Disease relevance of Calciol

• Vitamin D3 and calcium to prevent hip fractures in the elderly women [1].
• Characterization of 1 alpha-hydroxylation of vitamin D3 sterols by cultured alveolar macrophages from patients with sarcoidosis [2].
• In sarcoidosis, 1,25(OH)2D is produced by alveolar macrophages in response to gamma-interferon, and patients may develop hypercalcemia after prolonged exposure to sunlight and increased dermal production of vitamin D3 [3].
• Treatment with 1alpha(OH)D5 resulted in a dose-related (0.01-10.0 microM) inhibition without any toxicity, whereas the vitamin D3 analogue was highly potent but toxic at concentrations of 1.0 microM or higher [4].
• In nine patients with pseudohypoparathyroidism during the treatment with active vitamin D3, serum osteocalcin and plasma 1,25(OH)2D were normal (6.8 +/- 1.47 ng/ml and 27.2 +/- 6.0 pg/ml, respectively) [5].

Psychiatry related information on Calciol

• Numerous examples of such biphasic responses were documented, including osteoclast differentiation, various vascular responses, neutrophil migration, superoxide anion formation, exploratory behavior in rodents, vitamin D3 levels in macrophages, human sperm motility and mobility, myocardial contraction, and other functions [6].
• Physical activity, use of high-risk medication, and the use of vitamin D3, which was randomly allocated to the participants, were not strongly related to either falls or recurrent falls [7].
• 1,25 (OH)2 vitamin D3 levels in seasonal affective disorder: effects of light [8].
• In Experiment 2, vitamin D3 was provided at the low dosage for the first 5 d after hatch, followed by treatment with the high dosage for 12 h before and 12 h after each stressful event, which included weekly weighings and two DEX treatments [9].
• 4. The experiments demonstrate that vitamin D3, a steroid in structure, given in the critical period of hormonal imprinting may influence steroid hormone-receptor commanded events for life, in a way similar to the effects exhibited by synthetic steroid hormone analogues and benzpyrene in earlier studies [10].

High impact information on Calciol

• We show that 25-(OH) vitamin D3 in complex with its plasma carrier, the vitamin D-binding protein, is filtered through the glomerulus and reabsorbed in the proximal tubules by the endocytic receptor megalin [11].
• Endocytosis is required to preserve 25-(OH) vitamin D3 and to deliver to the cells the precursor for generation of 1,25-(OH)2 vitamin D3, a regulator of the calcium metabolism [11].
• The ligand for osteoprotegerin has been identified, and it is a TNF-related cytokine that replaces the requirement for stromal cells, vitamin D3, and glucocorticoids in the coculture model of in vitro osteoclastogenesis [12].
• Osf2/Cbfa1 expression is initiated in the mesenchymal condensations of the developing skeleton, is strictly restricted to cells of the osteoblast lineage thereafter, and is regulated by BMP7 and vitamin D3 [13].
• We expressed the PML-RAR alpha protein in U937 myeloid precursor cells and showed that they lost the capacity to differentiate under the action of different stimuli (vitamin D3 and transforming growth factor beta 1), acquired enhanced sensitivity to retinoic acid, and exhibited a higher growth rate consequent to diminished apoptotic cell death [14].

Chemical compound and disease context of Calciol

• Complete resistance to HIV-1 infection was observed in monocytes that had been treated for 5 d with rIL-4, and comparable results were obtained with other differentiation inducers such as dexamethasone or 1,25(OH)2 vitamin D3 (1,25(OH)2vitD3) [15].
• Circulating concentrations of hydroxylated metabolites of vitamin D were measured in seven Asian patients with histologically proven osteomalacia before and during treatment with either cholecalciferol (vitamin D3) or 1,25-dihydroxycholecalciferol [16].
• After vitamin D3-induced calcinosis, the elastin elastic modulus was unaffected, whereas the collagen elastic modulus decreased significantly during occlusion maneuvers (58.6%, p less than 0.01) and during bolus injections of angiotensin (37.2%, p less than 0.05) [17].
• Different types of acute myeloid leukemia blast cells were induced to differentiate in vitro with all-trans-retinoic acid (ATRA) and vitamin D3 (VD) [18].
• Antiproliferative responses to two human colon cancer cell lines to vitamin D3 are differently modified by 9-cis-retinoic acid [19].

Biological context of Calciol

• The bone density of the proximal femur increased 2.7 percent in the vitamin D3-calcium group and decreased 4.6 percent in the placebo group (P < 0.001) [1].
• Decreasing the half-site spacing by 1 nucleotide converts the TRE to a vitamin D3 response element, while eliminating response to T3 [20].
• Direct repeats as selective response elements for the thyroid hormone, retinoic acid, and vitamin D3 receptors [20].
• Impaired effects of active vitamin D3 may contribute to the relatively enhanced secretion and cell proliferation seen in hyperparathyroidism (HPT) [21].
• Active vitamin D3 constitutes a principal regulator of parathyroid cell growth, and polymorphism in the VDR gene has recently been related to bone mineral density and suggested as predisposing to osteoporosis [21].

Anatomical context of Calciol

• They are related to each other and similar to the group of receptors that includes those for thyroid hormones, retinoids, and vitamin D3 [22].
• The hormonal form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], at picomolar concentrations, inhibited the growth-promoting lymphokine interleukin-2, which is produced by human T lymphocytes activated in vitro by the mitogen phytohemagglutinin [23].
• Vitamin D3-induced calcium binding protein in bone tissue [24].
• Transcriptional activation of the Cdk inhibitor p21 by vitamin D3 leads to the induced differentiation of the myelomonocytic cell line U937 [25].
• Synergistic induction of HL60 cell differentiation by ketoconazole and 1-desoxy analogues of vitamin D3 [26].

Associations of Calciol with other chemical compounds

• These findings, together with the demonstration of cutaneous production of numerous other hormones including vitamin D3, PTH-related protein (PTHrP), catecholamines, and acetylcholine that share regulation by environmental stressors such as UV light, underlie a role for these agents in the skin response to stress [27].
• The effect on phosphate excretion of graded doses of parathyroid hormone (PTH) and the biologically active vitamin D3 metabolite, 25-hydroxycholecalciferol (25-HCC), administered singly and in combination, were studied in the nonexpanded, vitamin D-depleted thyroparathyroidectomized rat [28].
• The active hormonal form of vitamin D3, 1,25-dihydroxyvitamin D3[1,25(OH), which regulates cellular replication and function in many tissues and has a role in bone and calcium homeostasis, acts through a hormone receptor homologous with other steroid and thyroid hormone receptors [29].
• Upper and lower phases and serial fractions were analyzed for vitamin D3 (extraction, HPLC), cholesterol (enzyme assay), and human DBP (hDBP) (radial immunodiffusion) [30].
• Synergistic decrease of clonal proliferation, induction of differentiation, and apoptosis of acute promyelocytic leukemia cells after combined treatment with novel 20-epi vitamin D3 analogs and 9-cis retinoic acid [31].
• Vitamin D3 up-regulates Beclin1, which binds to class III phosphatidylinositol 3-kinase to trigger autophagy [32].

Gene context of Calciol

• In hemopoietic cells from PMLRARalpha TM, PML inactivation resulted in impaired response to differentiating agents such as RA and vitamin D3 as well as in a marked survival advantage upon proapoptotic stimuli [33].
• Here, we report a novel cytoplasmic localization of p21(Cip1/WAF1) in peripheral blood monocytes (PBMs) and in U937 cells undergoing monocytic differentiation by in vitro treatment with vitamin D3 or ectopic expression of p21(Cip1/WAF1), and analyze the biological consequences of this cytoplasmic expression [34].
• The expression of hTAF(II)28 also potentiated transactivation by several nuclear receptors, notably the oestrogen and vitamin D3 receptors (ER and VDR), whereas other classes of activator were not affected [35].
• These results indicate that this 24-bp sequence containing two 9-bp motifs binds to the vitamin D receptor and mediates the vitamin D3 enhancement of murine Spp-1 gene expression [36].
• A pathway for the metabolism of vitamin D3: unique hydroxylated metabolites formed during catalysis with cytochrome P450scc (CYP11A1) [37].

Analytical, diagnostic and therapeutic context of Calciol

• As detected by radioimmunoassay with antiserums against chick intestinal calcium binding protein (CaBP), administration of vitamin D3 to rachitic chicks causes a 25- to 100-fold increase in immunoreactive CaBP in chick bone [24].
• Oral administration of 10 mug (400 U) of cholecalciferol 7 h before incubation increased leucine incorporation into diaphragm muscle protein by 136% (P less than 0.001) of the preparation from untreated animals [38].
• Hepatectomy drastically disrupts vitamin D3 metabolism as revealed by prolonged high levels of [3H] vitamin D3 in the plasma compartment even 12 h after dose in contrast to sham-operated controls [39].
• Both cells express similar patterns of differentiation-specific antigens after treatment with vitamin D3, and both express the retinoblastoma gene product (p110Rb) [40].
• Deglycosylation of serum vitamin D3-binding protein leads to immunosuppression in cancer patients [41].

References