PECAM1 is a member of the immunoglobulin (Ig) superfamily that is expressed on the surface of circulating platelets,
monocytes, neutrophils, and particular T-cell subsets. It is also a major constituent of the endothelial cell intercellular
junction, where up to an estimated 1 million molecules are concentrated. Because of this cellular expression pattern,
PECAM1 is implicated in several functions, including transendothelial migration of leukocytes, angiogenesis, and
integrin activation.
NCBI Summary:
The protein encoded by this gene is found on the surface of platelets, monocytes, neutrophils, and some types of T-cells, and makes up a large portion of endothelial cell intercellular junctions. The encoded protein is a member of the immunoglobulin superfamily and is likely involved in leukocyte migration, angiogenesis, and integrin activation. [provided by RefSeq, May 2010]
General function
Cell adhesion molecule
Comment
Cellular localization
Extracellular Matrix, Plasma membrane
Comment
Soluble platelet/endothelial cell adhesion molecule (sPECAM)-1 is increased in polycystic ovary syndrome and related to endothelial dysfunction. Pepene CE et al. Striking evidence indicates endothelial impairment in polycystic ovary syndrome (PCOS) but the mechanisms linking PCOS status to cardiovascular risk remain elusive. Platelet/endothelial cell adhesion molecule (PECAM)-1 is a soluble (s) signaling molecule involved in inflammation and angiogenesis with predictive value for endothelial dysfunction in patients at risk. In a prospective, controlled study, sPECAM-1 levels and the relationships to metabolic, inflammatory and vascular PCOS traits were evaluated in 26 patients and 29-age- and body mass index-matched controls. To assess endothelial injury, carotid artery intimae-media thickness (CIMT) and brachial artery flow-mediated vasodilatation (FMD) were employed. Of the 26 women with PCOS, 25 completed a six-month metformin combined with ethinylestradiol 0.3?mg/drospirenone 3?mg therapy. Soluble PECAM-1 levels were increased in PCOS (p?=?0.018 vs. Controls) and significantly decreased at follow-up (p?=?0.0002). Smoking and weight had no effect on sPECAM-1 dynamics. In both univariate and multivariate analysis, basal sPECAM-1 was inversely related to FMD (r?=?-0.311, p?=?0.021) but not CIMT. To conclude, sPECAM-1 is increased in PCOS, an effect reversed by combined metformin and anti-androgenic contraceptive therapy. Elevated sPECAM-1 contributes to endothelial dysfunction however further studies are inquired to assess its relevance as biomarker and potential therapeutic target in PCOS.
Ovarian function
Comment
Expression regulated by
Comment
Rapid and Transient Upregulation of CCL11 (Eotaxin-1) in Mouse Ovary During Terminal Stages of Follicular Development. Kuwabara Y et al. PROBLEM: This study aimed to investigate the regulation of expression, localization and physiological role of the CCL11/CCR3 axis in mouse ovary during the periovulatory period. METHOD OF STUDY: CCL11/CCR3 expression in the mouse ovary after treatment with pregnant mare serum gonadotropin (PMSG) followed by human chorionic gonadotropin (hCG) 48?hr later was assessed in vivo and in 3-dimensional cultures in vitro. RESULTS: Real-time RT-PCR analyses revealed transient CCL11 mRNA upregulation 6?hr after hCG treatment. Immunohistochemical staining of serial ovarian sections demonstrated overlapping expression of CCL11, CCR3 and CD31 endothelial cell marker in the theca-interstitial layer at 10?hr after hCG treatment. In vitro 3-dimensional cultures of periovulatory ovarian tissues demonstrated that treatment with anti-CCL11 neutralizing antibody significantly decreased CD31 transcript. CONCLUSIONS: Gonadotropin surge leads to transient CCL11/CCR3 axis upregulation in the ovarian theca-interstitial layer, suggesting that it is involved in periovulatory physiological processes by affecting follicular vessels.
Ovarian localization
, Follicular Fluid
Comment
Benifla JL, et al 2001 reported the presence of Vascular endothelial growth factor, platelet endothelial cell adhesion molecule-1 and vascular cell adhesion molecule-1 in the
follicular fluid of patients undergoing IVF.
The aim of this study was to measure concentrations of vascular
endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1
(PECAM-1) CD31 and vascular cell adhesion molecules (VCAM-1) in the
follicular fluid of women treated with assisted reproduction technology to
determine whether these proteins might be outcome markers. Nineteen
women became pregnant (defined by human chorionic gonadotrophin
concentrations and embryonic cardiac activity 1 month after follicular aspiration);
56 did not. Women did not differ significantly in their follicular fluid
concentrations of VEGF, sCD31 and VCAM-1 according to cause of infertility, or assisted reproduction outcome, or age. Follicular fluid concentrations of VEGF were significantly correlated with the number of gonadotrophin ampoules
administered (P < 0.012), and follicular fluid concentrations of sVCAM-1 with
the fertilization rate (P < 0.01). Follicular fluid concentrations of VEGF and sVCAM-1 were also correlated (P < 0.007). The results do not
suggest that VEGF, CD31, or sVCAM-1 in follicular fluid predict assisted
reproduction outcome, especially among patients
Follicle stages
Comment
Phenotypes
PCO (polycystic ovarian syndrome)
Mutations
1 mutations
Species: mouse
Mutation name: type: null mutation fertility: fertile Comment: Bone marrow monocyte PECAM-1 deficiency elicits increased osteoclastogenesis resulting in trabecular bone loss. Wu Y et al. (2009) In our investigations of the bone marrow (BM) of PECAM-1 null (knockout, KO) mice, we observed that the trabecular bone volume and number of trabeculae were significantly reduced in femoral and tibial long bones. Further studies in vitro revealed increased numbers and size of osteoclasts, enhanced bone resorption on dentin substrates, and hypersensitivity to macrophage CSF and receptor activator of NF-kappaB ligand in BM-derived osteoclast precursor cultures from KO mice. Associations among PECAM-1, Syk, and SHP-1 were found in wild-type BM monocyte derived osteoclast-like cells. The absence of PECAM-1 and SHP-1 interactions in the KO cells leads to the dysregulation of Syk kinases and/or phosphatases, possibly SHP-1. Indeed, KO derived osteoclast-like cells exhibited increased Syk tyrosine phosphorylation levels compared with WT cells. Lastly, WT mice engrafted with marrow from KO kindred showed loss of trabecular bone analogous to KO mice, consistent with increased osteoclastogenesis.//////////////////