In the course of studying crosstalk between inflammation and angiogenesis, high doses of pro inflammatory factors have been reported to induce apoptosis in cells. Under normal circumstances also the pro-inflammatory cytokines are being released in low doses and are actively involved in cell signaling pathways. We studied the effects of low grade inflammation in growth factor induced angiogenesis using tumor necrosis factor alfa (TNF alpha) and vascular endothelial growth factor A (VEGF) respectively. We found that low dose of TNF alpha can inhibit VEGF induced angiogenesis in human umbilical vein endothelial cells (HUVECs). Low dose of TNF alpha induces mild upregulation and moreover nuclear localization of tumor suppressor protein 53 (P53) which causes decrease in inhibitor of DNA binding-1 (Idl) expression and shuttling to the cytoplasm. In absence of Idl, HUVECs fail to upregulate beta(3)-integrin and cell migration is decreased. Connecting low dose of TNF alpha induced p53 to beta(3)a-integrin through Idl, we present additional link in cross talk between inflammation and angiogenesis. (C) 2016 Elsevier Inc. All rights reserved.