contacts with pericytes. communication between endothelial cells and pericytes is vital. inhibiting the pdgf pathway leads to pericyte deficiency. this causes endothelial hyperplasia, abnormal junctions, and diabetic retinopathy. a lack of pericytes also causes an upregulation of vascular endothelial growth factor (vegf), leading to vascular leakage and hemorrhage. angiopoietin 2 can act as an antagonist to tie-2, destabilizing the endothelial cells, which results in less endothelial cell and pericyte interaction. this occasionally leads to the formation of tumors. similar to the inhibition of the pdgf pathway, angiopoietin 2 reduces levels of pericytes, leading to diabetic retinopathy. scarring usually, astrocytes are associated with the scarring process in the central nervous system, forming glial scars. it has been proposed that a subtype of pericytes participates in this scarring in a glial-independent manner. through lineage tracking studies, these subtype of pericytes were followed after stroke, revealing that they contribute to the glial scar by differentiating into myofibroblasts and depositing extracellular matrix. however, this remains controversial, as more recent studies suggest that the cell type followed in these scar studies is likely to be not pericytes, but fibroblasts. contribution to adult neurogenesis the emerging evidence (as of 2019) suggests that neural microvascular pericytes, under instruction from resident glial cells, are reprogrammed into interneurons and enrich local neuronal microcircuits. this response is amplified by concomitant angiogenesis.