The Proton-Sensing GPR4 Receptor Regulates Paracellular Gap Formation and Permeability of Vascular Endothelial Cells

dc.contributor.author	Krewson, Elizabeth A.
dc.contributor.author	Sanderlin, Edward J.
dc.contributor.author	Marie, Mona A.
dc.contributor.author	Akhtar, Shayan Nik
dc.contributor.author	Velcicky, Juraj
dc.contributor.author	Loetscher, Pius
dc.contributor.author	Yang, Li V.
dc.date.accessioned	2020-04-02T19:21:32Z
dc.date.available	2020-04-02T19:21:32Z
dc.date.issued	2020-02-21
dc.description.abstract	be activated by protons in the inflamed tissue microenvironment. Herein, we report that acidosis-induced GPR4 activation increases paracellular gap formation and permeability of vascular endothelialcells through the Ga12/13/Rho GTPase signaling pathway. Evaluation of GPR4 in the inflammatoryresponse using the acute hindlimb ischemia-reperfusion mouse model revealed that GPR4 mediatestissue edema, inflammatory exudate formation, endothelial adhesion molecule expression, and leuko-cyte infiltration in the inflamed tissue. Genetic knockout and pharmacologic inhibition of GPR4alleviate tissue inflammation. These results suggest GPR4 is a pro-inflammatory receptor and couldbe targeted for therapeutic intervention.	en_US
dc.identifier.doi	10.1016/j.isci.2020.100848
dc.identifier.uri	http://hdl.handle.net/10342/7827
dc.title	The Proton-Sensing GPR4 Receptor Regulates Paracellular Gap Formation and Permeability of Vascular Endothelial Cells	en_US
dc.type	Article	en_US
ecu.journal.issue	2	en_US
ecu.journal.name	iScience	en_US
ecu.journal.volume	23	en_US

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