Insulin does not disrupt actin microfilaments, microtubules, and in vitro aortic endothelial wound repair

In the face of small denuding injuries, the endothelium undergoes a process of rapid repair involving actin microfilaments, microtubules, and centrosomes to reestablish an intact monolayer. Failure to maintain an intact endothelial monolayer is an important factor in the pathogenesis of the atherosclerotic plaque. It was hypothesized that increased susceptibility to atherosclerosis in diabetes mellitus may be, in part, due to delayed reendothelialization following endothelial injury. To test this, the effects of high insulin concentrations on the reendothelialization of small wounds were examined using an in vitro porcine aortic endothelial cell wound model. Elevated concentrations of insulin did not disrupt the confluent endothelial monolayer or alter endothelial cell shape. Insulin also did not induce detectable alterations in the distribution of microtubules and microfilaments in the confluent monolayer. High insulin did not reduce the extent of reendothelialization of a linear wound made in the confluent monolayer. Centrosomal reorientation was similar to that of control wounded cultures as was the reorganization of the microfilaments and microtubules. The data suggest that the atherogenic effects of hyperinsulinemia are not due to disruption of endothelial repair.