Endothelial cell Pannexin1 modulates severity of ischemic stroke by regulating cerebral inflammation and myogenic tone.

摘要: Ischemic stroke is a leading cause of morbidity and mortality in the US; however, there currently exists only one effective acute pharmacological therapeutic intervention. Purinergic signaling has been shown to regulate vascular function pathological processes, including inflammation arterial myogenic reactivity, plays role ischemic outcome. requires extracellular purines; mechanism purine release from cells unclear. Pannexin1 (Panx1) channels are potentially novel expressed throughout tree that couples regulated with purinergic signaling. Therefore, we examined smooth muscle endothelial cell Panx1, using conditional type-specific transgenic mice, cerebral ischemia/reperfusion injury outcomes. Deletion but not significantly reduced infarct volume after ischemia/reperfusion. Infiltration leukocytes into brain tissue development tone were both when mice lacked Panx1. Panx1 regulation was unique circulation, as mesenteric reactivity blood pressure independent Overall, deletion mitigated by reducing development, indicating possible target for intervention stroke.