Tumor angiogenesis, the ability of tumor cells to stimulate blood vessel growth, is one the most critical steps of tumor progression. To support the growth of the expanding tumor, the “angiogenic switch” is turned on, which is often triggered by hypoxia (i.e., low oxygen)-mediated events such as expression of vascular endothelial growth factor (VEGF), causing normally quiescent endothelial cells to proliferate and sprout. An emerging picture of angiogenesis suggests that while governed by complex mechanisms, cell adhesion molecules (CAMs) plays a pivotal role in the regulation of angiogenesis. Our laboratory recently identified multiple previously unknown proteins including, transmembrane and immunoglobulin domain containing 1 (TMIGD1) and immunoglobulin-containing and proline-rich receptor 1 (IGPR1). Immunoglobulin-containing and cysteine-rich receptor 1 (IGCR1) represents the third remember of IGPR-1 family proteins. To investigate the expression and function of IGCR1, we have developed a rabbit polyclonal anti-IGCR1 antibody and demonstrated that IGCR1 is expressed in the endothelial cells of human blood vessels. To examine possible function of IGCR1, we have generated porcine aortic endothelial (PAE) cells over-expressing IGCR1. We demonstrate that IGCR1 expression in PAE cells inhibited cell proliferation and capillary tube formation as measured by colorimetric MTT and matrigel tube formation assays, respectively. In contrast, over-expression of IGCR1 in PAE cells inhibited cell migration as measured by wounding assay. Taken together, this study identifies IGCR1 as a novel regulator of angiogenesis. Given, angiogenesis is a highly coordinated cellular processes controlled spatially and temporally by a myriad of cell surface receptors and ligands, IGCR1 by modulating the rate of endothelial cell proliferation and migration, plays a significant role in the formation of blood vessels. / 2018-07-11T00:00:00Z