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dc.contributor.authorPang, Paul Danielen_US
dc.date.accessioned2015-08-04T15:59:20Z
dc.date.available2015-08-04T15:59:20Z
dc.date.issued2013
dc.date.submitted2013
dc.identifier.other
dc.identifier.urihttps://hdl.handle.net/2144/12179
dc.descriptionThesis (M.A.)--Boston Universityen_US
dc.description.abstractRegulator of G protein Signaling 4 (RGS4) has previously been shown to prevent prolonged vasoconstriction by binding to the Gq heterodimer. However, the known anti-inflammatory role of RGS4 has not been applied to reperfusion injury in the context of G protein signaling. The aims of this study is to elucidate the expression pattern of RGS4 in renal reperfusion injury to determine if cell signaling initiated by Angiotensin II, a known ligand of Gαq coupled-receptors, is modulated by RGS4. LacZ reporter animals were used to characterize RGS4 expression during reperfusion. Human smooth muscle cells co-cultured with human endothelial cells demonstrated that AngII induces apoptosis in the absence of RGS4 and initiates RANTES expression in smooth muscle cells. SMMHC-Cre rgs4fl/fl confirmed the role of vascular smooth muscle cells to inhibit macrophage localization during reperfusion injury. RGS4 expression in vascular smooth muscle cells therefore inhibits AngII-mediated oxidative stress, leukocyte recruitment by the same cell type, and endothelial damage prior to tubular epithelial injury.en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.titleRole of the Regulator of G protein Signaling 4 in renal ischemic reperfusion injury and repairen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameMaster of Artsen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


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