scholarly journals Comparing the Expressions of Vitamin D Receptor, Cell Proliferation, and Apoptosis in Gastric Mucosa With Gastritis, Intestinal Metaplasia, or Adenocarcinoma Change

2021 ◽  
Vol 8 ◽  
Author(s):  
Li-Wei Chen ◽  
Liang-Che Chang ◽  
Chung-Ching Hua ◽  
Tzu-Chien Cheng ◽  
Chin-Chan Lee
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Gastric Mucosa ◽  
Intestinal Metaplasia ◽  
Vitamin D Receptor ◽  
Statistical Significance ◽  
Tumor Stage ◽  
Chang Gung Memorial Hospital ◽  
Proliferation And Apoptosis ◽  
The Mean

Background: This study aimed to compare the expression of vitamin D receptor (VDR), cell proliferation, and apoptosis in the gastric mucosa of patients with gastritis, intestinal metaplasia (IM), and adenocarcinoma using artificial intelligence.Material and Methods: This study retrospectively enrolled patients at the Keelung Chang Gung Memorial Hospital from November of 2016 to June, 2017, who were diagnosed with gastric adenocarcinoma. The inclusion criteria were patients' pathologic reports that revealed all compartments of Helicobacter pylori infection, gastritis, IM, and adenocarcinoma simultaneously in the same gastric sample. Tissue slides after immunohistochemical (IHC) staining were transformed into digital images using a scanner and counted using computer software (QuPath and ImageJ). IHC staining included PA1-711 antibody for VDR, Ki67 antigen for proliferation, and M30 antibody CK18 for apoptosis.Results: Twenty-nine patients were included in the IHC staining quantitative analysis. The mean age was 69.1 ± 11.3 y/o. Most (25/29, 86.2%) patients had poorly differentiated adenocarcinoma. The mean expression of Ki67 and CK18 increased progressively from gastritis and IM to adenocarcinoma, with statistical significance (P < 0.05). VDR expression did not correlate with Ki67 or CK18 expression. Survival time was only correlated with tumor stage (correlation coefficient = −0.423, P value < 0.05), but was not correlated with the expression of VDR, Ki67, and CK18.Conclusion: Ki67 expression and CK18 expression progressively increased in the areas of gastritis, IM, and adenocarcinoma. No correlation between VDR expression and Ki67 or CK18 expression was found in this study.

scholarly journals Helicobacter pylori-Related Metabolic Parameters and Premalignant Gastric Mucosa Histological Lesions in Swiss Bariatric Patients

2021 ◽  
Vol 9 (7) ◽  
pp. 1361
Author(s):  
Michael Doulberis ◽  
Noah Thierry Pierre ◽  
Giulia Manzini ◽  
Apostolis Papaefthymiou ◽  
Jannis Kountouras ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Risk Factor ◽  
Gastric Mucosa ◽  
Arterial Hypertension ◽  
Intestinal Metaplasia ◽  
Large Scale ◽  
Statistical Significance ◽  
Bariatric Patients ◽  
The Mean ◽  
First Time

Obesity, as a major risk factor of metabolic syndrome (MetS), represents a pandemic, especially in Western societies, and is considered a risk factor for malignancies. Helicobacter pylori (Hp), is a definite carcinogen with global distribution. We aimed to investigate, for the first time in Switzerland, the main gastric mucosa premalignant histological lesions of bariatric patients in correlation with MetS components and Hp Infection (Hp-I). By reviewing retrospectively 94304 patient cases, a total of 116 eligible patients having undergone bariatric surgery were identified. The mean patient age was 48.66 years. Hp(+) patients were 24% (28/116). Presence of gastric mucosa atrophy was documented in 8/28 Hp(+) patients (29%) and (2/88) Hp(−) ones (2%) (p = 0.006). Gastric mucosa intestinal metaplasia was observed in 14/28 (50%) Hp(+) patients versus 3/88 (3.4%) of Hp(-) group (p < 0.0001). Hp(+) patients exhibited statistically higher arterial hypertension (p = 0.033). The homeostatic model of assessment insulin resistance was also statistically significantly higher for the Hp(+) group (p < 0.001). In a multivariate analysis, including arterial hypertension, gastric mucosa atrophy, and intestinal metaplasia as variables, statistical significance remained only for intestinal metaplasia (p = 0.001). In conclusion, Hp-I is associated with premalignant gastric mucosa histologic lesions and MetS components, including arterial hypertension and IR. Further large-scale prospective studies are required to confirm these findings.

scholarly journals Analysis of Vitamin D Receptor Gene Polymorphism in Chronic Periodontitis among Saudi Population

2021 ◽  
Vol 2 (01) ◽  
pp. 12-16
Author(s):  
Fathy M. Elfasakhany ◽  
Omaima N. Al-Qahtani ◽  
Asmaa M. Badri ◽  
Hala A. Abuelela
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Gene ◽  
Equilibrium Analysis ◽  
Plaque Index ◽  
Control Group ◽  
Saudi Population ◽  
Bleeding On Probing ◽  
Probing Depth ◽  
The Mean

Abstract Objective Genetic and environmental factors have important roles in the development of periodontitis. We aimed to assess the relation of vitamin D receptor (VDR) ApaI and TaqI polymorphisms and the susceptibility of periodontitis in Saudi population in Makkah region. Materials and Methods In total, 86 unrelated patients with moderate-to-severe periodontitis and 86 controls were enrolled in this study. Evaluation of the periodontal state was performed by using plaque index, bleeding on probing, probing depth, and attachment loss. Extraction of genomic DNA from peripheral blood and genotyping of VDR gene ApaI G/T (rs7975232) and TaqI T/C (rs731236) polymorphisms were performed by utilizing polymerase chain reaction and restriction digestion. Results There were statistically significant differences between both groups regarding the mean bleeding on probing, mean probing depth, mean plaque index, and the mean attachment level (p < 0.001) indicating that the matching based on the investigated groups was adequate. The examined populations were in Hardy-Weinberg equilibrium. Analysis of the genotype and allele frequencies of both VDR ApaI and TaqI single nucleotide polymorphisms revealed that they were statistically indifferent between the control group and the periodontitis subjects (p> 0.05). Conclusion These results suggested that VDR ApaI and TaqI polymorphisms might not be related to the susceptibility of periodontal disease in the Saudi subjects in Makkah region.

scholarly journals Vitamin D levels in children with COVID-19: a report from Turkey

2021 ◽  
Vol 149 ◽  
Author(s):  
Aysegul Alpcan ◽  
Serkan Tursun ◽  
Yaşar Kandur
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Statistical Significance ◽  
Serum Vitamin ◽  
University Hospital ◽  
Control Group ◽  
Serum Vitamin D ◽  
Vitamin D Levels ◽  
Normal Vitamin ◽  
The Mean

Abstract Several studies have demonstrated that higher levels of vitamin D are associated with better prognosis and outcomes in infectious diseases. We aimed to compare the vitamin D levels of paediatric patients with mild/moderate coronavirus disease 2019 (COVID-19) disease and a healthy control group. We retrospectively reviewed the medical records of patients who were hospitalised at our university hospital with the diagnosis of COVID-19 during the period between 25 May 2020 and 24 December 2020. The mean age of the COVID-19 patients was 10.7 ± 5.5 years (range 1–18 years); 43 (57.3%) COVID-19 patients were male. The mean serum vitamin D level was significantly lower in the COVID-19 group than the control group (21.5 ± 10.0 vs. 28.0 ± 11.0 IU, P < 0.001). The proportion of patients with vitamin D deficiency was significantly higher in the COVID-19 group than the control group (44% vs. 17.5%, P < 0.001). Patients with low vitamin D levels were older than the patients with normal vitamin D levels (11.6 ± 4.9 vs. 6.2 ± 1.8 years, P = 0.016). There was a significant male preponderance in the normal vitamin D group compared with the low vitamin D group (91.7% vs. 50.8%, P = 0.03). C-reactive protein level was higher in the low vitamin D group, although the difference did not reach statistical significance (9.6 ± 2.2 vs. 4.5 ± 1.6 mg/l, P = 0.074). Our study provides an insight into the relationship between vitamin D deficiency and COVID-19 for future studies. Empiric intervention with vitamin D can be justified by low serum vitamin D levels.

Vitamin D receptor gene polymorphisms in ocular surface squamous cell neoplasms

2019 ◽  
Vol 30 (5) ◽  
pp. 901-907
Author(s):  
Nergiz Ismayilova ◽  
Melis Palamar ◽  
Huseyin Onay ◽  
Emine Ipek Ceylan ◽  
Tahir Atik ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Squamous Cell ◽  
Ocular Surface ◽  
Gene Polymorphisms ◽  
Receptor Gene ◽  
Tumor Stage ◽  
Study Group ◽  
Vitamin D Receptor Gene ◽  
Cell Neoplasm

Purpose: To investigate vitamin D receptor polymorphisms in ocular surface squamous cell neoplasm and to evaluate the relationship between the identified polymorphisms and susceptibility to ocular surface squamous cell neoplasm and the clinical course. Materials and Methods: A totala of 70 patients with ocular surface squamous cell neoplasm (study group) and 75 healthy age and gender-matched individuals (control group) were included in the study. Vitamin D receptor FokI and BsmI polymorphisms were examined. The relationships between histopathological diagnosis, recurrence rates, tumor stage, and identified polymorphisms were investigated. Results: Histopathologically, 43 of the cases were squamous cell carcinoma and 27 of the cases were conjunctival intraepithelial neoplasia. The frequency of FokI (FF, Ff, ff) and BsmI (BB, Bb, bb) polymorphism genotype of vitamin D receptor gene were similar in the groups. The frequency of polymorphism (heterozygous or homozygous) for BsmI (Bb and bb) was significantly higher (p = 0.046) in the study group, while no difference was found between the groups in terms of polymorphic carriers (heterozygous or homozygous) for FokI. There was no correlation between tumor stage, recurrence-polymorphism frequency, and patient age-polymorphism frequency. Conclusion: It is known that active vitamin D inhibits the growth of cancer cells by binding to vitamin D receptor with regulation of genes responsible for cell proliferation. The presence of BsmI polymorphism in vitamin D receptor, in particular bb genotype and b allele, appears to be associated with the susceptibility of ocular surface squamous cell neoplasm. BsmI gene polymorphisms of vitamin D receptor might play an effective role in the formation, progression, and in the course of ocular surface squamous cell neoplasm.

scholarly journals Stimulation of Sirt1-Regulated FoxO Protein Function by the Ligand-Bound Vitamin D Receptor

2010 ◽  
Vol 30 (20) ◽  
pp. 4890-4900 ◽  
Author(s):  
Beum-Soo An ◽  
Luz E. Tavera-Mendoza ◽  
Vassil Dimitrov ◽  
Xiaofeng Wang ◽  
Mario R. Calderon ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Phosphatase Activity ◽  
Vitamin D Receptor ◽  
Nuclear Export ◽  
Target Genes ◽  
Trichostatin A ◽  
Control Cell ◽  
Sirtuin 1 ◽  
Foxo Protein

ABSTRACT Hormonal vitamin D, 1,25-dihydroxyvitamin D (1,25D), signals through the nuclear vitamin D receptor (VDR). 1,25D regulates cell proliferation and differentiation and has been identified as a cancer chemopreventive agent. FoxO proteins are transcription factors that control cell proliferation and survival. They function as tumor suppressors and are associated with longevity in several organisms. Accumulating data have revealed that 1,25D and FoxO proteins regulate similarly common target genes. We show here that the ligand-bound VDR regulates the posttranslational modification and function of FoxO proteins. 1,25D treatment enhances binding of FoxO3a and FoxO4 within 4 h to promoters of FoxO target genes and blocks mitogen-induced FoxO protein nuclear export. The VDR associates directly with FoxO proteins and regulators, the sirtuin 1 (Sirt1) class III histone deacetylase (HDAC), and protein phosphatase 1. In addition, phosphatase activity and trichostatin A-resistant HDAC activity coimmunoprecipitate with the VDR. 1,25D treatment rapidly (in <4 h) induces FoxO deacetylation and dephosphorylation, consistent with activation. In contrast, ablation of VDR expression enhances FoxO3a phosphorylation, as does knockdown of Sirt1, consistent with the coupling of FoxO acetylation and phosphorylation. 1,25D regulation of common VDR/FoxO target genes is attenuated by blockade of phosphatase activity or by small interfering RNA (siRNA)-mediated knockdown of Sirt1 or FoxO protein expression. Finally, 1,25D-dependent cell cycle arrest is blocked in FoxO3a-deficient cells, indicating that FoxO proteins are key downstream mediators of the antiproliferative actions of 1,25D. These studies link 1,25D signaling through the VDR directly to Sirt1 and FoxO function and provide a molecular basis for the cancer chemopreventive actions of 1,25D.

scholarly journals Prediagnostic Plasma 25-Hydroxyvitamin D and Pancreatic Cancer Survival

2016 ◽  
Vol 34 (24) ◽  
pp. 2899-2905 ◽  
Author(s):  
Chen Yuan ◽  
Zhi Rong Qian ◽  
Ana Babic ◽  
Vicente Morales-Oyarvide ◽  
Douglas A. Rubinson ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Vitamin D ◽  
Plasma Level ◽  
Vitamin D Receptor ◽  
Statistical Significance ◽  
Receptor Gene ◽  
Vitamin D Receptor Gene ◽  
Single Nucleotide ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D

Purpose Although vitamin D inhibits pancreatic cancer proliferation in laboratory models, the association of plasma 25-hydroxyvitamin D [25(OH)D] with patient survival is largely unexplored. Patients and Methods We analyzed survival among 493 patients from five prospective US cohorts who were diagnosed with pancreatic cancer from 1984 to 2008. We estimated hazard ratios (HRs) for death by plasma level of 25(OH)D (insufficient, < 20 ng/mL; relative insufficiency, 20 to < 30 ng/mL; sufficient ≥ 30 ng/mL) by using Cox proportional hazards regression models adjusted for age, cohort, race and ethnicity, smoking, diagnosis year, stage, and blood collection month. We also evaluated 30 tagging single-nucleotide polymorphisms in the vitamin D receptor gene, requiring P < .002 (0.05 divided by 30 genotyped variants) for statistical significance. Results Mean prediagnostic plasma level of 25(OH)D was 24.6 ng/mL, and 165 patients (33%) were vitamin D insufficient. Compared with patients with insufficient levels, multivariable-adjusted HRs for death were 0.79 (95% CI, 0.48 to 1.29) for patients with relative insufficiency and 0.66 (95% CI, 0.49 to 0.90) for patients with sufficient levels (P trend = .01). These results were unchanged after further adjustment for body mass index and history of diabetes (P trend = .02). The association was strongest among patients with blood collected within 5 years of diagnosis, with an HR of 0.58 (95% CI, 0.35 to 0.98) comparing patients with sufficient to patients with insufficient 25(OH)D levels. No single-nucleotide polymorphism at the vitamin D receptor gene met our corrected significance threshold of P < .002; rs7299460 was most strongly associated with survival (HR per minor allele, 0.80; 95% CI, 0.68 to 0.95; P = .01). Conclusion We observed longer overall survival in patients with pancreatic cancer who had sufficient prediagnostic plasma levels of 25(OH)D.

scholarly journals 1,25(OH)2Vitamin D3 Stimulates Myogenic Differentiation by Inhibiting Cell Proliferation and Modulating the Expression of Promyogenic Growth Factors and Myostatin in C2C12 Skeletal Muscle Cells

Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 2976-2986 ◽  
Author(s):  
Leah A. Garcia ◽  
Keisha K. King ◽  
Monica G. Ferrini ◽  
Keith C. Norris ◽  
Jorge N. Artaza
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Cell Proliferation ◽  
Vitamin D Receptor ◽  
Myogenic Differentiation ◽  
Receptor Expression ◽  
Negative Regulator ◽  
Muscle Performance ◽  
Rt Pcr ◽  
C2c12 Myoblasts

Skeletal muscle wasting is an important public health problem associated with aging, chronic disease, cancer, kidney dialysis, and HIV/AIDS. 1,25-Dihydroxyvitamin D (1,25-D3), the active form of vitamin D, is widely recognized for its regulation of calcium and phosphate homeostasis in relation to bone development and maintenance and for its calcemic effects on target organs, such as intestine, kidney, and parathyroid glands. Emerging evidence has shown that vitamin D administration improves muscle performance and reduces falls in vitamin D-deficient older adults. However, little is known of the underlying mechanism or the role 1,25-D3 plays in promoting myogenic differentiation at the cellular and/or molecular level. In this study, we examined the effect of 1,25-D3 on myoblast cell proliferation, progression, and differentiation into myotubes. C2C12 myoblasts were treated with 1,25-D3 or placebo for 1, 3, 4, 7, and 10 d. Vitamin D receptor expression was analyzed by quantitative RT-PCR, Western blottings and immunofluorescence. Expression of muscle lineage, pro- and antimyogenic, and proliferation markers was assessed by immunocytochemistry, PCR arrays, quantitative RT-PCR, and Western blottings. Addition of 1,25-D3 to C2C12 myoblasts 1) increased expression and nuclear translocation of the vitamin D receptor, 2) decreased cell proliferation, 3) decreased IGF-I expression, and 4) promoted myogenic differentiation by increasing IGF-II and follistatin expression and decreasing the expression of myostatin, the only known negative regulator of muscle mass, without changing growth differentiation factor 11 expression. This study identifies key vitamin D-related molecular pathways for muscle regulation and supports the rationale for vitamin D intervention studies in select muscle disorder conditions.

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