Targeting Gαi2 in neutrophils protects from myocardial ischemia reperfusion injury

Neutrophils are not only involved in immune defense against infection but also contribute to the exacerbation of tissue damage after ischemia and reperfusion. We have previously shown that genetic ablation of regulatory Gα i proteins in mice has both protective and deleterious effects on myocardial ischemia reperfusion injury (mIRI), depending on which isoform is deleted. To deepen and analyze these findings in more detail the contribution of Gα i2 proteins in resident cardiac vs circulating blood cells for mIRI was first studied in bone marrow chimeras. In fact, the absence of Gα i2 in all blood cells reduced the extent of mIRI (22,9% infarct size of area at risk (AAR) Gnai2 −/− → wt vs 44.0% wt → wt; p