Disease relevance of 1alpha,25-dihydroxy-20-epivitamin D_3 / 1alpha,25-dihydroxy-20-epicholecalciferol

• In vivo it produced hypercalcemia, acted on bone and kidney, and stimulated 1,25-dihydroxy-vitamin D3 formation [1].
• The effects of short-term treatment with 1,25-dihydroxy-vitamin D3 [1,25(0H)2D3] or 1 alpha-hydroxy-vitamin D3 [1 alpha(OH)D3] on intestinal absorption of 47Ca were compared in 41 experiments in normals and 72 experiments in patients with chronic renal failure [2].
• The specific activity of alkaline phosphatase was increased in two human osteogenic sarcoma cell lines, SAOS and TE85, after treatment with 1,25 dihydroxy-vitamin D3 (1,25(OH)2D3) [3].
• 1,25-Dihydroxy-vitamin D3 [1,25-(OH)2D3] suppresses the secretion and synthesis of parathyroid hormone (PTH) and has been used in the treatment of secondary hyperparathyroidism [4].
• Without 1,25-dihydroxy-vitamin D3 [1,25-(OH)2D3], a hormone that induces osteoclastic differentiation in vitro, bone marrow cultures showed very little bone resorption, and only small numbers of CT receptor-positive cells developed [5].

High impact information on 1alpha,25-dihydroxy-20-epivitamin D_3 / 1alpha,25-dihydroxy-20-epicholecalciferol

• Treatment of duodenal tissue from rats deficient in vitamin D with 1,25-dihydroxy-vitamin D3 [1,25-(OH)2-D3] led to more than a doubling of calcium uptake by the isolated cells and the appearacne in those cells of previously undetectable calcium-binding protein (CaBP) [6].
• The genomic action of calcitriol (1,25-dihydroxy-vitamin D3) is mediated through the interaction of the calcitriol receptor (VDR) with vitamin D response elements (VDREs) [7].
• This study asks whether arterial blood ionized calcium concentration (Ca++) can regulate the serum level of 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] independently of serum phosphorus and parathyroid hormone (PTH) [8].
• In addition, expression of the c-src gene product increases when bone marrow cells are induced to express an osteoclast-like phenotype by 1,25-dihydroxy-vitamin D3, further suggesting that high expression of pp60c-src is part of the osteoclast phenotype [9].
• Since the osteoclast is thought to be derived from early marrow cells of the macrophage lineage, we cultured normal primate marrow mononuclear cells in medium containing 1,25-dihydroxy-vitamin D3 [10].

Chemical compound and disease context of 1alpha,25-dihydroxy-20-epivitamin D_3 / 1alpha,25-dihydroxy-20-epicholecalciferol

• In the present study, SK&F 86002 inhibited fetal rat long bone (FRLB) resorption induced by parathyroid hormone (PTH), 1,25-dihydroxy-vitamin D3, tumor necrosis factor alpha, and Escherichia coli lipopolysaccharide in a dose-dependent (IC50 of 0.5-1 microM) and reversible manner [11].

Biological context of 1alpha,25-dihydroxy-20-epivitamin D_3 / 1alpha,25-dihydroxy-20-epicholecalciferol

• Functional interactions between bile acids, all-trans retinoic acid, and 1,25-dihydroxy-vitamin D3 on monocytic differentiation and myeloblastin gene down-regulation in HL60 and THP-1 human leukemia cells [12].
• Dimethyl sulfoxide (DMSO), retinoic acid (RA) and 1,25-dihydroxy-vitamin D3, all of which induce the differentiation in HL-60 cells, did not cause any changes in protein phosphorylation [13].
• Because a role for ET in bone remodeling has been suggested, the present study was undertaken (a) to characterize ET receptors and their responses in the rat osteosarcoma cell line ROS 17/2.8 and (b) to study their regulation by 1,25-dihydroxy-vitamin D3 [14].
• Both cell lines produced material comigrating with 1,25 dihydroxy-vitamin D3 (1,25(OH)2D3) and 24,25 dihydroxyvitamin D3 (24,25(OH)2D3) in straight and reverse phase high performance liquid chromatography systems and displacing the relevant labeled ligands in competitive binding assays [15].
• We investigated the gene expression of 1,25-dihydroxy-vitamin D3 (1,25(OH)2D3) receptors (VDR) and 25-hydroxy-vitamin D3-24-hydroxylase (24-hydroxylase) in opossum kidney (OK) cells [16].

Anatomical context of 1alpha,25-dihydroxy-20-epivitamin D_3 / 1alpha,25-dihydroxy-20-epicholecalciferol

• It has been well established that human mononuclear phagocytes have the capacity to produce 1,25-dihydroxy-vitamin D3 [1,25(OH)3D3] and express the vitamin D receptor (VDR) [17].
• The K052 cells were capable of phenotypic or morphologic differentiation after being incubated with granulocyte colony-stimulating factor, interleukin-2, phorbol 12-myristate 13-acetate, or 1,25-dihydroxy-vitamin D3 [18].
• Treatment of ROS osteoblasts with 10 nM 1,25-dihydroxy-vitamin D3 for 14 hr resulted in a significant (> 50%) decrease in 125I-ET-1 and 125I-IRL-1620 binding [14].
• Its expression is stimulated by a number of agents including calcium and 1,25-dihydroxy-vitamin D3 that promote the differentiation process in keratinocytes [19].
• The active metabolite of this photosynthesized vitamin, 1,25-dihydroxy-vitamin D3 (1,25D), promotes maturation and activation of human monocytes and macrophages (MPs) [20].

Associations of 1alpha,25-dihydroxy-20-epivitamin D_3 / 1alpha,25-dihydroxy-20-epicholecalciferol with other chemical compounds

• Since duodenal Ca2+ influx at the brush border was regulated by 1,25-dihydroxy-vitamin D3 [1,25-(OH)2D3], we tested the effect of 1,25-(OH)2D3 administration on the uptake activity in isolated membrane vesicles [21].
• The 1,25-dihydroxy-vitamin D3 receptor is phosphorylated in response to 1,25-dihydroxy-vitamin D3 and 22-oxacalcitriol in rat osteoblasts, and by casein kinase II, in vitro [22].
• Evidence on the participation of the 3',5'-cyclic AMP pathway in the non-genomic action of 1,25-dihydroxy-vitamin D3 in cardiac muscle [23].
• In a previous double-blind, placebo-controlled study 1 micrograms alphacalcidol, a synthetic analogue of 1,25 dihydroxy-vitamin D3, induced a decrease in blood pressure in mild HPT subjects [24].
• Studies on the mechanism of action of calciferol VII. Localization of 1,25-dihydroxy-vitamin D3 in chick parathyroid glands [25].

Gene context of 1alpha,25-dihydroxy-20-epivitamin D_3 / 1alpha,25-dihydroxy-20-epicholecalciferol

• Identification and characterization of endothelin receptors on rat osteoblastic osteosarcoma cells: down-regulation by 1,25-dihydroxy-vitamin D3 [14].
• 1,25-Dihydroxy-vitamin-D3 enhances antiproliferative effect and transcription of TGF-beta1 on human keratinocytes in culture [26].
• Furthermore, the CSF-induced BMC proliferation was dose dependently inhibited by dexamethasone and 1,25-dihydroxy-vitamin D3 as well as by interferon-gamma and tumor necrosis factor-alpha [27].
• Induction of osteocalcin was primarily mediated by ETA receptors, and these receptors were also down-regulated at the mRNA level by 1,25-dihydroxy-vitamin D3 [14].
• Low-Pi diet, via stimulation of the activity of the renal 25-hydroxyvitamin-D3-1alpha-hydroxylase (1alphaOHase), leads to an increase in the level of 1,25-dihydroxy-vitamin D3 [1,25(OH)2D] [28].

Analytical, diagnostic and therapeutic context of 1alpha,25-dihydroxy-20-epivitamin D_3 / 1alpha,25-dihydroxy-20-epicholecalciferol

• The effect of 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] on the activity of peritoneal macrophages from CAPD patients and nonuremic controls was studied [29].
• After 12-18 months of transplantation, biochemical parameters (including 25-hydroxy- and 1,25-dihydroxy-vitamin D3) were studied [30].
• Calcitriol (1,25-dihydroxy-vitamin D3) coadministered with influenza vaccine does not enhance humoral immunity in human volunteers [31].
• Differential effects of acute administration of 19-Nor-1,25-dihydroxy-vitamin D2 and 1,25-dihydroxy-vitamin D3 on serum calcium and phosphorus in hemodialysis patients [32].
• Although tuberculosis can contribute to hypercalcemia, this possibility was ruled out in our patient by the low serum 1,25-dihydroxy-vitamin D3 levels and return to normal of serum calcium and renal function under hormone replacement therapy [33].

References