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Malik, Arif, Bushra Shaheen, Muhammad Shahzad Farooq, Qura-Tul Ain, and Sulayman Waquar. "VITAMIN-D DEFICIENCY;." Professional Medical Journal 24, no. 09 (September 8, 2017): 1437–43. http://dx.doi.org/10.29309/tpmj/2017.24.09.947.
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Background: Deficiency of vitamin D is characterized by the low bone masswhich leads to the bone fragility and high risk of fractures. Bone fractures causes the formationof free radicals, generated by the tissue damaged. Uncontrolled production of free radicalsaccelerates the oxidative stress and increased the bone remodeling process ultimatelycauses osteoporosis. One of the most damaging effects of free radicals is lipid peroxidation;end product of which is MDA, it also act as major factor in osteoblastic activity. Low level ofantioxidative defense system found in osteoporotic patients due to the deficiency of vitamin D.Many important mineral ions removed from bones and risk of bone fragility increases. Currentstudy is aim to check the antioxidative effect produced from excess reactive oxygen speciescompared with low level of vitamin D which is held responsible for higher or lower activityof bone cells. Study Design: Case Control Study. Setting: Study was conducted at Instituteof Molecular Biology and Biotechnology (IMBB), University of Lahore. Period of Study: Oneyear. Materials and Methods: Blood samples of 272 post-menopausal osteoporotic womenbetween the age 49-57 were collected from Jinnah hospital Lahore. While the samples of 92individuals were served as a control. Concentration of both enzymatic and non-enzymaticantioxidant such as CAT, GSH, SOD, GPx and GR, vitamin A, C and E and levels of MDAwere estimated spectrophotometrically. While the concentration of IL6, AOPPS, AGEs, TNF-α,MMP9, Isoprostanes, LDH, cholesterol, triglycerides, free fatty acids and phospholipid weremeasured by using commercially available Elisa kits. Results: Blood plasma levels of vitaminD were significantly lower in osteoporosis patients than in normal subjects. In addition, levelof stress biomarker such as MDA was found to be higher in patients as compared to control.Due to oxidative stress, level of antioxidants (GSH, CAT, and SOD) was found to be reduced.Blood cells and many other important minerals are also reduces in patient group from theirnormal amount. Conclusion: It concludes that excess production of free radicals over whelmsthe antioxidative system, thus it may leads to osteoporosis. Further more antioxidant speciessubjected to body might protect bone loss and also help in acceleration of healing of fracturedbones.
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Holzapfel, B. M., F. Jakob, A. A. Kurth, G. Maier, and K. Horas. "The Role of Vitamin D and the Vitamin D Receptor in Bone Oncology." Osteologie 27, no. 03 (September 2018): 129–34. http://dx.doi.org/10.1055/s-0038-1673534.
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SummaryVitamin D deficiency is a global health problem of enormous and increasing dimensions. In the past decades, numerous studies have centered on the role of vitamin D in the pathogenesis and course of many diseases including several types of cancer. Indeed, vitamin D has been widely acknowledged to be involved in the regulation of cell proliferation, differentiation and apoptosis in numerous cancer cells. While the full range of molecular mechanisms involveld in cancer cell growth and progression remains to be elucidated, recent research has deepened our understanding of the processes that may be affected by vitamin D or vitamin D deficiency.In this review, we consider the properties of bone that enable cancer cells to grow and thrive within the skeleton, and the role of vitamin D and the vitamin D receptor in the process of primary and secondary cancer growth in bone.
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AYDOĞAN, Tolga, Meltem HENDEK, and Ebru OLGUN. "Relationship between periodontal disease and vitamin D." Journal of Medicine and Palliative Care 3, no. 4 (December 26, 2022): 381–85. http://dx.doi.org/10.47582/jompac.1208868.
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Vitamin D is a hormone synthesized by human skin cells or consumed through diet with immunomodulatory, anti-inflammatory, and antiproliferative effects. Vitamin D deficiency may increase the risk of periodontal disease by causing decreased bone mineral density, osteoporosis, progression of periodontal diseases, and resorption of the jawbone. In addition, vitamin D is important for bone metabolism, alveolar bone resorption, and the prevention of tooth loss. It increases the antibacterial defense of gingival epithelial cells, reduces gingival inflammation, accelerates postoperative wound healing after periodontal surgery, and is a key supplement functioning as a prophylaxis in periodontology. The present review study aims to highlight the role of vitamin D in periodontal disease.
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Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.
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Bagchi, Subrata. "Vitamin D Deficiency – The Modern Epidemic." Journal of Comprehensive Health 2, no. 2 (October 24, 2020): 5–7. http://dx.doi.org/10.53553/jch.v02i02.001.
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Researchers have analyzed data on vitamin D status on adult population in USA and found Vit D deficiency or insufficiency in 50-78%1. In United Kingdom 90% of adult population had low vitamin D2. It is extremely common in Sunny Middle East because people cover their body with clothes. The causes of vitamin D deficiency are – modern life style, Sun phobia because of skin cancer, wrinkles, aging spots; obesity, medical illness e.g. mal-absorption, liver & kidney disease; medications e.g. phenytoin, phenobarbital, steroid. Natural vitamin has two forms, vitamin D3 (cholecaciferol) and vitamin D2 (ergocalciferol). Vitamin D3 is superior to vitamin D2.Vitamin D affects every system in human body. It plays a vital role in health of muscle and bones, normal functioning of immune system, controls growth of normal and cancerous cells, prevention & treatment of type 2 diabetes, prevention of heart disease, kidney disease & heart failure, prevention of coronary artery disease, treatment of psoriasis, prevention of dental problems and prevention & treatment of depression3 In people with Vit D deficiency the parathyroid glands produce more than normal amount of PTH, which cause excessive dissolving of calcium from bone leading to bone aches and pain. Vitamin D deficiency is a major cause of osteoporosis. There is a direct correlation between Vit D level and bone mineral density. Post menopausal women with osteoporosis had low level of Vit D. Steroids antagonize effects of Vit D.
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Anderson, Paul H., Gerald J. Atkins, Andrew G. Turner, Masakazu Kogawa, David M. Findlay, and Howard A. Morris. "Vitamin D metabolism within bone cells: Effects on bone structure and strength." Molecular and Cellular Endocrinology 347, no. 1-2 (December 2011): 42–47. http://dx.doi.org/10.1016/j.mce.2011.05.024.
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Bychkov, Aleksey, Vyacheslav Koptev, Varvara Zaharova, Polina Reshetnikova, Elena Trofimova, Elena Bychkova, Ekaterina Podgorbunskikh, and Oleg Lomovsky. "Experimental Testing of the Action of Vitamin D and Silicon Chelates in Bone Fracture Healing and Bone Turnover in Mice and Rats." Nutrients 14, no. 10 (May 10, 2022): 1992. http://dx.doi.org/10.3390/nu14101992.
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This study presents findings on the biological action of an integrated supplement containing the following components involved in osteogenesis and mineralization: vitamin D and silicon in the bioavailable and soluble form. A hypothesis that these components potentiate one another’s action and make calcium absorption by the body more efficient was tested. Biological tests of the effect of vitamin D and silicon chelates on bone fracture healing and bone turnover were conducted using ICR mice and albino Wistar rats. Radiographic and biochemical studies show that the supplement simultaneously containing silicon chelates and vitamin D stimulates bone tissue regeneration upon mechanical defects and accelerates differentiation of osteogenic cells, regeneration of spongy and compact bones, and restoration of bone structure due to activation of osteoblast performance. Bone structure restoration was accompanied by less damage to skeletal bones, apparently due to better absorption of calcium from food. The studied supplement has a similar effect when used to manage physiologically induced decalcification, thus holding potential for the treatment of osteomalacia during pregnancy or occupational diseases (e.g., for managing bone decalcification in astronauts).
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Jagelavičienė, Eglė, Inga Vaitkevičienė, Dovilė Šilingaitė, Eglė Šinkūnaitė, and Goda Daugėlaitė. "The Relationship between Vitamin D and Periodontal Pathology." Medicina 54, no. 3 (June 12, 2018): 45. http://dx.doi.org/10.3390/medicina54030045.
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Osteoporosis and periodontal diseases are common problems among the elderly population. Vitamin D is a secosteroid hormone that is either synthesized by human skin cells under the effect of UV radiation or consumed through diet. Deficiency in vitamin D leads to reduced bone mineral density, osteoporosis, the progression of periodontal diseases and causes resorption to occur in the jawbone. Sufficient intake of vitamin D can decrease the risk of gingivitis and chronic periodontitis, as it has been shown to have immunomodulatory, anti-inflammatory, antiproliferative effects and initiates cell apoptosis. In addition, vitamin D is also important for bone metabolism, alveolar bone resorption and preventing tooth loss. It increases antibacterial defense of gingival epithelial cells and decrease gingival inflammation, improves postoperative wound healing after periodontal surgery and is an important supplement used as prophylaxis in periodontology. This publication aims to update the recent advances, stress the clinical importance, and evaluate vitamin D in the prevention of periodontal diseases to reach a successful outcome of conservative and surgical treatment. An analysis of the literature shows that vitamin D plays a significant role in maintaining healthy periodontal and jaw bone tissues, alleviating inflammation processes, stimulating post-operative healing of periodontal tissues and the recovery of clinical parameters. However, further research is needed to clarify the required vitamin D concentration in plasma before starting periodontal treatment to achieve the best outcome.
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Bouillon, Roger, Geert Carmeliet, Lieve Verlinden, Evelyne van Etten, Annemieke Verstuyf, Hilary F. Luderer, Liesbet Lieben, Chantal Mathieu, and Marie Demay. "Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice." Endocrine Reviews 29, no. 6 (October 1, 2008): 726–76. http://dx.doi.org/10.1210/er.2008-0004.
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Abstract The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)2D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1α-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency. The intestine is the key target for the VDR because high calcium intake, or selective VDR rescue in the intestine, restores a normal bone and growth plate phenotype. The VDR is nearly ubiquitously expressed, and almost all cells respond to 1,25-(OH)2D exposure; about 3% of the mouse or human genome is regulated, directly and/or indirectly, by the vitamin D endocrine system, suggesting a more widespread function. VDR-deficient mice, but not vitamin D- or 1α-hydroxylase-deficient mice, and man develop total alopecia, indicating that the function of the VDR and its ligand is not fully overlapping. The immune system of VDR- or vitamin D-deficient mice is grossly normal but shows increased sensitivity to autoimmune diseases such as inflammatory bowel disease or type 1 diabetes after exposure to predisposing factors. VDR-deficient mice do not have a spontaneous increase in cancer but are more prone to oncogene- or chemocarcinogen-induced tumors. They also develop high renin hypertension, cardiac hypertrophy, and increased thrombogenicity. Vitamin D deficiency in humans is associated with increased prevalence of diseases, as predicted by the VDR null phenotype. Prospective vitamin D supplementation studies with multiple noncalcemic endpoints are needed to define the benefits of an optimal vitamin D status.
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Seiler, Jonas, Regina Ebert, Maximilian Rudert, Marietta Herrmann, Ellen Leich, Manuela Weißenberger, and Konstantin Horas. "Bone Metastases of Diverse Primary Origin Frequently Express the VDR (Vitamin D Receptor) and CYP24A1." Journal of Clinical Medicine 11, no. 21 (November 3, 2022): 6537. http://dx.doi.org/10.3390/jcm11216537.
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Active vitamin D (1,25(OH)2D3) is known to exert direct anti-cancer actions on various malignant tissues through binding to the vitamin D receptor (VDR). These effects have been demonstrated in breast, prostate, renal and thyroid cancers, which all have a high propensity to metastasise to bone. In addition, there is evidence that vitamin D catabolism via 24-hydroxylase (CYP24A1) is altered in tumour cells, thus, reducing local active vitamin D levels in cancer cells. The aim of this study was to assess VDR and CYP24A1 expression in various types of bone metastases by using immunohistochemistry. Overall, a high total VDR protein expression was detected in 59% of cases (39/66). There was a non-significant trend of high-grade tumours towards the low nuclear VDR expression (p = 0.07). Notably, patients with further distant metastases had a reduced nuclear VDR expression (p = 0.03). Furthermore, a high CYP24A1 expression was detected in 59% (39/66) of bone metastases. There was a significant positive correlation between nuclear VDR and CYP24A1 expression (p = 0.001). Collectively, the VDR and CYP24A1 were widely expressed in a multitude of bone metastases, pointing to a potential role of vitamin D signalling in cancer progression. This is of high clinical relevance, as vitamin D deficiency is frequent in patients with bone metastases.
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Langub, M. C., T. A. Reinhardt, R. L. Horst, H. H. Malluche, and N. J. Koszewski. "Characterization of vitamin D receptor immunoreactivity in human bone cells." Bone 27, no. 3 (September 2000): 383–87. http://dx.doi.org/10.1016/s8756-3282(00)00335-5.
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Dusso, Adriana S., Alex J. Brown, and Eduardo Slatopolsky. "Vitamin D." American Journal of Physiology-Renal Physiology 289, no. 1 (July 2005): F8—F28. http://dx.doi.org/10.1152/ajprenal.00336.2004.
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The vitamin D endocrine system plays an essential role in calcium homeostasis and bone metabolism, but research during the past two decades has revealed a diverse range of biological actions that include induction of cell differentiation, inhibition of cell growth, immunomodulation, and control of other hormonal systems. Vitamin D itself is a prohormone that is metabolically converted to the active metabolite, 1,25-dihydroxyvitamin D [1,25(OH)2D]. This vitamin D hormone activates its cellular receptor (vitamin D receptor or VDR), which alters the transcription rates of target genes responsible for the biological responses. This review focuses on several recent developments that extend our understanding of the complexities of vitamin D metabolism and actions: the final step in the activation of vitamin D, conversion of 25-hydroxyvitamin D to 1,25(OH)2D in renal proximal tubules, is now known to involve facilitated uptake and intracellular delivery of the precursor to 1α-hydroxylase. Emerging evidence using mice lacking the VDR and/or 1α-hydroxylase indicates both 1,25(OH)2D3-dependent and -independent actions of the VDR as well as VDR-dependent and -independent actions of 1,25(OH)2D3. Thus the vitamin D system may involve more than a single receptor and ligand. The presence of 1α-hydroxylase in many target cells indicates autocrine/paracrine functions for 1,25(OH)2D3in the control of cell proliferation and differentiation. This local production of 1,25(OH)2D3is dependent on circulating precursor levels, providing a potential explanation for the association of vitamin D deficiency with various cancers and autoimmune diseases.
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Schedlich, Lynette J., Anita Muthukaruppan, Michelle K. O’Han, and Robert C. Baxter. "Insulin-Like Growth Factor Binding Protein-5 Interacts with the Vitamin D Receptor and Modulates the Vitamin D Response in Osteoblasts." Molecular Endocrinology 21, no. 10 (October 1, 2007): 2378–90. http://dx.doi.org/10.1210/me.2006-0558.
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Abstract The 1,25 dihydroxyvitamin D3 [1,25(OH)2D3]-induced differentiation of osteoblasts comprises the sequential induction of cell cycle arrest at G0/G1 and the expression of bone matrix proteins. Reports differ on the effects of IGF binding protein (IGFBP)-5 on bone cell growth and osteoblastic function. IGFBP-5 can be growth stimulatory or inhibitory and can enhance or impair osteoblast function. In previous studies, we have shown that IGFBP-5 localizes to the nucleus and interacts with the retinoid receptors. We now show that IGFBP-5 interacts with nuclear vitamin D receptor (VDR) and blocks retinoid X receptor (RXR):VDR heterodimerization. VDR and IGFBP-5 were shown to colocalize to the nuclei of MG-63 and U2-OS cells and coimmunoprecipitate in nuclear extracts from these cells. Induction of osteocalcin promoter activity and alkaline phosphatase activity by 1,25(OH)2D3 were significantly enhanced when IGFBP-5 was down-regulated in U2-OS cells. Moreover, we found IGFBP-5 increased basal alkaline phosphatase activity and collagen α1 type 1 expression, and that 1,25(OH)2D3 was unable to further induce the expression of these bone differentiation markers in MG-63 cells. Expression of IGFBP-5 inhibited MG-63 cell growth and caused cell cycle arrest at G0/G1 and G2/M. Furthermore, IGFBP-5 reduced the effects of 1,25(OH)2D3 in blocking cell cycle progression at G0/G1 and decreased the expression of cyclin D1. These results demonstrate that IGFBP-5 can interact with VDR to prevent RXR:VDR heterodimerization and suggest that IGFBP-5 may attenuate the 1,25(OH)2D3-induced expression of bone differentiation markers while having a modest effect on the 1,25(OH)2D3-mediated inhibition of cell cycle progression in bone cells.
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Murdaca, Giuseppe, Alessandro Allegra, Alessandro Tonacci, Caterina Musolino, Luisa Ricciardi, and Sebastiano Gangemi. "Mast Cells and Vitamin D Status: A Clinical and Biological Link in the Onset of Allergy and Bone Diseases." Biomedicines 10, no. 8 (August 3, 2022): 1877. http://dx.doi.org/10.3390/biomedicines10081877.
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The immune system is made up by an extremely composite group of cells, whose regulated and harmonious activity is fundamental to maintain health. The mast cells are an essential effector of inflammatory response which is characterized by a massive release of mediators accumulated in cytoplasmic secretory granules. However, beyond the effects on immune response, mast cells can modify bone metabolism and are capable of intervening in the genesis of pathologies such as osteoporosis and osteopenia. Vitamin D is recognized to induce changes in bone metabolism, but it is also able to influence immune response, suppressing mast cell activation and IgE synthesis from B cells and increasing the number of dendritic cells and IL-10-generating regulatory T cells. Vitamin D deficit has been reported to worsen sensitization and allergic manifestations in several different experimental models. However, in clinical situations, contradictory findings have been described concerning the correlation between allergy and vitamin D deficit. The aim of this review was to analyze the close relationships between mast cells and vitamin D, which contribute, through the activation of different molecular or cellular activation pathways, to the determination of bone pathologies and the onset of allergic diseases.
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Hou, Yi-Chou, Chien-Lin Lu, Cai-Mei Zheng, Wen-Chih Liu, Tzung-Hai Yen, Ruei-Ming Chen, Yuh-Feng Lin, Chia-Ter Chao, and Kuo-Cheng Lu. "The Role of Vitamin D in Modulating Mesenchymal Stem Cells and Endothelial Progenitor Cells for Vascular Calcification." International Journal of Molecular Sciences 21, no. 7 (April 2, 2020): 2466. http://dx.doi.org/10.3390/ijms21072466.
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Vascular calcification, which involves the deposition of calcifying particles within the arterial wall, is mediated by atherosclerosis, vascular smooth muscle cell osteoblastic changes, adventitial mesenchymal stem cell osteoblastic differentiation, and insufficiency of the calcification inhibitors. Recent observations implied a role for mesenchymal stem cells and endothelial progenitor cells in vascular calcification. Mesenchymal stem cells reside in the bone marrow and the adventitial layer of arteries. Endothelial progenitor cells that originate from the bone marrow are an important mechanism for repairing injured endothelial cells. Mesenchymal stem cells may differentiate osteogenically by inflammation or by specific stimuli, which can activate calcification. However, the bioactive substances secreted from mesenchymal stem cells have been shown to mitigate vascular calcification by suppressing inflammation, bone morphogenetic protein 2, and the Wingless-INT signal. Vitamin D deficiency may contribute to vascular calcification. Vitamin D supplement has been used to modulate the osteoblastic differentiation of mesenchymal stem cells and to lessen vascular injury by stimulating adhesion and migration of endothelial progenitor cells. This narrative review clarifies the role of mesenchymal stem cells and the possible role of vitamin D in the mechanisms of vascular calcification.
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Liu, Wei, Lei Zhang, Hui-Jing Xu, Yan Li, Chuan-Min Hu, Jing-Yan Yang, and Mei-Yan Sun. "The Anti-Inflammatory Effects of Vitamin D in Tumorigenesis." International Journal of Molecular Sciences 19, no. 9 (September 13, 2018): 2736. http://dx.doi.org/10.3390/ijms19092736.
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In conjunction with the classical functions of regulating intestinal, bone, and kidney calcium and phosphorus absorption, as well as bone mineralization of vitamin D, the population-based association between low vitamin D status and increased cancer risk is now generally accepted. Inflammation is causally related to oncogenesis. It is widely thought that vitamin D plays an important role in the modulation of the inflammation system by regulating the production of inflammatory cytokines and immune cells, which are crucial for the pathogenesis of many immune-related diseases. Mechanistic studies have shown that vitamin D influences inflammatory processes involved in cancer progression, including cytokines, prostaglandins, MAP kinase phosphatase 5 (MKP5), the nuclear factor kappa B (NF-κB) pathway, and immune cells. Multiple studies have shown that vitamin D has the potential to inhibit tumor development by interfering with the inflammation system. The present review summarizes recent studies of the mechanisms of vitamin D on regulating the inflammation system, which contributes to its potential for cancer prevention and therapy. This review helps answer whether inflammation mediates a causal relationship between vitamin D and tumorigenesis.
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Pereira, Fábio, María Jesús Larriba, and Alberto Muñoz. "Vitamin D and colon cancer." Endocrine-Related Cancer 19, no. 3 (March 1, 2012): R51—R71. http://dx.doi.org/10.1530/erc-11-0388.
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The most active vitamin D metabolite, 1α,25-dihydroxyvitamin D3(1,25(OH)2D3), is a pleiotropic hormone with wide regulatory actions. Classically, vitamin D deficiency was known to alter calcium and phosphate metabolism and bone biology. In addition, recent epidemiological and experimental studies support the association of vitamin D deficiency with a large variety of human diseases, and particularly with the high risk of colorectal cancer. By regulating the expression of many genes via several mechanisms, 1,25(OH)2D3induces differentiation, controls the detoxification metabolism and cell phenotype, sensitises cells to apoptosis and inhibits the proliferation of cultured human colon carcinoma cells. Consistently, 1,25(OH)2D3and several of its analogues decrease intestinal tumourigenesis in animal models. Molecular, genetic and clinical data in humans are scarce but they suggest that vitamin D is protective against colon cancer. Clearly, the available evidence warrants new, well-designed, large-scale trials to clarify the role of vitamin D in the prevention and/or therapy of this important neoplasia.
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Gil, Ángel, Julio Plaza-Diaz, and María Dolores Mesa. "Vitamin D: Classic and Novel Actions." Annals of Nutrition and Metabolism 72, no. 2 (2018): 87–95. http://dx.doi.org/10.1159/000486536.
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Background: Classically, vitamin D has been implicated in bone health by promoting calcium absorption in the gut and maintenance of serum calcium and phosphate concentrations, as well as by its action on bone growth and reorganization through the action of osteoblasts and osteoclasts cells. However, in the last 2 decades, novel actions of vitamin D have been discovered. The present report summarizes both classic and novel actions of vitamin D. Summary: 1,25(OH)2 vitamin D, the active metabolite of vitamin D, also known as calcitriol, regulates not only calcium and phosphate homeostasis but also cell proliferation and differentiation, and has a key a role to play in the responses of the immune and nervous systems. Current effects of vitamin D include xenobiotic detoxification, oxidative stress reduction, neuroprotective functions, antimicrobial defense, immunoregulation, anti-inflammatory/anticancer actions, and cardiovascular benefits. The mechanism of action of calcitriol is mediated by the vitamin D receptor, a subfamily of nuclear receptors that act as transcription factors into the target cells after forming a heterodimer with the retinoid X receptor. This kind of receptors has been found in virtually all cell types, which may explain its multiple actions on different tissues. Key Messages: In addition to classic actions related to mineral homeostasis, vitamin D has novel actions in cell proliferation and differentiation, regulation of the innate and adaptative immune systems, preventive effects on cardiovascular and neurodegenerative diseases, and even antiaging effects.
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Khan, Sono S., Martin Petkovich, Rachel M. Holden, and Michael A. Adams. "Megalin and Vitamin D Metabolism—Implications in Non-Renal Tissues and Kidney Disease." Nutrients 14, no. 18 (September 7, 2022): 3690. http://dx.doi.org/10.3390/nu14183690.
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Megalin is an endocytic receptor abundantly expressed in proximal tubular epithelial cells and other calciotropic extrarenal cells expressing vitamin D metabolizing enzymes, such as bone and parathyroid cells. The receptor functions in the uptake of the vitamin D-binding protein (DBP) complexed to 25 hydroxyvitamin D3 (25(OH)D3), facilitating the intracellular conversion of precursor 25(OH)D3 to the active 1,25 dihydroxyvitamin D3 (1,25(OH)2D3). The significance of renal megalin-mediated reabsorption of 25(OH)D3 and 1,25(OH)2D3 has been well established experimentally, and other studies have demonstrated relevant roles of extrarenal megalin in regulating vitamin D homeostasis in mammary cells, fat, muscle, bone, and mesenchymal stem cells. Parathyroid gland megalin may regulate calcium signaling, suggesting intriguing possibilities for megalin-mediated cross-talk between calcium and vitamin D regulation in the parathyroid; however, parathyroid megalin functionality has not been assessed in the context of vitamin D. Within various models of chronic kidney disease (CKD), megalin expression appears to be downregulated; however, contradictory results have been observed between human and rodent models. This review aims to provide an overview of the current knowledge of megalin function in the context of vitamin D metabolism, with an emphasis on extrarenal megalin, an area that clearly requires further investigation.
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van Driel, Marjolein van, and Johannes P. T. M. van van Leeuwen. "Vitamin D and Bone: A Story of Endocrine and Auto/Paracrine Action in Osteoblasts." Nutrients 15, no. 3 (January 17, 2023): 480. http://dx.doi.org/10.3390/nu15030480.
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Despite its rigid structure, the bone is a dynamic organ, and is highly regulated by endocrine factors. One of the major bone regulatory hormones is vitamin D. Its renal metabolite 1α,25-OH2D3 has both direct and indirect effects on the maintenance of bone structure in health and disease. In this review, we describe the underlying processes that are directed by bone-forming cells, the osteoblasts. During the bone formation process, osteoblasts undergo different stages which play a central role in the signaling pathways that are activated via the vitamin D receptor. Vitamin D is involved in directing the osteoblasts towards proliferation or apoptosis, regulates their differentiation to bone matrix producing cells, and controls the subsequent mineralization of the bone matrix. The stage of differentiation/mineralization in osteoblasts is important for the vitamin D effect on gene transcription and the cellular response, and many genes are uniquely regulated either before or during mineralization. Moreover, osteoblasts contain the complete machinery to metabolize active 1α,25-OH2D3 to ensure a direct local effect. The enzyme 1α-hydroxylase (CYP27B1) that synthesizes the active 1α,25-OH2D3 metabolite is functional in osteoblasts, as well as the enzyme 24-hydroxylase (CYP24A1) that degrades 1α,25-OH2D3. This shows that in the past 100 years of vitamin D research, 1α,25-OH2D3 has evolved from an endocrine regulator into an autocrine/paracrine regulator of osteoblasts and bone formation.
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Goltzman, D. "Functions of vitamin D in bone." Histochemistry and Cell Biology 149, no. 4 (February 12, 2018): 305–12. http://dx.doi.org/10.1007/s00418-018-1648-y.
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Sassi, Francesca, Cristina Tamone, and Patrizia D’Amelio. "Vitamin D: Nutrient, Hormone, and Immunomodulator." Nutrients 10, no. 11 (November 3, 2018): 1656. http://dx.doi.org/10.3390/nu10111656.
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The classical functions of vitamin D are to regulate calcium-phosphorus homeostasis and control bone metabolism. However, vitamin D deficiency has been reported in several chronic conditions associated with increased inflammation and deregulation of the immune system, such as diabetes, asthma, and rheumatoid arthritis. These observations, together with experimental studies, suggest a critical role for vitamin D in the modulation of immune function. This leads to the hypothesis of a disease-specific alteration of vitamin D metabolism and reinforces the role of vitamin D in maintaining a healthy immune system. Two key observations validate this important non-classical action of vitamin D: first, vitamin D receptor (VDR) is expressed by the majority of immune cells, including B and T lymphocytes, monocytes, macrophages, and dendritic cells; second, there is an active vitamin D metabolism by immune cells that is able to locally convert 25(OH)D3 into 1,25(OH)2D3, its active form. Vitamin D and VDR signaling together have a suppressive role on autoimmunity and an anti-inflammatory effect, promoting dendritic cell and regulatory T-cell differentiation and reducing T helper Th 17 cell response and inflammatory cytokines secretion. This review summarizes experimental data and clinical observations on the potential immunomodulating properties of vitamin D.
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Cihan, Yasemin Benderli. "Does vitamin D prevent radiotherapy-induced toxicity?" Turkish Journal of Biochemistry 44, no. 5 (October 25, 2019): 575–77. http://dx.doi.org/10.1515/tjb-2018-0479.
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AbstractVitamin D is known as the bone hormone, it is also know that it has effects on cancer because of its anti-inflammatory and immunomodulatory characteristics and its effects on cytokine levels. It is seen that vitamin D use together with radiotherapy can have a positive effect on cancer treatment. It should be investigated whether toxicities due to radiation is prevented by vitamin D metabolites’ increasing the induction of immunomodulator cells and the capacities of immune response cells. Use of 1,25[OH]2 Vitamin D3 analogs as an adjuvant immunomodulator for patients receiving radiotherapy should be evaluated. There is a need for studies to be done in this regard.
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St-Arnaud, R., J. Prud'homme, C. Leung-Hagesteijn, and S. Dedhar. "Constitutive expression of calreticulin in osteoblasts inhibits mineralization." Journal of Cell Biology 131, no. 5 (December 1, 1995): 1351–59. http://dx.doi.org/10.1083/jcb.131.5.1351.
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Recent studies have shown that the multifunctional protein calreticulin can localize to the cell nucleus and regulate gene transcription via its ability to bind a protein motif in the DNA-binding domain of nuclear hormone receptors. A number of known modulators of bone cell function, including vitamin D, act through this receptor family, suggesting that calreticulin may regulate their action in bone cells. We have used a gain-of-function strategy to examine this putative role of calreticulin in MC3T3-E1 osteoblastic cells. Purified calreticulin inhibited the binding of the vitamin D receptor to characterized vitamin D response elements in gel retardation assays. This inhibition was due to direct protein-protein interactions between the vitamin D receptor and calreticulin. Expression of calreticulin transcripts declined during MC3T3-E1 osteoblastic differentiation. MC3T3-E1 cells were transfected with calreticulin expression vectors; stably transfected cell lines overexpressing recombinant calreticulin were established and assayed for vitamin D-induced gene expression and the capacity to mineralize. Constitutive calreticulin expression inhibited basal and vitamin D-induced expression of the osteocalcin gene, whereas osteopontin gene expression was unaffected. This pattern mimicked the gene expression pattern observed in parental cells before down-regulation of endogenous calreticulin expression. In long-term cultures of parental or vector-transfected cells, 1 alpha,25-dihydroxyvitamin D3 (1,25[OH]2D3) induced a two- to threefold stimulation of 45Ca accumulation into the matrix layer. Constitutive expression of calreticulin inhibited the 1,25(OH)2D3-induced 45Ca accumulation. This result correlated with the complete absence of mineralization nodules in long-term cultures of calreticulin-transfected cells. These data suggest that calreticulin can regulate bone cell function by interacting with specific nuclear hormone receptor-mediated pathways.
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Lee, Hyun-Jin, Young-Min Song, Seunghoon Baek, Yoon-Hee Park, and Jun-Beom Park. "Vitamin D Enhanced the Osteogenic Differentiation of Cell Spheroids Composed of Bone Marrow Stem Cells." Medicina 57, no. 11 (November 19, 2021): 1271. http://dx.doi.org/10.3390/medicina57111271.
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Background and Objectives: Vitamin D is a bone modulator widely used in regenerative medicine. This study aimed to analyze the effects of vitamin D on the osteogenic differentiation and mineralization of human mesenchymal stem cells. Materials and Methods: Spheroids were fabricated using human bone marrow-derived stem cells, and were cultured in the presence of vitamin D at concentrations of 0, 0.1, 1, 10, and 100 nM. Stem cell spheroids were fabricated and the morphological evaluation was conducted on days 1, 3, 7 and 14. Determination of qualitative cellular viability was performed with Live/Dead Kit assay on days 1 and 7. Quantitative cellular viability was evaluated with Cell Counting Kit-8 on days 1, 3, 7, and 14. To analyze the osteogenic differentiation of cell spheroids, alkaline phosphatase activity assays were performed with commercially available kit on days 7 and 14. Real-time polymerase chain reaction was used to determine the expression levels of RUNX2, BSP, OCN, and COL1A1 on days 7 and 14. Results: The stem cells produced well-formed spheroids, and addition of vitamin D did not result in any noticeable changes in the shape. The addition of vitamin D did not significantly change the diameter of the spheroids at 0, 0.1, 1, 10, or 100 nM concentrations. Quantitative cell viability results from days 1, 3, 7 and 14 showed no significant difference between groups (p > 0.05). There was significantly higher alkaline phosphatase activity in the 0.1 nM group when compared with the control group on day 14 (p < 0.05). Real-time polymerase chain reaction results demonstrated that the mRNA expression levels of RUNX2, OCN, and COL1A1 were significantly increased when vitamin D was added to the culture. Conclusions: Based on these findings, we concluded that vitamin D could be applied to the increased osteogenicity of stem cell spheroids.
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De Kok, I. J., K. C. Hicok, R. J. Padilla, R. G. Young, and L. F. Cooper. "Effect of Vitamin D Pretreatment of Human Mesenchymal Stem Cells on Ectopic Bone Formation." Journal of Oral Implantology 32, no. 3 (June 1, 2006): 103–9. http://dx.doi.org/10.1563/760.1.
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Abstract Adult mesenchymal stem cells (MSCs) are used in contemporary strategies for tissue engineering. The MSC is able to form bone following implantation as undifferentiated cells adherent to hydroxyapatite (HA)/tricalcium phosphate (TCP) scaffolds. Previous investigators have demonstrated that human MSCs (hMSCs) can be differentiated to osteoblasts in vitro by the inclusion of vitamin D and ascorbic acid. The aim of this study was to compare the osteogenic potential of predifferentiated and undifferentiated bone marrow–derived, culture-expanded hMSCs adherent to synthetic HA/TCP (60%/40%) following subcutaneous engraftment in severe combined immunodeficiency (SCID) mice. During the final 3 days of culture, cells were grown in Dulbecco's modified Eagle's medium containing 10% fetal calf serum and antibiotics or media containing 25-mM calcium supplementation with vitamin D and ascorbic acid. Four weeks following implantation in SCID mice, scoring analysis of bone formation within the cubes revealed the absence of bone formation in unloaded cubes. Bone formation compared by a qualitative bone index was 7.23% for undifferentiated cells compared to 5.20% for differentiated cells. Minimal resorption was observed at this early time point. In this ectopic model, predifferentiation using a combination of vitamin D and ascorbic acid failed to increase subsequent bone formation by implanted cells. Following implantation of hMSCs adherent to an osteoconductive scaffold, host factors may contribute dominant osteoinductive signals or impose inhibitory signals to control the fate of the implanted cell. Predifferentiation strategies require confirmation in vivo.
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Jovičić, Snežana, Svetlana Ignjatović, and Nada Majkić-Singh. "Biochemistry and metabolism of vitamin D / Biohemija i metabolizam vitamina D." Journal of Medical Biochemistry 31, no. 4 (October 1, 2012): 309–15. http://dx.doi.org/10.2478/v10011-012-0028-8.
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Summary Vitamin D is not technically a vitamin, since it is not an essential dietary factor. It is rather a prohormone produced photochemically in the skin from 7-dehydrocholesterol. Vitamin D and its metabolites may be categorized as either cholecalciferols or ergocalciferols. Cholecalciferol (vi - tamin D3) is the parent compound of the naturally occurring family and is produced in the skin from 7-dehydrocholesterol on exposure to the ultraviolet B portion of sunlight. Vitamin D2 (ergocalciferol), the parent compound of the other family, is manufactured by irradiation of ergosterol produced by yeasts and its potency is less than one-third of vitamin D3’s potency. The steps in the vitamin D endocrine system include the following: 1) the photoconversion of 7- dehydrocholesterol to vitamin D3 in the skin or dietary intake of vitamin D3; 2) metabolism of vitamin D3 by the liver to 25-hydroxyvitamin-D3 [25(OH)D3 ], the major form of vitamin D circulating in the blood compartment; 3) conversion of 25(OH)D3 by the kidney (functioning as an endocrine gland) to the hormone 1,25-dihydroxyvitamin D3 [1,25(OH)2D3 ]; 4) systemic transport of the dihydroxylated metabolite 1,25(OH)2D3 to distal target organs; and 5) binding of 1,25(OH)2D3 to a nuclear receptor (VDR) at target organs, followed by generation of appropriate biological responses. The activation of vitamin D to its hormonal form is mediated by cytochrome P450 enzymes. Six cytochrome P450 (CYP) isoforms have been shown to hydroxylate vitamin D. Four of these, CYP27A1, CYP2R1, CYP3A4 and CYP2J3, are candidates for the enzyme vitamin D 25-hy - droxylase that is involved in the first step of activation. The highly regulated, renal enzyme 25-hydroxyvitamin D-1a-hy - dro xylase contains the component CYP27B1, which completes the activation pathway to the hormonal form 1,25(OH)2D3. A five-step inactivation pathway from 1,25(OH)2D3 to calcitroic acid is attributed to a single multifunctional CYP, CYP24A1, which is transcriptionally in du - ced in vitamin D target cells by the action of 1,25(OH)2D3. An additional key component in the operation of the vitamin D endocrine system is the plasma vitamin D binding protein (DBP), which carries vitamin D3 and its metabolites to their metabolism and target organs. DBP is a specific, high-affinity transport protein. It is synthesized by the liver and circulates in great excess, with fewer than 5% of the binding sites normally occupied. 1,25(OH)2D3, acts as a ligand for a nuclear transcription factor, vitamin D receptor - VDR, which like all other nuclear receptors, regulates gene transcription and cell function. The widespread presence of VDR, and the key activating (1a-hydroxylase, CYP27B1) and inactivating (24-hydroxylase, CYP24A1) en - zy mes in most mammalian cells means that the cells in these tissues have the potential to produce biological res pon ses, depending on the availability of appropriate amounts of vi - tamin D3. Thanks to this widespread presence of elements of vitamin D endocrine system, its biological features are being recognized outside bone tissue, i.e. calcium and pho - sphate metabolism.
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Geng, Shuo, Shuanhu Zhou, Zhenggang Bi, and Julie Glowacki. "Vitamin D metabolism in human bone marrow stromal (mesenchymal stem) cells." Metabolism 62, no. 6 (June 2013): 768–77. http://dx.doi.org/10.1016/j.metabol.2013.01.003.
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Evans, DB, M. Thavarajah, and JA Kanis. "P27. Proliferative effect of vitamin D metabolites on human bone cells." Bone 10, no. 6 (January 1989): 483. http://dx.doi.org/10.1016/8756-3282(89)90119-1.
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Zhou, Shuanhu, Meryl S. LeBoff, and Julie Glowacki. "Vitamin D Metabolism and Action in Human Bone Marrow Stromal Cells." Endocrinology 151, no. 1 (January 1, 2010): 14–22. http://dx.doi.org/10.1210/en.2009-0969.
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Caballero-García, Alberto, Alfredo Córdova-Martínez, Néstor Vicente-Salar, Enrique Roche, and Daniel Pérez-Valdecantos. "Vitamin D, Its Role in Recovery after Muscular Damage Following Exercise." Nutrients 13, no. 7 (July 8, 2021): 2336. http://dx.doi.org/10.3390/nu13072336.
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Aside from its role in bone metabolism, vitamin D is a key immunomodulatory micronutrient. The active form of vitamin D (1,25(OH)D) seems to modulate the innate immune system through different mechanisms. The vitamin is involved in the differentiation of monocytes into macrophages, increasing the phagocytic and chemotactic functions of these cells. At the same time, vitamin D enables efferocytosis and prevents immunopathology. In addition, vitamin D is involved in other processes related to immune function, such as inflammation. Regarding muscle tissue, vitamin D plays an active role in muscle inflammatory response, protein synthesis, and regulation of skeletal muscle function. Two mechanisms have been proposed: A direct role of 1,25(OH)D binding to vitamin D receptors (VDRs) in muscle cells and the modulation of calcium transport in the sarcoplasmic reticulum. This second mechanism needs additional investigation. In conclusion, vitamin D seems to be effective in cases of deficiency and/or if there is a great muscular commitment, such as in high intensity exercises.
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Manikam, Nurul Ratna Mutu. "Vitamin D and immune responses: how much is too much?" World Nutrition Journal 5, S3 (May 31, 2022): 30. http://dx.doi.org/10.25220/wnj.v05.s3.0019.
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Vitamin D is a sunshine vitamin that is widely known for bone health. The main source of vitamin D from exposure to ultraviolet B radiation, whereas only 20% from natural and fortified food. Recent studies concluded that vitamin D has a putative role in reducing the risk of viral respiratory infection by suppressing pro-inflammatory cytokines and delaying increasing anti-inflammatory cytokines response. Whereas, vitamin D regulates innate immunity through macrophage and dendrite cell activity as well as an adaptive immune response through lymphocyte T cells response.
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Pritulo, Olga A., Dmitri V. Brodavkin, Darya А. Ravlyuk, Elvira Y. Bekirova, and Alexey А. Petrov. "The role of Vitamin D in the pathogenesis of some immune-mediated dermatoses." Russian Journal of Skin and Venereal Diseases 25, no. 4 (November 29, 2022): 323–32. http://dx.doi.org/10.17816/dv111799.
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In recent years, the sunlight vitamin has become extremely popular and almost mandatory to use, especially because of its pleiotropic effects, although until recently its use was limited to the prevention of the development of pathology of the bone system, in particular rickets in children. Being actually a fat-soluble prohormone of a steroid nature, Vitamin D participates in the endocrine, paracrine and autocrine regulation of the body. The pharmacotherapeutic renaissance of calciferol is associated with the discovery of Vitamin D receptors in most cells of the body, and the presence of enzymes synthesizing the active form of Vitamin D extrarenally, in particular, in the skin, has led to renewed interest and broad discussion in the dermatological community. Is the role of non-bone effects of calciferol, mainly its role in the pathogenesis of autoimmune skin diseases, really justified from the point of view of evidence-based medicine, and is the tendency to consume Vitamin D safe?
This article presents the most up-to-date information about the role of Vitamin D deficiency in the mechanisms of immune response development, in some dermatoses. In addition to generalizing the bone and extra-bone functions of Vitamin D to the macroorganism, the mechanisms of formation of some of the most common dermatoses, such as psoriasis, atopic dermatitis and vitiligo are discussed in detail. The review details the biological effects of Vitamin D in the skin. The article analyzes the legality of the use of Vitamin D-based drugs and their effectiveness in dermatological practice.
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Yu, Sanhong, and Margherita T. Cantorna. "Regulation of CD1d expression by vitamin D results in fewer hyporesponsive iNKT cells in the vitamin D receptor knockout mouse. (89.7)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S149—S150. http://dx.doi.org/10.4049/jimmunol.178.supp.89.7.
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Abstract CD1d-reactive natural killer T (NKT) cells with an invariant T cell receptor Vα14 rearrangement (i) are a unique subset of lymphocytes, which play important roles in immune regulation, tumor surveillance and host defense against pathogens. Vitamin D and the vitamin D receptor (VDR) are important regulators of T cell function, yet their role in iNKT cells remains unknown. Expression of the vitamin D receptor (VDR) is required for normal development of iNKT cells. Mice lacking the VDR had significantly fewer iNKT cells and the remaining iNKT cells were hyporesponsive. iNKT cell development is blocked at a late stage in iNKT cell development, the CD44high NK1.1− stage. Bone marrow transplantation showed that VDR knockout (KO) hematopoetic cells fail to repopulate iNKT cells in the wild type thymus. The block was not due to fewer iNKT precursors in the VDR KO mice but instead CD1d expression was diminished in the VDR KO thymus. The decreased CD1d results in fewer, hyporesponsive iNKT cells in the VDR KO mouse. The data suggest that vitamin D through the vitamin D receptor is critical for proper iNKT cell development and function.
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Suda, Tatsuo, Naoyuki Takahashi, and Etsuko Abe. "Role of vitamin D in bone resorption." Journal of Cellular Biochemistry 49, no. 1 (May 1992): 53–58. http://dx.doi.org/10.1002/jcb.240490110.
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White, C. P., N. A. Morrison, E. M. Gardiner, and J. A. Eisman. "Vitamin D receptor alleles and bone physiology." Journal of Cellular Biochemistry 56, no. 3 (November 1994): 307–14. http://dx.doi.org/10.1002/jcb.240560306.
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Misiorowski, Waldemar. "Vitamin D, infections and immunity." Wiedza Medyczna 2, no. 2 (December 8, 2020): 6–15. http://dx.doi.org/10.36553/wm.55.
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Vitamin D (VD) is a steroid prohormone that regulates the body's calcium and phosphate levels in bone mineralization. It is also well described as a fat-soluble vitamin playing an important role in immunomodulation, regulation of cytokines, and cell proliferation. Thus, VD is a powerful hormone with pleiotropic effects, which acts to maintain optimal health. Recent studies demonstrate that VD deficiency is associated with the development of autoimmune disorders. Vitamin D generates many extraskeletal effects due to the vitamin D receptor (VDR) which is present in most tissues throughout the body. This paper reviews the recent data on the role of vitamin D in the genesis of various immunological disorders. The possible role of vitamin D in infections is implied from its impact on the innate and adaptive immune responses. A significant effect is the suppression of inflammatory processes. It inhibits immune reactions in general, but it enhances the transcription of "endogenous antibiotics" such as cathelicidin and defensins. VD inhibits the genesis of both Th1 – and Th2-cell mediated diseases. Th1 – dependent autoimmune diseases (e.g., multiple sclerosis, Type 1 diabetes, Crohn's disease, rheumatoid arthritis and so on) are also inhibited by VD due to inhibition of antigen presentation, reduced polarization of Th0 cells to Th1 cells and reduced production of cytokines from the latter cells. VD seems to also be a useful adjunct in the prevention of allograft rejection. Cardiac and coagulopathic features of COVID-19 disease deserve attention as they may be related to vitamin D. There are also intriguing potential links to vitamin D as a factor in the cytokine storm that consist some of the most serious consequences of SARS-CoV-2 infection, such as the acute respiratory distress syndrome. Finally, the current clinical data strongly associate vitamin D with SARS-CoV-2 infection, however a putative clinical link that at this time must still be considered hypothetical.
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Innao, Vanessa, Alessandro Allegra, Lia Ginaldi, Giovanni Pioggia, Massimo De Martinis, Caterina Musolino, and Sebastiano Gangemi. "Reviewing the Significance of Vitamin D Substitution in Monoclonal Gammopathies." International Journal of Molecular Sciences 22, no. 9 (May 6, 2021): 4922. http://dx.doi.org/10.3390/ijms22094922.
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Vitamin D is a steroid hormone that is essential for bone mineral metabolism and it has several other effects in the body, including anti-cancer actions. Vitamin D causes a reduction in cell growth by interrupting the cell cycle. Moreover, the active form of vitamin D, i.e., 1,25-dihydroxyvitamin D, exerts various effects via its interaction with the vitamin D receptor on the innate and adaptive immune system, which could be relevant in the onset of tumors. Multiple myeloma is a treatable but incurable malignancy characterized by the growth of clonal plasma cells in protective niches in the bone marrow. In patients affected by multiple myeloma, vitamin D deficiency is commonly correlated with an advanced stage of the disease, greater risk of progression, the development of pathological fractures, and a worse prognosis. Changes in the vitamin D receptor often contribute to the occurrence and progress of deficiencies, which can be overcome by supplementation with vitamin D or analogues. However, in spite of the findings available in the literature, there is no clear standard of care and clinical practice varies. Further research is needed to better understand how vitamin D influences outcomes in patients with monoclonal gammopathies.
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Jeanson, Nathaniel T., and David T. Scadden. "Vitamin D receptor deletion leads to increased hematopoietic stem and progenitor cells residing in the spleen." Blood 116, no. 20 (November 18, 2010): 4126–29. http://dx.doi.org/10.1182/blood-2010-04-280552.
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Abstract Bone components participate in the regulation of hematopoietic stem cells in the adult mammal. Vitamin D regulates bone mineralization and is associated with pleiotropic effects in many cell types, including putative roles in hematopoietic differentiation. We report that deletion of the vitamin D receptor (VDR) in hematopoietic cells did not result in cell autonomous perturbation of hematopoietic stem cell or progenitor function. However, deletion of VDR in the microenvironment resulted in a marked accumulation of hematopoietic stem cells in the spleen that could be reversed by calcium dietary supplementation. These data suggest that VDR participates in restricting splenic hematopoiesis through maintenance of bone calcium homeostasis and are consistent with the concept that calcium regulation through VDR is a central participant in localizing adult hematopoiesis preferentially to bone marrow.
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Lipińska-Opałka, Agnieszka, Joanna Milart, Jacek Z. Kubiak, and Bolesław Kalicki. "Vitamin D deficiency and the course of SARS-CoV-2 infection." Pediatria i Medycyna Rodzinna 17, no. 1 (March 5, 2021): 17–21. http://dx.doi.org/10.15557/pimr.2021.0002.
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Vitamin D is a fat-soluble steroid hormone. Its main role is to regulate calcium and phosphate levels, which are strictly associated with ossification and bone homeostasis. However, due to the presence of a nuclear vitamin D receptor (VDR) in the majority of cells of the human body, vitamin D also displays multiple effects beyond the bones. Calcitriol (1,25(OH)2D) not only affects cell growth and differentiation, but also stimulates the immune system by, for example, modulating the production of IL-4 and IL-5 anti-inflammatory cytokines. High numbers of VDRs have been found on macrophages, dendritic cells and lymphocytes, among other cells, which can be considered a very strong argument for the participation of vitamin D in autoimmune and anti-inflammatory processes. In recent months we have been witnessing the development of the COVID-19 pandemic. One of the most dangerous consequences of SARS-CoV-2 infection is acute respiratory distress syndrome caused by the activation of lung macrophages and the so-called cytokine storm. A recent study on COVID-19 patients suggests that vitamin D activates the innate immune response and suppresses the acquired immune response; the resultant decreased cytokine expression can reduce the severity of inflammation associated with COVID-19. Among older children and adults, vitamin D deficiency is widespread and observed worldwide, including in the Polish population. Based on numerous studies, normal serum vitamin D levels were established. Vitamin D concentration below 20 ng/mL is considered deficient and a level between 20 and 30 ng/mL is regarded as suboptimal. An optimal vitamin D concentration is 30–50 ng/mL.
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Schröder-Heurich, Bianca, Clara Juliane Pacifica Springer, and Frauke von Versen-Höynck. "Vitamin D Effects on the Immune System from Periconception through Pregnancy." Nutrients 12, no. 5 (May 15, 2020): 1432. http://dx.doi.org/10.3390/nu12051432.
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Vitamin D is a well-known secosteroid and guardian of bone health and calcium homeostasis. Studies on its role in immunomodulatory functions have expanded its field in recent years. In addition to its impact on human physiology, vitamin D influences the differentiation and proliferation of immune system modulators, interleukin expression and antimicrobial responses. Furthermore, it has been shown that vitamin D is synthesized in female reproductive tissues and, by modulating the immune system, affects the periconception period and reproductive outcomes. B cells, T cells, macrophages and dendritic cells can all synthesize active vitamin D and are involved in processes which occur from fertilization, implantation and maintenance of pregnancy. Components of vitamin D synthesis are expressed in the ovary, decidua, endometrium and placenta. An inadequate vitamin D level has been associated with recurrent implantation failure and pregnancy loss and is associated with pregnancy-related disorders like preeclampsia. This paper reviews the most important data on immunomodulatory vitamin D effects in relation to the immune system from periconception to pregnancy and provides an insight into the possible consequences of vitamin D deficiency before and during pregnancy.
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Siddiqui, Maheen, Judhell S. Manansala, Hana A. Abdulrahman, Gheyath K. Nasrallah, Maria K. Smatti, Nadin Younes, Asmaa A. Althani, and Hadi M. Yassine. "Immune Modulatory Effects of Vitamin D on Viral Infections." Nutrients 12, no. 9 (September 21, 2020): 2879. http://dx.doi.org/10.3390/nu12092879.
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Viral infections have been a cause of mortality for several centuries and continue to endanger the lives of many, specifically of the younger population. Vitamin D has long been recognized as a crucial element to the skeletal system in the human body. Recent evidence has indicated that vitamin D also plays an essential role in the immune response against viral infections and suggested that vitamin D deficiency increases susceptibility to viral infections as well as the risk of recurrent infections. For instance, low serum vitamin D levels were linked to increased occurrence of high burdens viral diseases such as hepatitis, influenza, Covid-19, and AIDS. As immune cells in infected patients are responsive to the ameliorative effects of vitamin D, the beneficial effects of supplementing vitamin D-deficient individuals with an infectious disease may extend beyond the impact on bone and calcium homeostasis. Even though numerous studies have highlighted the effect of vitamin D on the immune cells, vitamin D’s antiviral mechanism has not been fully established. This paper reviews the recent mechanisms by which vitamin D regulates the immune system, both innate and adaptive systems, and reflects on the link between serum vitamin D levels and viral infections.
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FAUCHEUX, Corinne, Reine BAREILLE, and Joëlle AMEDEE. "Synthesis of calbindin-D28K during mineralization in human bone marrow stromal cells." Biochemical Journal 333, no. 3 (August 1, 1998): 817–23. http://dx.doi.org/10.1042/bj3330817.
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1α,25-Dihydroxyvitamin D3 [1,25(OH)2D3] is known to modulate Ca2+ metabolism in several cell types. Vitamin-D-dependent calcium binding proteins such as calbindin-D28K (28 kDa calcium binding proteins) have been shown to be regulated by 1,25(OH)2D3 but the mechanisms controlling calbindin synthesis are still poorly understood in human osteoblast cell culture models. The human bone marrow stromal cells (HBMSC) described in this paper developed a calcified matrix, expressed osteocalcin (OC), osteopontin (OP) and responded to 1,25(OH)2D3. The expression of vitamin D receptor mRNA was demonstrated by reverse transcription-PCR. Calbindin-D28K protein was identified only in cells arising from the sixth subculture, which exhibited a calcified matrix and all of the osteoblastic markers, e.g. OC and OP. It was demonstrated by dot-immunodetection using immunological probes, and by in situ hybridization using labelled cDNA probes. Moreover, vitamin D3 enhanced calbindin-D28K synthesis as well as OC synthesis and alkaline phosphatase activity. Uptake of 45Ca induced into the matrix by 1,25(OH)2D3 supports the hypothesis that the calcium-enriched matrix could trap calbindin-D proteins. In conclusion, the studies in vitro described in the present paper indicate, for the first time, a possible role of calbindin-D28K in mineralized matrix formation in HBMSC.
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Kaiser, Martin, Maren Mieth, Orhan Sezer, and Ulrike Heider. "The Proteasome Inhibitor Bortezomib Stimulates Osteoblastic Differentiation of Human Osteoblast Precursor Cells Via Upregulation of Vitamin D Receptor Signaling." Blood 116, no. 21 (November 19, 2010): 1899. http://dx.doi.org/10.1182/blood.v116.21.1899.1899.
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Abstract Abstract 1899 Introduction In multiple myeloma (MM), interactions of the malignant plasma cell clone with the bone marrow microenvironment lead to an enhanced osteoclast recruitment and impaired osteoblast activity. The proteasome inhibitor bortezomib has been shown to suppress osteoclast activity, and there is recent evidence that bortezomib enhances osteoblast differentiation. The aim of this study was to investigate the effects of bortezomib on human osteoblast precursors, focusing on vitamin D (VD) dependent osteoblastic differentiation. Since vitamin D receptor (VDR) is degraded by the proteasome, we hypothesized that bortezomib could influence its signaling and hence vitamin D induced osteoblastic differentiation. This might be of clinical importance, since an increased rate of vitamin D deficiency has recently been reported in patients with MM. Methods Primary human mesenchymal stem cells (hMSC) and primary human osteoblasts (hOB) were isolated from bone marrow aspirates or from bone fragments of healthy donors undergoing orthopedic surgery, respectively. Ascorbic acid and β-glycerolphosphate were used for osteoblastic stimulation (OS), either in combination with or without vitamin D. In order to analyze the effects of proteasome inhibition on osteoblastic differentiation and activity, hMSC and hOB were incubated with bortezomib at subapoptotic doses (1 - 5 nM). In addition, coculture experiments of hMSC, hOB and myeloma cells were performed. Expression of osteocalcin and osteopontin (OPN) were quantified by real-time PCR as markers of osteoblastic lineage differentiation. Expression of VDR was analyzed by western blot in subcellular fractions and VDR signaling was investigated using luciferase reporter assays. Results In coculture experiments, myeloma cells inhibited the vitamin D dependent differentiation and activity of osteoblast precursors, e.g. coculture of hMSC with the myeloma cell line LP-1 for 4 days decreased their osteocalcin expression by 58%. Treatment with bortezomib led to an increased osteoblastic differentiation of hMSC and hOB by OS, represented by an enhanced expression of osteoblast markers osteocalcin and OPN. Importantly, this effect could be further increased, when vitamin D was added. In hMSC stimulated with OS only, addition of 5 nM bortezomib led to an 18.3 fold increase in OPN mRNA expression. In comparison, hMSC stimulated with OS + vitamin D showed a 27.5 fold increase in OPN mRNA with the addition of bortezomib. Osteocalcin expression was increased 1.9 fold by bortezomib in the presence of OS and vitamin D, but not with OS alone. Similar results were obtained with osteoblasts: Incubation with bortezomib slightly increased osteocalcin and OPN mRNA expression in cells stimulated with OS only (1.3 fold and 2.4 fold, respectively). In comparison, in cells stimulated with OS and vitamin D, bortezomib elevated osteocalcin and OPN expression 2.9 fold and 5.5 fold, respectively. Bortezomib led to an increase in nuclear VDR levels in hMSC in western blot analyses. Primary hMSC transfected with a VDR luciferase reporter construct showed a 3.7 fold increase in VDR signaling with bortezomib. Conclusion Our data show that bortezomib stimulates osteoblastic differentiation of hMSCs and hOBs and acts, at least in part, through VDR signaling. Substitution of vitamin D in multiple myeloma patients treated with bortezomib may be beneficial for bone turnover and needs clinical evaluation. Disclosures: Kaiser: Johnson & Johnson: Research Funding. Mieth:Johnson & Johnson: Research Funding. Sezer:Johnson & Johnson: Research Funding. Heider:Johnson & Johnson: Research Funding.
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Lin, Rui. "Crosstalk between Vitamin D Metabolism, VDR Signalling, and Innate Immunity." BioMed Research International 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/1375858.
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The primary function of vitamin D is to regulate calcium homeostasis, which is essential for bone formation and resorption. Although diet is a source of vitamin D, most foods are naturally lacking vitamin D. Vitamin D is also manufactured in the skin through a photolysis process, leading to a process called the “sunshine vitamin.” The active form of vitamin D, 1,25-dihydroxyvitamin D (calcitriol), is biosynthesised in the kidney through the hydroxylation of 25-hydroxycholecalciferol by the CYP27B1 enzyme. It has been found that several immune cells express the vitamin D receptor (VDR) and CYP27B1; of the latter, synthesis is determined by several immune-specific signals. The realisation that vitamin D employs several molecular mechanisms to regulate innate immune responses is more recent. Furthermore, evidence collected from intervention studies indicates that vitamin D supplements may boost clinical responses to infections. This review considers the current knowledge of how immune signals regulate vitamin D metabolism and how innate immune system function is modulated by ligand-bound VDR.
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Muresan, Giorgiana Corina, Mihaela Hedesiu, Ondine Lucaciu, Sanda Boca, and Nausica Petrescu. "Effect of Vitamin D on Bone Regeneration: A Review." Medicina 58, no. 10 (September 23, 2022): 1337. http://dx.doi.org/10.3390/medicina58101337.
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Background and Objectives: Vitamin D (Vit. D) is known for its role in the skeletal system. Vit. D deficiency is also widely researched for its effects on the healing of fractures, bone defects, and osseointegration of implants. In the literature, there are studies that investigated the effects of dietary supplementation with Vit. D to reduce Vit. D deficiency, but increasing the serum level of this vitamin takes time. Therefore, an attempt has been made to combat the effect of Vit. D deficiency through topical applications. The aim of this article was to conduct a review of the existing bibliographic data that investigate the effect of Vit. D on bone regeneration. Materials and Methods: In order to carry out this review, an electronic search was made in several databases and the articles found were selected and analyzed. Results: The in vitro studies’ results demonstrated that Vit. D has a high therapeutic potential by enhancing the differentiation of stem cells in osteoblasts. Human and animal studies were conducting using various methods, but most of them revealed that Vit. D has a positive influence on the process of bone regeneration. Conclusions: The overall results of the research showed that, indeed, Vit. D is beneficial for bone regeneration; however, most of the studies imply that a thorough research is still needed for finding the most effective mode of administration and the dose needed in order to achieve the desired effect.
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Halfon, Matthieu, Olivier Phan, and Daniel Teta. "Vitamin D: A Review on Its Effects on Muscle Strength, the Risk of Fall, and Frailty." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/953241.
Full textAbstract:
Vitamin D is the main hormone of bone metabolism. However, the ubiquitary nature of vitamin D receptor (VDR) suggests potential for widespread effects, which has led to new research exploring the effects of vitamin D on a variety of tissues, especially in the skeletal muscle.In vitrostudies have shown that the active form of vitamin D, calcitriol, acts in myocytes through genomic effects involving VDR activation in the cell nucleus to drive cellular differentiation and proliferation. A putative transmembrane receptor may be responsible for nongenomic effects leading to rapid influx of calcium within muscle cells. Hypovitaminosis D is consistently associated with decrease in muscle function and performance and increase in disability. On the contrary, vitamin D supplementation has been shown to improve muscle strength and gait in different settings, especially in elderly patients. Despite some controversies in the interpretation of meta-analysis, a reduced risk of falls has been attributed to vitamin D supplementation due to direct effects on muscle cells. Finally, a low vitamin D status is consistently associated with the frail phenotype. This is why many authorities recommend vitamin D supplementation in the frail patient.
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Sung, Chih-Chien, Min-Tser Liao, Kuo-Cheng Lu, and Chia-Chao Wu. "Role of Vitamin D in Insulin Resistance." Journal of Biomedicine and Biotechnology 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/634195.
Full textAbstract:
Vitamin D is characterized as a regulator of homeostasis of bone and mineral metabolism, but it can also provide nonskeletal actions because vitamin D receptors have been found in various tissues including the brain, prostate, breast, colon, pancreas, and immune cells. Bone metabolism, modulation of the immune response, and regulation of cell proliferation and differentiation are all biological functions of vitamin D. Vitamin D may play an important role in modifying the risk of cardiometabolic outcomes, including diabetes mellitus (DM), hypertension, and cardiovascular disease. The incidence of type 2 DM is increasing worldwide and results from a lack of insulin or inadequate insulin secretion following increases in insulin resistance. Therefore, it has been proposed that vitamin D deficiency plays an important role in insulin resistance resulting in diabetes. The potential role of vitamin D deficiency in insulin resistance has been proposed to be associated with inherited gene polymorphisms including vitamin D-binding protein, vitamin D receptor, and vitamin D 1alpha-hydroxylase gene. Other roles have been proposed to involve immunoregulatory function by activating innate and adaptive immunity and cytokine release, activating inflammation by upregulation of nuclear factorκB and inducing tumor necrosis factorα, and other molecular actions to maintain glucose homeostasis and mediate insulin sensitivity by a low calcium status, obesity, or by elevating serum levels of parathyroid hormone. These effects of vitamin D deficiency, either acting in concert or alone, all serve to increase insulin resistance. Although there is evidence to support a relationship between vitamin D status and insulin resistance, the underlying mechanism requires further exploration. The purpose of this paper was to review the current information available concerning the role of vitamin D in insulin resistance.
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Dobreva, Ivelina, Pavlina Teneva, and Valya Trencheva. "INFLUENCE OF SUNSHINE ON THE SERUM LEVELS OF VITAMIN D." Teacher of the future 31, no. 4 (June 5, 2019): 1081–85. http://dx.doi.org/10.35120/kij31041081d.
Full textAbstract:
Vitamin D - anti-rheumatic vitamin - directly related to calcium and phosphate metabolism and bone formation. In recent years, it has been proven to be much more important because it also has an impact on cells of the immune system, heart, endocrine and muscle cells. Vitamin deficiency also involves mental illness such as depression and schizophrenia. For the synthesis of enough vitamin D it is necessary to have a daily, all year round direct exposure to direct sunlight for at least 20-30 minutes a day. The geographic location of Republic of Bulgaria provides the average annual sunshine duration around 2150 hours and it is about 49% of the maximum possible sunshine. However, the majority (58.33%) of the study participants had a "deficiency" in serum levels of vitamin D, snd there is also a large percentage of those who are less often outdoors.
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Kito, Hiroaki, Haruka Morihiro, Yuka Sakakibara, Kyoko Endo, Junko Kajikuri, Takayoshi Suzuki, and Susumu Ohya. "Downregulation of the Ca2+-activated K+ channel KCa3.1 in mouse preosteoblast cells treated with vitamin D receptor agonist." American Journal of Physiology-Cell Physiology 319, no. 2 (August 1, 2020): C345—C358. http://dx.doi.org/10.1152/ajpcell.00587.2019.
Full textAbstract:
The maturity of osteoblasts by proliferation and differentiation in preosteoblasts is essential for maintaining bone homeostasis. The beneficial effects of vitamin D on bone homeostasis in mammals have been demonstrated experimentally and clinically. However, the direct actions of vitamin D on preosteoblasts remain to be fully elucidated. In this study, we found that the functional activity of intermediate-conductance Ca2+-activated K+ channels (KCa3.1) positively regulated cell proliferation in MC3T3-E1 cells derived from mouse preosteoblasts by enhancing intracellular Ca2+ signaling. We examined the effects of treatment with vitamin D receptor (VDR) agonist on the expression and activity of KCa3.1 by real-time PCR examination, Western blotting, Ca2+ imaging, and patch clamp analyses in mouse MC3T3-E1 cells. Following the downregulation of KCa3.1 transcriptional modulators such as Fra-1 and HDAC2, KCa3.1 activity was suppressed in MC3T3-E1 cells treated with VDR agonists. Furthermore, application of the KCa3.1 activator DCEBIO attenuated the VDR agonist-evoked suppression of cell proliferation rate. These findings suggest that a decrease in KCa3.1 activity is involved in the suppression of cell proliferation rate in VDR agonist-treated preosteoblasts. Therefore, KCa3.1 plays an important role in bone formation by promoting osteoblastic proliferation under physiological conditions.