Different roles of CD31/PECAM1

Platelet endothelial cell adhesion molecule 1 (PECAM1), also known as cluster of differentiation 31 (CD31), is a cell-surface glycoprotein expressed on platelets, monocytes, neutrophils, some types of T-cells and NK (natural killer) cells. It makes up a large portion of the endothelial cell intercellular junctions. CD31/PECAM1 is a member of the immunoglobulin superfamily and plays many different roles involving leukocyte migration under most inflammatory conditions, angiogenesis, integrin activation, atherosclerosis and thrombopoiesis.

Diseases associated with CD31/PECAM1 include angiosarcoma and pulmonary vein stenosis. Among its related super-pathways are response to elevated platelet cytosolic Ca2+ and hemostasis.

CD31/PECAM1 is commonly used as an endothelial marker, particularly in angiogenesis. It has an important role in assisting placental and endometrial vascular development. However, it is also associated with many negative angiogenic occurrences, particularly those within or related to tumors and other disease lesions. These include MS, cardiac angiosarcoma and prostate cancer.

Novus CD31/PECAM antibody NB600-562 was used in a study about quantification and prognostic relevance of angiogenic parameters in invasive cervical cancer. Tumor stromal neovascularization was investigated in carcinomas of the uterine cervix by staining representative sections with the specific endothelial marker anti CD31 (clone JC/70A, isotope IgG1). It has been shown that all angiogenesis parameters had prognostic value. In the future these criteria may be used for selection of patients for anti-angiogenesis therapy. (1)

Western Blot: CD31/PECAM1 Antibody (JC/70A) [NB600-562]

CD31 is thought to contribute to the physiological regulation T cell homeostasis due to the presence of two immunotyrosine-based inhibitory motifs in its cytoplasmic tail. Loss of CD31 expression leads to uncontrolled T cell-mediated inflammation and certain CD31 polymorphisms correlate with increased disease severity in human graft-versus-host disease and atherosclerosis. Kishore’s group used the Novus CD31 antibody NB100-92205 in their study proposing that CD31-mediated modulation of memory T cell chemokinesis is a key mechanism by which this molecule contributes to the homeostatic regulation of effector T cell immunity. (2)

PECAM-1 (CD31) might also play an important role in regulating antigen-specific T cells trafficking in CNS inflammatory diseases. (3)