4.5 Review Retracted Publication

被撤回的出版物: Endothelial PECAM-1 and its function in vascular physiology and atherogenic pathology (Retracted article. See vol. 127, 2022)

期刊

EXPERIMENTAL AND MOLECULAR PATHOLOGY
卷 100, 期 3, 页码 409-415

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yexmp.2016.03.012

关键词

Endothelial cell adhesion molecules; Platelet endothelial cell adhesion molecule-1; PECAM-1; Endothelial barrier function; Vascular physiology Atherosclerosis; Inflammation

资金

  1. Russian Science Foundation, Russian Federation [14-15-00112]
  2. Russian Science Foundation [14-15-00112] Funding Source: Russian Science Foundation

向作者/读者索取更多资源

Platelet endothelial cell adhesion molecule (PECAM-1) is highly expressed in vascular cells such as endothelial cells (ECs) and blood-borne cells like platelets and leukocytes. In ECs, this molecule controls junctional and adhesive properties. In physiological conditions, PECAM-1 supports the endothelial battier function. In inflammation that is observed in vessels affected by atherosclerosis, the function of PECAM-1 is impaired, an event that leads to increased adhesion of neutrophils and other leukocytes to ECs, decreased vascular integrity, and higher leukocyte transmigration to the intima media. PECAM-1 has six extracellular immunoglobulin (Ig)-like domains that support attraction and adhesion of leukocytes to ECs. The cytoplasmic tail of PECAM-1 contains two tyrosine residues (Tyr-663 and Tyr-686) that could be phosphorylated by Src family protein kinases is involved in the intracellular signaling. Actually, those tyrosines are the part of the immunoreceptor tyrosine-based inhibition motifs (ITIMs) that inhibit inflammation. However, in atherosclerosis, the PECAM-1-dependent immune suppression is disturbed. This in turn facilitates recruitment of leukocytes and supports proatherogenic inflammation. (C) 2016 Elsevier Inc. All rights reserved.

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