Estradiol Regulates Expression of Polysialated Neural Cell Adhesion Molecule by Human Vascular Endothelial Cells
REPRODUCTIVE SCIENCES, vol.17, no.12, pp.1090-1098, 2010 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 17 Issue: 12
- Publication Date: 2010
- Doi Number: 10.1177/1933719110379649
- Journal Name: REPRODUCTIVE SCIENCES
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Page Numbers: pp.1090-1098
- Keywords: cardiovascular, atherosclerosis, estrogen, adhesion, inflammation, VERTEBRATE NERVOUS-SYSTEM, BLOOD-BRAIN-BARRIER, TUMOR-CELLS, NCAM POLYSIALYLATION, SYNAPTIC PLASTICITY, PSA-NCAM, ACID, ADULT, INVASIVENESS, NEUROGENESIS
- Akdeniz University Affiliated: Yes
Abstract
Rationale: The mechanism of atherogenesis includes leukocyte adhesion to endothelial cells followed by migration into the subendothelial space. The polysialylated neural cell adhesion molecules (PSA-nCAMs) are a group of hydrophilic neural cell adhesion molecule (NCAM) isoforms that inhibit NCAM: NCAM association, thereby blocking cell: cell adhesion. During previous studies, we demonstrated that sialylation of specific NCAMs are upregulated at proestrus in the rat and that PSA-nCAM is expressed by the rat vascular endothelium. Methods and Results: In this study, we sought the presence of PSA-nCAM in human vessels and regulation of its expression in estradiol-treated human umbilical vascular endothelial cells (HUVEC). Immunoreactive PSA-nCAM (ir-PSA-nCAM) was shown in blood and lymph vessels of adult rats and human brain, skin, liver, lung, cervix, endometrium, and ovary. Staining for ir-PSA-nCAM was present on the glycocalyceal surface of estradiol-treated HUVEC, but not in the presence of the estrogen receptor (ER)-blocker fulvestrant. Western blotting confirmed these findings. Conclusions: PSA-nCAM is widely present in the glycocalyx of human and rat vascular endothelium. It also is expressed by HUVEC, in which it is induced by estradiol. The estrogen-regulated presence of vascular PSA-nCAM could diminish NCAM-dependent interactions between vessels and circulating leukocytes, thereby impeding vascular inflammation and atherogenesis, and, contributing to estrogen-induced cardioprotection. This hypothesized action is presently under study.