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Vascular progenitor cells with decalcifying potential: a step toward prevention or treatment of atherosclerotic vascular calcification?

Vascular calcification (VC) is an important feature of progressive atherosclerosis and is commonly seen in patients with various vascular diseases, diabetes and renal disease. Furthermore, VC is considered to be a prognostic marker of future adverse cardiovascular events. A meta-analysis has shown that patients with VC have a threefold higher risk of cardiovascular events [1]. In past reports, VC has usually been accompanied by other diseases and aging. However, recent studies have shown that the pathophysiologic process of VC is a tightly regulated, active process that resembles bone formation [2]. But despite the clinical importance of calcification, no therapy has yet been shown to ameliorate the process [3]. Previous studies to reverse VC were focused on the regulation of inflammation signaling pathway and vascular smooth muscle cells (VSMCs) as a key cell type of vascular calcification process. Evidence from research has demonstrated that inflammatory signals result in VC [3,4]. VMSCs were considered key cells in developing VC, specifically intimal or subintimal (atherosclerotic) calcification [5–7]. Statin use, targeting the inflammation to prevent or reverse VC, has been expected to decrease inflammatory cytokines, increase VSMCs survival and viability, as well as tissue remodeling. Therapy with bisphosphonates, sevelamer and calcimimetics, as well as thyroidectomy for regulating mineral balance were anticipated to prevent calcium accumulation and inhibit VMSC apoptosis. However, studies have failed to show a response with these approaches [8–11], resulting in the therapeutic nihilism of vascular calcification. To explain the cause of calcium buildup in vessel walls, we paid attention to the possibility of vascular calcifying progenitor cells, instead of VSMCs, to modulate or reverse VC. We first isolated vessel-resident calcifying progenitor cells from the mouse aorta [12] using antibodies for stem cell antigen-1 (Sca-1) and platelet-derived growth factor receptor alpha (PDGFRα). Sca-1 is a marker of hematopoietic [13] and mesenchymal stem cells [14] in mice. Vesselresident Sca-1+ progenitor cells originated from bone marrow (BM) and could be clonally expanded. There are two kinds of BM-derived progenitors in the artery that are positive for stem cell antigen-1 (Sca1+). Sca-1+/PDGFRα+ progenitor cells are more committed to differentiate only into osteoblasts, whereas Sca-1+/PDGFRαprogenitor cells differentiate into osteoblasts Vascular progenitor cells with decalcifying potential: a step toward prevention or treatment of atherosclerotic vascular calcification?