The Proton-Sensing GPR4 Receptor Regulates Paracellular Gap Formation and Permeability of Vascular Endothelial Cells
- ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
- Elizabeth A.,Sanderlin,Edward J.,Marie,Mona A.,Akhtar,Shayan Krewson (Creator)
- Institution
- East Carolina University (ECU )
- Web Site: http://www.ecu.edu/lib/
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.
Additional Information
- Publication
- Other
- Language: English
- Date: 2020
| Title | Location & Link | Type of Relationship |
| The Proton-Sensing GPR4 Receptor Regulates Paracellular Gap Formation and Permeability of Vascular Endothelial Cells | http://hdl.handle.net/10342/7827 | The described resource references, cites, or otherwise points to the related resource. |