Hypoxia favors maintenance of the vascular smooth muscle cell phenotype in culture

摘要

Vascular smooth muscle cells (VSMCs) are derived from mesenchymal cells and differentiate into osteoblast-like cells at sites of atherosclerosis/arterial calcification [1-4]. VSMCs in the medial layer of arteries are normally protected from the high oxygen levels in arterial blood by the endothelium and in-tima. If the endothelium is damaged by atherosclerosis, however, VSMCs are possibly exposed to relatively high oxygen levels. Recently, we reported that relatively high oxygen tension promotes osteoblas-tic differentiation of mesenchymal stem cells [5]. Although certain stimuli, such as inorganic pyrophos-phate, low-density lipoprotein levels, high glucose levels, and oxidative stress, can transform VSMCs into "calcifying vascular cells," that is, osteogenic cell [6-9], we hypothesized that exposure to excess oxygen also enhances the commitment of VSMCs to osteogenic differentiation, while keeping cells under a hypoxic condition maintains the VSMC phenotype.