biostudies-literatureMcCrary MRNational Institute of Neurological Disorders and StrokeAmerican Heart AssociationRRD VANINDS NIH HHSNIGMS NIH HHS10680-10691https://www.ebi.ac.uk/biostudies/studies/S-EPMC6766648biostudies-literatureUnknown33(10)GPCR 37 (GPR37) is a GPCR expressed in the CNS; its physiological and pathophysiological functions are largely unknown. We tested the role of GPR37 in the ischemic brain of GPR37 knockout (KO) mice, exploring the idea that GPR37 might be protective against ischemic damage. In an ischemic stroke model, GPR37 KO mice exhibited increased infarction and cell death compared with wild-type (WT) mice, measured by 2,3,5-triphenyl-2H-tetrazolium chloride and TUNEL staining 24 h after stroke. Moreover, more severe functional deficits were detected in GPR37 KO mice in the adhesive-removal and corner tests. In the peri-infarct region of GPR37 KO mice, there was significantly more apoptotic and autophagic cell death accompanied by caspase-3 activation and attenuated mechanistic target of rapamycin signFASEB journal : official publication of the Federation of American Societies for Experimental BiologyProtective effects of GPR37 <i>via</i> regulation of inflammation and multiple cell death pathways after ischemic stroke in mice.PMC6766648R01 NS085568NS073378R01 NS088413R44 NS073378I01 RX000666NS091585NS088413R42 NS073378R01 NS091585T32 GM008169NS085568POST25710112R41 NS073378Wei ZZJiang MQGu XMcCrary MRZhang JYGiddens MMZhong WYu SPXin HHall RAOwino SWei LfalseProtective effects of GPR37 <i>via</i> regulation of inflammation and multiple cell death pathways after ischemic stroke in mice.GPCR 37 (GPR37) is a GPCR expressed in the CNS; its physiological and pathophysiological functions are largely unknown. We tested the role of GPR37 in the ischemic brain of GPR37 knockout (KO) mice, exploring the idea that GPR37 might be protective against ischemic damage. In an ischemic stroke model, GPR37 KO mice exhibited increased infarction and cell death compared with wild-type (WT) mice, measured by 2,3,5-triphenyl-2H-tetrazolium chloride and TUNEL staining 24 h after stroke. Moreover, more severe functional deficits were detected in GPR37 KO mice in the adhesive-removal and corner tests. In the peri-infarct region of GPR37 KO mice, there was significantly more apoptotic and autophagic cell death accompanied by caspase-3 activation and attenuated mechanistic target of rapamycin sign2019-01-01T00:00:00Z2019 Oct2026-06-04T00:58:39.373Z2020-07-06T07:04:12ZS-EPMC67666483126873610.1096/fj.201900070R10.1096/fj.201900070r