Several lines of evidence suggests that neovascularization in adult organism may be mediated by circulating progenitor cells. During ischemia and brain injury, populations of endothelial progenitor cells are mobilized and recruited to ischemic and injured areas, accelerating the neovascularization process. Surgical brain injury causes neovascularization in the disrupted brain parenchyma, which occurs with participation of endothelial-like cells. The aim of study was comparison of ultrastructural and immunohistochemical features of endothelial progenitor cells participated in new vessel formation following surgical brain injury in non-diabetic and diabetic rats. We investigated subcellular localization of protein markers: Flk-1, AC133 and vimentin. We detected the presence of immature endothelial cells showing positive immunostaining for all investigated markers in the proximity to the injured brain area in diabetic rats. Only few these cells were observed in the brains of non-diabetic animals. Ultrastructural studies showed many morphological changes within capillaries in the injured brain derived from diabetic animals. Our results point to the diabetes related dysfunction of the brain capillaries. The number of progenitors and, probably, their abnormal differentiation contribute to disorders in the process of repair following the injury in diabetes-affected rats.
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