Nucleolin positively regulates spontaneous cell proliferation but is not involved in inhibition of proliferation by lead in cultured bovine aortic endothelial cells

Abstract

Nucleolin (NCL) is an abundant DNA-, RNA-, and protein-binding protein that is expressed ubiquitously in eukaryotic cells, implicating it in many cellular functions such as gene silencing, senescence, cytokinesis, and proliferation. NCL is also involved in angiogenesis events including vascular endothelial cell migration and proliferation. We previously found that lead, an environmental pollutant with vascular toxicity, inhibits the repair process of injured vascular endothelium via suppression of cell proliferation as a result of a lower proliferative response of cells to endogenous fibroblast growth factor-2. The present study investigated the expression of NCL in proliferating bovine aortic vascular endothelial cells and the role of NCL in proliferation of the cells in the presence or absence of lead. We found that the expression of NCL protein was independent of cell density. Both siRNA-mediated NCL knockdown and an anti-NCL-neutralizing antibody inhibited the proliferation of vascular endothelial cells without non-specific cell damage, indicating that NCL was involved in endothelial cell proliferation. However, lead significantly inhibited the proliferation of vascular endothelial cells without changing the expression level of NCL. Therefore, NCL may positively regulate spontaneous proliferation, but is not involved in the inhibition of proliferation by lead in vascular endothelial cells.