| Leukocyte diapedesis |
PECAM-1 helps leukocytes transmigrate through the cell-cell junction and basement membrane |
(Thompson et al. 2001;Wang et al. 2005;Woodfin et al. 2009;Duncan et al. 1999;Bixel et al. 2010) |
| ICAM-1-activated Src and eNOS signaling sequentially induce PECAM-1-mediated PMN transendothelial migration through Tyr686 phosphorylation and increased EC PECAM-1 surface expression |
(Liu et al. 2012) |
| PECAM-1 is part of the LBRC, a surface connected membrane compartment, that promotes leukocyte transmigration |
(Mamdouh et al. 2003;Mamdouh et al. 2008;Mamdouh et al. 2009;Dasgupta et al. 2009;Sullivan et al. 2013) |
| Monocyte diapedesis alters endothelial junctional organization to a more monocyte-permeable state (increased PECAM-1 and decreased VE-cadherin expression), which augments transmigratory activity |
(Hashimoto et al. 2011) |
| Mechanotransduction and atherogenesis |
PECAM-1 transmits mechanical force in a mechanosensory complex with VE-cadherin and VEGFR2 to confer responsiveness to flow in endothelial cells and activate pro-inflammatory signaling pathways in response to disturbed flow |
(Tzima et al. 2005) |
| PECAM-1 and Gαq11 are part of a sensory complex at EC junctions that respond to rapid changes in fluid shear stress |
(Otte et al. 2009) |
| Localized tensional forces on PECAM-1 result in activation of PI3K, cell-wide activation of integrins and the small GTPase RhoA, which facilitates changes in cytoskeletal architecture and focal adhesions |
(Collins et al. 2012) |
| PECAM-1 expression is correlated with more plaques in atherosusceptible regions of the aorta |
(Harry et al. 2008;Stevens et al. 2008) |
| Expression of PECAM-1 is correlated with decreased atherosclerotic lesion area in the total aorta with preferential protection in the aortic sinus, descending aorta, and the branching arteries of the aortic arch |
(Goel et al. 2008) |
| PECAM-1 mechanotransduction is essential for fibronectin gene expression and assembly into matrix fibrils in response to fluid shear stress |
(Feaver et al. 2010) |
| EC conditioned by shear stress recruit fewer flowing neutrophils after stimulation with TNF, a response that is less effective in the absence of PECAM-1. Expression of CD31 is not required for the shear-induced modification of wound closure |
(Glen et al. 2012) |
| Paracellular permeability |
PECAM-1-specific antibody fragments augment albumin transit across endothelial cell junctions both in cultured cells and in mice, expression of PECAM-1 makes non-PECAM-1-expressing cells less permeable to albumin |
(Ferrero et al. 1995) |
| Expression of PECAM-1 delays the onset of EAE by promoting vascular integrity and decreasing parenchymal inflammatory cell infiltration |
(Graesser et al. 2002) |
| Expression of PECAM-1 is associated with increased vascular integrity in LPS-induced endotoxemia |
(Carrithers et al. 2005;Maas et al. 2005) |
| PECAM-1 facilitates the dephosphorylation and stabilization of β-catenin through ITIM-mediated recruitment of SHP-2 and activation of GSK-3β thus promoting reconstitution of adherens junctions |
(Biswas et al. 2006) |
| PECAM-1 homophilic interactions are more important than its signaling function for maintaining the integrity of endothelial cell junctions |
(Privratsky et al. 2011) |
| CD44 regulates vascular permeability and integrity through a PECAM-1 dependent mechanism |
(Flynn et al. 2013) |
| Gamma radiation decreases endothelial barrier function, which is correlated with a transient loss of PECAM-1 and cell detachment |
(Sharma et al. 2013) |
| Reticular AJ act coordinately with PECAM-1 to maintain endothelial barrier function in regions of low actomyosin-mediated tension |
(Fernandez-Martin et al. 2012) |
| Angiogenesis |
PECAM-1 engagement on the cell surface can transduce "outside-in" signals and activate MAPK/ERKs and small GTPases, impacting both cadherin-mediated cell-cell and integrin-mediated cell-matrix interactions |
(Wang and Sheibani 2006) |
| PECAM-1 expression has a significant impact on endothelial cell-cell and cell-matrix interactions by augmenting cell migration and capillary morphogenesis by increasing eNOS expression and NO availability |
(Park et al. 2010) |
| PECAM-1 stimulates EC cell migration and the formation of filopodia through SHP-2- and paxillin-mediated MAPK pathway activation and the turnover of focal adhesions |
(Zhu et al. 2010;O'Brien et al. 2004) |
| PECAM-1 expression and its potential interactions with EphB4/ephrin B2 and eNOS are important for survival, migration, and functional organization of EC during retinal vascular development and angiogenesis |
(Dimaio et al. 2008) |
| PECAM-1 isoforms lacking ITIM, as opposed to isoforms containing the ITIM, in PECAM-1−/− bEND cells activated MAPK/ERKs, disrupted adherens junctions, and enhanced cell migration and capillary morphogenesis in Matrigel |
(Dimaio and Sheibani 2008) |
| PECAM-1-expression in EC is correlated with increased migration, more ability to undergo capillary morphogenesis, and more dense peripheral focal adhesions and peripheral cortical actin distribution |
(Kondo et al. 2007) |
| Sustained activation of MAPK/ERKs results in disruption of cadherin-mediated cell-cell adhesion, down-regulation of PECAM-1 expression, and enhanced cell migration in microvascular endothelial cells |
(Wu and Sheibani 2003) |
| Antibodies against PECAM-1 decrease angiogenesis in transplanted tumors, inhibit tube formation and migration of HUVEC, and block in vitro tube formation by rat capillary endothelial cells during cytokine-induced rat corneal neovascularization |
(Cao et al. 2002;Delisser et al. 1997) |
| PECAM-1 is strongly expressed at cell borders in confluent monolayers whereas little or no PECAM-1 immunostaining is detected in sparse or migrating cultured EC |
(RayChaudhury et al. 2001) |
