essential flow sensor in arteriolar endothelium and is a critical signaling component in cardiovascular pathophysiology.
[Display omitted]
•Design of a novel high-throughput assay for cellular mechanosensation•An RNAi screen identifies GPR68 as a mechanosensor•GPR68 is necessary and sufficient for responses to fluid shear stress•GPR68 is required for flow-induced dilation and remodeling in mice
A GPCR is a critical sensor for fluid shear stress in blood vessels. |
| doi_str_mv | 10.1016/j.cell.2018.03.076 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5951615</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0092867418304483</els_id><sourcerecordid>2028948661</sourcerecordid><originalsourceid>FETCH-LOGICAL-c455t-119ee6f1e5813d72a360f09ca552beaa47071ff66c8c83ec588344a264a83eac3</originalsourceid><addsrcrecordid>eNp9kFtLAzEQhYMoWqt_wAfZR192nWQ3lxURpNQLCBZvryHNztaU7UaTttJ_75aq6ItPwzDnnDl8hBxRyChQcTrNLDZNxoCqDPIMpNgiPQqlTAsq2TbpAZQsVUIWe2Q_xikAKM75LtljpZCSU9kjZ9ejB6GSR2wjxuSq8R-JaavkNibDGLGdO9MktQ_Ji4l20ZiQjF5X0fnGT1YHZKc2TcTDr9knz1fDp8FNend_fTu4vEttwfk8pbREFDVFrmheSWZyATWU1nDOxmhMIUHSuhbCKqtytFypvCgME4XpVmPzPrnY5L4txjOsbNcqmEa_BTczYaW9cfrvpXWveuKXmpecCsq7gJOvgODfFxjneubiGp1p0S-iZsBUWSghaCdlG6kNPsaA9c8bCnoNXU_12qnX0DXkuoPemY5_F_yxfFPuBOcbAXaYlg6DjtZha7FyAe1cV979l_8Jh0uSvw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2028948661</pqid></control><display><type>article</type><title>GPR68 Senses Flow and Is Essential for Vascular Physiology</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><source>Cell Press Free Archives</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Xu, Jie ; Mathur, Jayanti ; Vessières, Emilie ; Hammack, Scott ; Nonomura, Keiko ; Favre, Julie ; Grimaud, Linda ; Petrus, Matt ; Francisco, Allain ; Li, Jingyuan ; Lee, Van ; Xiang, Fu-li ; Mainquist, James K. ; Cahalan, Stuart M. ; Orth, Anthony P. ; Walker, John R. ; Ma, Shang ; Lukacs, Viktor ; Bordone, Laura ; Bandell, Michael ; Laffitte, Bryan ; Xu, Yan ; Chien, Shu ; Henrion, Daniel ; Patapoutian, Ardem</creator><creatorcontrib>Xu, Jie ; Mathur, Jayanti ; Vessières, Emilie ; Hammack, Scott ; Nonomura, Keiko ; Favre, Julie ; Grimaud, Linda ; Petrus, Matt ; Francisco, Allain ; Li, Jingyuan ; Lee, Van ; Xiang, Fu-li ; Mainquist, James K. ; Cahalan, Stuart M. ; Orth, Anthony P. ; Walker, John R. ; Ma, Shang ; Lukacs, Viktor ; Bordone, Laura ; Bandell, Michael ; Laffitte, Bryan ; Xu, Yan ; Chien, Shu ; Henrion, Daniel ; Patapoutian, Ardem</creatorcontrib><description>Mechanotransduction plays a crucial role in vascular biology. One example of this is the local regulation of vascular resistance via flow-mediated dilation (FMD). Impairment of this process is a hallmark of endothelial dysfunction and a precursor to a wide array of vascular diseases, such as hypertension and atherosclerosis. Yet the molecules responsible for sensing flow (shear stress) within endothelial cells remain largely unknown. We designed a 384-well screening system that applies shear stress on cultured cells. We identified a mechanosensitive cell line that exhibits shear stress-activated calcium transients, screened a focused RNAi library, and identified GPR68 as necessary and sufficient for shear stress responses. GPR68 is expressed in endothelial cells of small-diameter (resistance) arteries. Importantly, Gpr68-deficient mice display markedly impaired acute FMD and chronic flow-mediated outward remodeling in mesenteric arterioles. Therefore, GPR68 is an essential flow sensor in arteriolar endothelium and is a critical signaling component in cardiovascular pathophysiology.
[Display omitted]
•Design of a novel high-throughput assay for cellular mechanosensation•An RNAi screen identifies GPR68 as a mechanosensor•GPR68 is necessary and sufficient for responses to fluid shear stress•GPR68 is required for flow-induced dilation and remodeling in mice
A GPCR is a critical sensor for fluid shear stress in blood vessels.</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/j.cell.2018.03.076</identifier><identifier>PMID: 29677517</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Biocompatible Materials ; blood flow ; Calcium - metabolism ; Cell Line, Tumor ; Endothelial Cells - physiology ; Endothelium, Vascular - cytology ; GPCR ; HEK293 Cells ; Human Umbilical Vein Endothelial Cells ; Humans ; Hydrogen-Ion Concentration ; mechanosensation ; mechanotransduction ; Mechanotransduction, Cellular ; Mesenteric Arteries - physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nitric Oxide - metabolism ; outward remodeling ; Receptors, G-Protein-Coupled - genetics ; Receptors, G-Protein-Coupled - physiology ; RNA Interference ; RNA, Small Interfering - metabolism ; Shear Strength ; shear stress ; Stress, Mechanical ; vascular biology ; Vascular Resistance ; vasodilation</subject><ispartof>Cell, 2018-04, Vol.173 (3), p.762-775.e16</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-119ee6f1e5813d72a360f09ca552beaa47071ff66c8c83ec588344a264a83eac3</citedby><cites>FETCH-LOGICAL-c455t-119ee6f1e5813d72a360f09ca552beaa47071ff66c8c83ec588344a264a83eac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cell.2018.03.076$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29677517$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Jie</creatorcontrib><creatorcontrib>Mathur, Jayanti</creatorcontrib><creatorcontrib>Vessières, Emilie</creatorcontrib><creatorcontrib>Hammack, Scott</creatorcontrib><creatorcontrib>Nonomura, Keiko</creatorcontrib><creatorcontrib>Favre, Julie</creatorcontrib><creatorcontrib>Grimaud, Linda</creatorcontrib><creatorcontrib>Petrus, Matt</creatorcontrib><creatorcontrib>Francisco, Allain</creatorcontrib><creatorcontrib>Li, Jingyuan</creatorcontrib><creatorcontrib>Lee, Van</creatorcontrib><creatorcontrib>Xiang, Fu-li</creatorcontrib><creatorcontrib>Mainquist, James K.</creatorcontrib><creatorcontrib>Cahalan, Stuart M.</creatorcontrib><creatorcontrib>Orth, Anthony P.</creatorcontrib><creatorcontrib>Walker, John R.</creatorcontrib><creatorcontrib>Ma, Shang</creatorcontrib><creatorcontrib>Lukacs, Viktor</creatorcontrib><creatorcontrib>Bordone, Laura</creatorcontrib><creatorcontrib>Bandell, Michael</creatorcontrib><creatorcontrib>Laffitte, Bryan</creatorcontrib><creatorcontrib>Xu, Yan</creatorcontrib><creatorcontrib>Chien, Shu</creatorcontrib><creatorcontrib>Henrion, Daniel</creatorcontrib><creatorcontrib>Patapoutian, Ardem</creatorcontrib><title>GPR68 Senses Flow and Is Essential for Vascular Physiology</title><title>Cell</title><addtitle>Cell</addtitle><description>Mechanotransduction plays a crucial role in vascular biology. One example of this is the local regulation of vascular resistance via flow-mediated dilation (FMD). Impairment of this process is a hallmark of endothelial dysfunction and a precursor to a wide array of vascular diseases, such as hypertension and atherosclerosis. Yet the molecules responsible for sensing flow (shear stress) within endothelial cells remain largely unknown. We designed a 384-well screening system that applies shear stress on cultured cells. We identified a mechanosensitive cell line that exhibits shear stress-activated calcium transients, screened a focused RNAi library, and identified GPR68 as necessary and sufficient for shear stress responses. GPR68 is expressed in endothelial cells of small-diameter (resistance) arteries. Importantly, Gpr68-deficient mice display markedly impaired acute FMD and chronic flow-mediated outward remodeling in mesenteric arterioles. Therefore, GPR68 is an essential flow sensor in arteriolar endothelium and is a critical signaling component in cardiovascular pathophysiology.
[Display omitted]
•Design of a novel high-throughput assay for cellular mechanosensation•An RNAi screen identifies GPR68 as a mechanosensor•GPR68 is necessary and sufficient for responses to fluid shear stress•GPR68 is required for flow-induced dilation and remodeling in mice
A GPCR is a critical sensor for fluid shear stress in blood vessels.</description><subject>Animals</subject><subject>Biocompatible Materials</subject><subject>blood flow</subject><subject>Calcium - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Endothelial Cells - physiology</subject><subject>Endothelium, Vascular - cytology</subject><subject>GPCR</subject><subject>HEK293 Cells</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>Hydrogen-Ion Concentration</subject><subject>mechanosensation</subject><subject>mechanotransduction</subject><subject>Mechanotransduction, Cellular</subject><subject>Mesenteric Arteries - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nitric Oxide - metabolism</subject><subject>outward remodeling</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>Receptors, G-Protein-Coupled - physiology</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Shear Strength</subject><subject>shear stress</subject><subject>Stress, Mechanical</subject><subject>vascular biology</subject><subject>Vascular Resistance</subject><subject>vasodilation</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kFtLAzEQhYMoWqt_wAfZR192nWQ3lxURpNQLCBZvryHNztaU7UaTttJ_75aq6ItPwzDnnDl8hBxRyChQcTrNLDZNxoCqDPIMpNgiPQqlTAsq2TbpAZQsVUIWe2Q_xikAKM75LtljpZCSU9kjZ9ejB6GSR2wjxuSq8R-JaavkNibDGLGdO9MktQ_Ji4l20ZiQjF5X0fnGT1YHZKc2TcTDr9knz1fDp8FNend_fTu4vEttwfk8pbREFDVFrmheSWZyATWU1nDOxmhMIUHSuhbCKqtytFypvCgME4XpVmPzPrnY5L4txjOsbNcqmEa_BTczYaW9cfrvpXWveuKXmpecCsq7gJOvgODfFxjneubiGp1p0S-iZsBUWSghaCdlG6kNPsaA9c8bCnoNXU_12qnX0DXkuoPemY5_F_yxfFPuBOcbAXaYlg6DjtZha7FyAe1cV979l_8Jh0uSvw</recordid><startdate>20180419</startdate><enddate>20180419</enddate><creator>Xu, Jie</creator><creator>Mathur, Jayanti</creator><creator>Vessières, Emilie</creator><creator>Hammack, Scott</creator><creator>Nonomura, Keiko</creator><creator>Favre, Julie</creator><creator>Grimaud, Linda</creator><creator>Petrus, Matt</creator><creator>Francisco, Allain</creator><creator>Li, Jingyuan</creator><creator>Lee, Van</creator><creator>Xiang, Fu-li</creator><creator>Mainquist, James K.</creator><creator>Cahalan, Stuart M.</creator><creator>Orth, Anthony P.</creator><creator>Walker, John R.</creator><creator>Ma, Shang</creator><creator>Lukacs, Viktor</creator><creator>Bordone, Laura</creator><creator>Bandell, Michael</creator><creator>Laffitte, Bryan</creator><creator>Xu, Yan</creator><creator>Chien, Shu</creator><creator>Henrion, Daniel</creator><creator>Patapoutian, Ardem</creator><general>Elsevier Inc</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><scope>5PM</scope></search><sort><creationdate>20180419</creationdate><title>GPR68 Senses Flow and Is Essential for Vascular Physiology</title><author>Xu, Jie ; 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One example of this is the local regulation of vascular resistance via flow-mediated dilation (FMD). Impairment of this process is a hallmark of endothelial dysfunction and a precursor to a wide array of vascular diseases, such as hypertension and atherosclerosis. Yet the molecules responsible for sensing flow (shear stress) within endothelial cells remain largely unknown. We designed a 384-well screening system that applies shear stress on cultured cells. We identified a mechanosensitive cell line that exhibits shear stress-activated calcium transients, screened a focused RNAi library, and identified GPR68 as necessary and sufficient for shear stress responses. GPR68 is expressed in endothelial cells of small-diameter (resistance) arteries. Importantly, Gpr68-deficient mice display markedly impaired acute FMD and chronic flow-mediated outward remodeling in mesenteric arterioles. Therefore, GPR68 is an essential flow sensor in arteriolar endothelium and is a critical signaling component in cardiovascular pathophysiology.
[Display omitted]
•Design of a novel high-throughput assay for cellular mechanosensation•An RNAi screen identifies GPR68 as a mechanosensor•GPR68 is necessary and sufficient for responses to fluid shear stress•GPR68 is required for flow-induced dilation and remodeling in mice
A GPCR is a critical sensor for fluid shear stress in blood vessels.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>29677517</pmid><doi>10.1016/j.cell.2018.03.076</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biocompatible Materials blood flow Calcium - metabolism Cell Line, Tumor Endothelial Cells - physiology Endothelium, Vascular - cytology GPCR HEK293 Cells Human Umbilical Vein Endothelial Cells Humans Hydrogen-Ion Concentration mechanosensation mechanotransduction Mechanotransduction, Cellular Mesenteric Arteries - physiology Mice Mice, Inbred C57BL Mice, Knockout Nitric Oxide - metabolism outward remodeling Receptors, G-Protein-Coupled - genetics Receptors, G-Protein-Coupled - physiology RNA Interference RNA, Small Interfering - metabolism Shear Strength shear stress Stress, Mechanical vascular biology Vascular Resistance vasodilation |
| title | GPR68 Senses Flow and Is Essential for Vascular Physiology |
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