• Title/Summary/Keyword: Vitamin D receptor

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Association of Calcium Intake and Bone Mineral Density by Vitamin D Receptor Genotype among Elderly Women Living in Rural a Area (노년기 농촌여성의 비타민 D 수용체 유전자형에 따른 칼슘 섭취량과 골밀도와의 관계)

  • Kim Ji-Sun;Kim Hee-Seon
    • Korean Journal of Community Nutrition
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    • v.11 no.4
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    • pp.534-540
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    • 2006
  • Recent studies have shown that environmental, biochemical, nutritional or genetic factors affect bone mineral density (BMD). The purpose of the present study was to investigate the effect of vitamin D receptor (VDR) gentotype and nutritional status on BMD of elderly women living in a rural area. Three hundred thirty five elderly women over 65 years in Asan participated the study. Data for demographic and nutrient intakes were obtained by survey with a two day 24 hr recall method. BMD was measured by broadband ultrasound attenuation (BUA) using quantitative ultrasound (QUS). VDR genotypes of the subjects analyzed with Bsm I restriction enzyme were bb (92%), Bb (7%) and BB (1%). No differences were found between genotypes bb and Bb/BB in age, menopausal age, body mass index and body fat. BUA of bb genotype was higher (62.5 $\pm$ 15.6 dB/MHz) than Bb/BB genotype (56.1 $\pm$ 17.6 dB/MHz) by Student's t-tests. Correlation analyses showed strong negative correlation of BMD and age, but positive correlation with BMI, energy and calcium intake. When subgroup analyses were conducted after stratification by the median calcium intake level (412.9 mg/d), the above median calcium intake group showed significant difference in BUA by VDR genotype while the lower median calcium intake group did not show significant difference. The current study confirmed interaction of calcium intake and VDR genotype in association with BMD. Further nutritional intervention will be needed to improve calcium status of the elderly women living in rural areas.

Vitamin D Receptor Gene TaqI, BsmI and FokI Polymorphisms in Korean Patients with Tuberculosis

  • Kang, Tae-Jin;Jin, Song-Hou;Yeum, Chung-Eun;Lee, Seong-Beom;Kim, Chi-Hong;Lee, Sang-Haak;Kim, Kwan-Hyoung;Shin, Eun-Soon;Chae, Gue-Tae
    • IMMUNE NETWORK
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    • v.11 no.5
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    • pp.253-257
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    • 2011
  • Background: The active metabolite (1, 25- dihydroxycholecalciferol) of vitamin D (25-hydroxycholecalciferol) leads to activation of macrophages and deficiency of vitamin D seems to be involved in the risk of tuberculosis. The effects of vitamin D are exerted by interaction with the vitamin D receptor (VDR) and may be influenced by polymorphism in the VDR gene. In this study, variation in the VDR gene was investigated in Korean population with tuberculosis. Methods: We typed three VDR polymorphisms of restriction endonuclease sites for TaqI, BsmI and FokI in 155 patients with tuberculosis and 105 healthy volunteers. Results: The frequencies of FokI genotypes determined from TB patients were 29.13% for FF, 56.31% for Ff, and 14.56% for ff. We observed 1.4-fold increased prevalence of the Ff genotype in TB patients compared with normal healthy groups (p=0.0857). However, there was no significant association between the genotype groups, TB patient and normal control, for FokI polymorphism. There was also no significant association between VDR gene and tuberculosis in another polymorphism (BsmI and TaqI). Conclusion: Three polymorphisms (TaqI, BsmI and FokI) in the VDR gene do not appear to be responsible for host susceptibility to human tuberculosis in Korean population.

Associations between Vitamin D Receptor (VDR) Gene Polymorphisms and Colorectal Cancer Risk and Effect Modifications of Dietary Calcium and Vitamin D in a Japanese Population

  • Takeshige, Nobuyuki;Yin, Guang;Ohnaka, Keizo;Kono, Suminori;Ueki, Takashi;Tanaka, Masao;Maehara, Yoshihiko;Okamura, Takeshi;Ikejiri, Koji;Maekawa, Takafumi;Yasunami, Yohichi;Takenaka, Kenji;Ichimiya, Hitoshi;Terasaka, Reiji
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.5
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    • pp.2019-2026
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    • 2015
  • Much interest has been drawn to possible associations between vitamin D receptor (VDR) gene polymorphisms and colorectal cancer risk in conjunction with potentially protective effects of calcium and vitamin D. In a study of 685 cases of colorectal cancer and 778 community controls in Japan, we examined the associations of the FokI, BsmI, ApaI, and TaqI polymorphisms with colorectal cancer risk and effect modification by dietary calcium and vitamin D. Genotypes were determined by the PCR-RFLP method. The ApaI polymorphism seemed to be associated with a decreased risk of colorectal cancer, particularly of rectal cancer. The adjusted odds ratio of colorectal cancer for the ApaI AA and Aa genotypes combined versus the aa genotype was 0.83 (95% confidence interval [CI] 0.67-1.02), and the corresponding value for rectal cancer was 0.75 (95%CI 0.56-0.99). A decreased risk of colorectal cancer for the ApaI AA and Aa genotypes combined was more evident in individuals with high calcium intake (interaction p=0.055). The FokI polymorphism seemed to be associated with a decreased risk of colon cancer among those with high vitamin D intake (interaction p=0.09). The BsmI and TaqI polymorphisms were unrelated to colorectal cancer risk, and the null associations were not modified by calcium or vitamin D intake. In conclusion, the ApaI polymorphism may be associated with a decreased risk of colorectal cancer in Japanese, dependent on dietary calcium intake.

A Case of Vitamin D-Dependent Rickets, Type 1 (제 1형 비타민 D 의존성 구루병 1례)

  • Hur, Ji Hye;Lee, Chong Guk;Sur, Chung Wook
    • Clinical and Experimental Pediatrics
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    • v.48 no.6
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    • pp.665-668
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    • 2005
  • "Rickets" is the term applied to impaired mineralization at epiphyseal growth plate, resulting in deformity and impaired linear growth of long bones. Rickets may arise as a result of vitamin D deficiency or abnormality in metabolism. Vitamin D-dependent rickets(VDDR) is rare autosomal recessive disorder in which affected individuals have clinical features of vitamin D deficiency. In 1961, Prader first described this disorder including severe clinical features of rickets, such as hypophosphatemia, hypocalcemia, muscle weakness and seizure. Two distinctive hereditary defects, type I VDDR and type II VDDR have been recognized in vitamin D metabolism. Type I VDDR may be due to congenital defects of renal 1 ${\alpha}$-hydroxylase, the enzyme responsible for conversion of $25(OH)D_3$. These patients have low to detectable $1,25(OH)_2D_3$ in presence of normal to raised $25(OH)D_3$. In type II VDDR, renal production of $1,25(OH)_2D_3$ is intact but $1,25(OH)_2D_3$ is not used effectively and target organ resistant to $1,25(OH)_2D_3$ is respectively derived from the abnormality in the vitamin D receptor. We report a case of a 25 month-old girl with typical clinical features of VDDR type I rickets, hypocalcemia, increased alkaline phosphatase and secondary hyperparathyroidism.

Vitamin D Proliferates Vaginal Epithelium through RhoA Expression in Postmenopausal Atrophic Vagina tissue

  • Lee, Arum;Lee, Man Ryul;Lee, Hae-Hyeog;Kim, Yeon-Suk;Kim, Jun-Mo;Enkhbold, Temuulee;Kim, Tae-Hee
    • Molecules and Cells
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    • v.40 no.9
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    • pp.677-684
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    • 2017
  • Postmenopausal atrophic vagina (PAV) is the thinning of the walls of the vagina and decreased lugae of the vagina. PAV is caused by decreased estrogen levels in postmenopausal women. However, the harmful effects of hormone replacement therapy (HRT) have resulted in considerable caution in its use. Various estrogen agonist treatment options are available. Vitamin D is influences the regulation of differentiation and proliferation of various cells, especially tissues lining stratified squamous epithelium, such as the vaginal epithelium. In this study, we hypothesized that vitamin D could provide an alternative and a safe treatment option for PAV by promoting the proliferation and differentiation of the vaginal epithelium. Thirty six patients were enrolled in this case-control study. Vitamin D associated proteins in a vitamin D and sex hormone treated vaginal epithelial cell line as well as normal and PAV tissues were measured. To confirm of cell-to-cell junction protein expression, cell line and tissue studies included RT-PCR, immunohistochemistry staining, and immunoblot analyses. The expression of cell-to-cell junction proteins was higher in women with symptoms of atrophic vagina tissue compared to women without the symptoms. Vitamin D stimulated the proliferation of the vaginal epithelium by activating p-RhoA and Erzin through the vitamin D receptor (VDR). The results suggest that vitamin D positively regulates cell-to-cell junction by increasing the VDR/p-RhoA/p-Ezrin pathway. This is the first study to verify the relationship of the expression of RhoA and Ezrin proteins in vaginal tissue of PAV.

Role of vitamin D for orthodontic tooth movement, external apical root resorption, and bone biomarker expression and remodeling: A systematic review

  • Martina Ferrillo;Dario Calafiore;Lorenzo Lippi;Francesco Agostini;Mario Migliario;Marco Invernizzi;Amerigo Giudice;Alessandro de Sire
    • The korean journal of orthodontics
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    • v.54 no.1
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    • pp.26-47
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    • 2024
  • Objective: This systematic review aimed to evaluate the correlation between vitamin D levels and the rate of tooth movement, external apical root resorption, bone biomarker expression, and bone remodeling. Methods: Three databases (PubMed, Scopus, and Web of Science) were systematically searched from inception until 14th March 2023 to identify studies investigating the correlation between orthodontic tooth movement and vitamin D in animals and humans. The quality assessment was made in accordance with the Joanna Briggs Institute Critical Appraisal Checklist. Results: Overall, 519 records were identified, and 19 were selected for the qualitative synthesis. Eleven studies investigated the effect of local administration (injections in the periodontal ligament, to the gingiva distal to the teeth, or submucosae palatal area) and systemic administration (oral supplementation) of vitamin D on tooth movement, external apical root movement, pro-inflammatory cytokines, and bone remodeling factors. The remaining eight studies investigated the correlation between serum vitamin D levels and salivary vitamin D levels on bone turnover markers and tooth movement. Conclusions: The findings of this systematic review support that vitamin D3 local injections might increase the rate of tooth movement via the receptor activator of the nuclear factor-kB/osteoprotegerin axis. However, the non-uniform study designs and the different protocols and outcome methods make it challenging to draw reliable conclusions.

Inhibition of Vitamin D Receptor Translocation by Cigarette Smoking Extracts

  • Uh, Soo-Taek;Koo, So-My;Kim, Yang Ki;Kim, Ki Up;Park, Sung Woo;Jang, An Soo;Kim, Do Jin;Kim, Yong Hoon;Park, Choon Sik
    • Tuberculosis and Respiratory Diseases
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    • v.73 no.5
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    • pp.258-265
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    • 2012
  • Background: Vitamin D can translocate a vitamin D receptor (VDR) from the nucleus to the cell membranes. The meaning of this translocation is not elucidated in terms of a role in pathogenesis of chronic obstructive pulmonary disease (COPD) till now. VDR deficient mice are prone to develop emphysema, suggesting that abnormal function of VDR might influence a generation of COPD. The blood levels of vitamin D have known to be well correlated with that of lung function in patients with COPD, and smoking is the most important risk factor in development of COPD. This study was performed to investigate whether cigarette smoke extracts (CSE) can inhibit the translocation of VDR and whether mitogen activated protein kinases (MAPKs) are involved in this inhibition. Methods: Human alveolar basal epithelial cell line (A549) was used in this study. 1,25-$(OH_2)D_3$ and/or MAPKs inhibitors and antioxidants were pre-incubated before stimulation with 10% CSE, and then nucleus and microsomal proteins were extracted for a Western blot of VDR. Results: Five minutes treatment of 1,25-(OH2)D3 induced translocation of VDR from nucleus to microsomes by a dose-dependent manner. CSE inhibited 1,25-$(OH_2)D_3$-induced translocation of VDR in both concentrations of 10% and 20%. All MAPKs inhibitors did not suppress the inhibitory effects of CSE on the 1,25-$(OH_2)D_3$-induced translocation of VDR. Quercetin suppressed the inhibitory effects of CSE on the 1,25-$(OH_2)D_3$-induced translocation of VDR, but not in n-acetylcysteine. Conclusion: CSE has an ability to inhibit vitamin D-induced VDR translocation, but MAPKs are not involved in this inhibition.

The Effect of Chrysin on the Transcriptional Activity of Vitamin D Receptor in Human Keratinocytes (각질형성세포에서 Chrysin이 Vitamin D Receptor의 전사 활성화에 미치는 영향)

  • Choo, Jung Ha;Lee, Sang Hwa
    • Journal of the Society of Cosmetic Scientists of Korea
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    • v.39 no.1
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    • pp.75-81
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    • 2013
  • Chrysin (5,7-dihydroxyflavone) is a natural flavonoid found in various plants and foods such as propolis and honey. It has been reported that chrysin has various biological effects including antioxidant, anti-aging, anti-inflammatory and anti-cancer. In this study, we investigated the effect of chrysin on the transcriptional activity of VDR in human epidermal keratinocytes by performing dual-luciferase assay. Chrysin significantly induced the transcriptional activity of VDR in a concentration-dependent manner. The VDR mRNA expression was investigated by quantitative real time PCR and chrysin increased the VDR mRNA expression in normal human epidermal keratinocytes. We also found that chrysin increased the expression of keratinocyte differentiation markers such as keratin 10, involucrin and filaggrin. Therefore, the results suggest that chrysin can stimulate the differentiation of human keratinocytes by increasing transcriptional activity of VDR.

Vitamin D maintains E-cadherin intercellular junctions by downregulating MMP-9 production in human gingival keratinocytes treated by TNF-α

  • Oh, Changseok;Kim, Hyun Jung;Kim, Hyun-Man
    • Journal of Periodontal and Implant Science
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    • v.49 no.5
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    • pp.270-286
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    • 2019
  • Purpose: Despite the well-known anti-inflammatory effects of vitamin D in periodontal health, its mechanism has not been fully elucidated. In the present study, the effect of vitamin D on strengthening E-cadherin junctions (ECJs) was explored in human gingival keratinocytes (HGKs). ECJs are the major type of intercellular junction within the junctional epithelium, where loose intercellular junctions develop and microbial invasion primarily occurs. Methods: HOK-16B cells, an immortalized normal human gingival cell line, were used for the study. To mimic the inflammatory environment, cells were treated with tumor necrosis factor-alpha ($TNF-{\alpha}$). Matrix metalloproteinases (MMPs) in the culture medium were assessed by an MMP antibody microarray and gelatin zymography. The expression of various molecules was investigated using western blotting. The extent of ECJ development was evaluated by comparing the average relative extent of the ECJs around the periphery of each cell after immunocytochemical E-cadherin staining. Vitamin D receptor (VDR) expression was examined via immunohistochemical analysis. Results: $TNF-{\alpha}$ downregulated the development of the ECJs of the HGKs. Dissociation of the ECJs by $TNF-{\alpha}$ was accompanied by the upregulation of MMP-9 production and suppressed by a specific MMP-9 inhibitor, Bay 11-7082. Exogenous MMP-9 decreased the development of ECJs. Vitamin D reduced the production of MMP-9 and attenuated the breakdown of ECJs in the HGKs treated with $TNF-{\alpha}$. In addition, vitamin D downregulated $TNF-{\alpha}$-induced nuclear factor kappa B ($NF-{\kappa}B$) signaling in the HGKs. VDR was expressed in the gingival epithelium, including the junctional epithelium. Conclusions: These results suggest that vitamin D may avert $TNF-{\alpha}$-induced downregulation of the development of ECJs in HGKs by decreasing the production of MMP-9, which was upregulated by $TNF-{\alpha}$. Vitamin D may reinforce ECJs by downregulating $NF-{\kappa}B$ signaling, which is upregulated by $TNF-{\alpha}$. Strengthening the epithelial barrier may be a way for vitamin D to protect the periodontium from bacterial invasion.