Demonstration of 1,25(OH)2 vitamin D3 receptors and actions in vascular smooth muscle cellsIn vitro

Abstract

Binding of [3H] 1,25(OH)2D3 and effects of 1,25(OH)2D3 on cell ultrastructure were evaluated in vascular smooth muscle cells (VSMC) primary cultures (aortic media). Specific reversible binding of [3H] 1,25(OH)2D3 by a 3.5 S macromolecule with DNA binding, KD 6.2 X 10(-10) M and Nmax 16 fmol/mg protein was demonstrated. Incubation of VSMC with 10(-8) M 1,25(OH)2D3, but not 25(OH)D3, in the presence of 10% FCS for up to three weeks caused rapid reversible appearance in the cytoplasm of membrane-bounded electron-dense lysosomal particles which on electronspectroscopic imaging contained Ca and Pi. VSMC are targets for vitamin D.

Reducing the Burden of Cardiovascular Calcification in Patients with Chronic Kidney Disease

“…Reprinted from reference (29), with permission. (29). Vitamin D has also been shown to increase calcification in VSMC in vitro (30).…”

“…Clinical studies have also reported an association between vascular calcification and use of vitamin D therapy in hyperphosphatemic patients with renal failure (27,28). Vascular smooth muscle cells (VSMC) have been shown to express vitamin D receptors (29). Although vitamin D inhibits VSMC proliferation by enhancing Ca flux into cells, it induces VSMC to exhibit an osteoblastic phenotype Figure 1.…”

Impact of Treatment with Calcimimetics on Hyperparathyroidism and Vascular Mineralization

“…Further administration of vitamin D may induce hypercalcemia, thereby increasing the risk for VC in affected patients (23). A second mechanism for inducing VC is that the active vitamin D sterol calcitriol may act on specific vitamin D receptors that are constitutively expressed by VSMC (32). Calcitriol has been shown to increase expression of several proteins that are involved in calcification (e.g., alkaline phosphatase) and to decrease expression of proteins that inhibit calcification (e.g., PTH-related peptide [28,33]).…”

25-Hydroxyvitamin D 3 -1α-Hydroxylase Is Expressed in Human Vascular Smooth Muscle Cells and Is Upregulated by Parathyroid Hormone and Estrogenic Compounds

“…9 On the other hand, 1,25(OH) 2 vitamin D 3 may accelerate cell migration 10 and promote the transition of contractile VSMCs into a secretory cell phenotype. 11 Finally, 1,25(OH) 2 D 3 has been linked to the formation of arterial calcifications in a complex and poorly understood manner; although hypervitaminosis D induces vascular calcifications 12,13 and 1,25(OH) 2 vitamin D 3 increases the expression of bone proteins such as osteopontin in VSMCs, 10,13 coronary calcifications appear to be inversely related to circulating 1,25(OH) 2 vitamin D 3 . 14 Furthermore, a consistent association between osteoporosis and vascular calcification has been noted in a number of reports.…”