Abstract
Vascular calcification is an active process of osteoblastic differentiation of vascular smooth muscle cells; however, its definite mechanism remains unknown. Vinpocetine, a derivative of the alkaloid vincamine, has been demonstrated to inhibit the high glucose-induced proliferation of vascular smooth muscle cells; however, it remains unknown whether vinpocetine can affect the osteoblastic differentiation of vascular smooth muscle cells. We hereby investigated the effect of vinpocetine on vascular calcification using a beta-glycerophosphate-induced cell model. Our results showed that vinpocetine significantly reduced the osteoblast-like phenotypes of vascular smooth muscle cells including ALP activity, osteocalcin, collagen type I, Runx2 and BMP-2 expression as well as the formation of mineralized nodule. Vinpocetine, binding to translocation protein, induced phosphorylation of extracellular signal-related kinase and Akt and thus inhibited the translocation of nuclear factor-kappa B into the nucleus. Silencing of translocator protein significantly attenuated the inhibitory effect of vinpocetine on osteoblastic differentiation of vascular smooth muscle cells. Taken together, vinpocetine may be a promising candidate for the clinical therapy of vascular calcification.
Highlights
Vascular calcification is a common problem among the aged with diabetes, heart failure and end-stage renal disease [1]
There was significant less expression of both the mRNA and protein of Runx2 and bone morphogenetic protein-2 (BMP-2) in vascular smooth muscle cells (VSMCs) treated with β-GP and vinpocetine than those treated with β-GP only (Fig 2C–2F, the data of western bloting analysis of Runx2 and BMP-2 on day 3, 9 and 12 were not shown)
Osteocalcin and collagen type I are critical for the osteoblastic differentiation of VSMCs [15]
Summary
Vascular calcification is a common problem among the aged with diabetes, heart failure and end-stage renal disease [1]. It is correlated with a number of clinical complications such as myocardial infarction, impaired vascular tone, angioplasty dissection and poor surgical outcome [2]. Recent progresses suggest that vascular calcification is an active process in vascular smooth muscle cells (VSMCs) being similar to bone formation [3]. This process includes the expression of osteoblast-like phenotypes and the presence of the bone mineral hydroxyl apatite. It is necessary to explore the mechanism of osteoblastic differentiation of VSMCs and develop effective strategies
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