Ethanol and Vitamin D Receptor in T Cell Apoptosis

Rehman, Shabina; Chandel, Nirupama; Salhan, Divya; Rai, Partab; Sharma, Bipin; Singh, Tejinder; Husain, Mohammad; Malhotra, Ashwani; Singhal, Pravin C.

doi:10.1007/s11481-012-9393-9

Cited by 14 publications

(8 citation statements)

References 58 publications

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“…In agreement with the findings of the present study, a previous study demonstrated that the protective activity of 1,25(OH) 2 D 3 was mediated by antioxidant ROS inhibition and associated with reduced tumor necrosis factor-α and nuclear factor-κB levels (19). It has also been previously demonstrated that T cell apoptosis was mediated via ROS generation in response to the downregulation of vitamin D receptor (20). However, to the best of our knowledge, this is the first report demonstrating the protective role of 1,25(OH) 2 D 3 against HG-induced apoptosis and ROS production in HPMCs.…”

Section: Discussionsupporting

confidence: 93%

1,25(OH)2D3 inhibits high glucose-induced apoptosis and ROS production in human peritoneal mesothelial cells via the MAPK/P38 pathway

Yang

et al. 2016

Molecular Medicine Reports

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The regulation of cell proliferation, differentiation and immunomodulation are affected by 1,25(OH)2D3. However, its function during apoptosis and oxidative stress in human peritoneal mesothelial cells (HPMCs) remains unknown. The aim of the present study was to investigate whether the regulation of apoptosis and oxidative stress have therapeutic relevance in peritoneal dialysis (PD) therapy. The present study investigated the effects of 1,25(OH)2D3 on high glucose (HG)-induced apoptosis and reactive oxygen species (ROS) production in HPMCs, and examined the underlying molecular mechanisms. Flow cytometry and western blotting were performed to detect cell apoptosis, 2,7-dichlorofluorescein diacetate was used to measure reactive oxygen species production and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was used to measure cell viability. The results of the present study demonstrated that exposure to HG increased apoptosis and ROS production in HPMCs, whereas pretreatment with 1,25(OH)2D3 significantly inhibited HG‑induced apoptosis and ROS production. Further analysis revealed that 1,25(OH)2D3 facilitated cell survival via the MAPK/P38 pathway. The results of the present study indicate that 1,25(OH)2D3 inhibits apoptosis and ROS production in HG‑induced HPMCs via inhibition of the MAPK/P38 pathway.

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Section: Discussionsupporting

confidence: 93%

1,25(OH)2D3 inhibits high glucose-induced apoptosis and ROS production in human peritoneal mesothelial cells via the MAPK/P38 pathway

Yang

et al. 2016

Molecular Medicine Reports

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“…The silencing of VDR with siRNA displayed the activation of the RAS, and the activation of the VDR resulted in the downregulation of the RAS. ROS generation was inhibited if VDR was activated or if AngII was blocked by Losartan (Rehman et al 2013). In this context, we show that mitochondrial injury linked to AT 1 /VDR uncoupling was improved when paricalcitol, enalapril, or, better still, the combination of both was used.…”

Section: Discussionmentioning

confidence: 74%

Vitamin D receptor-modulated Hsp70/AT1 expression may protect the kidneys of SHRs at the structural and functional levels

García

Altamirano

Mazzei

et al. 2014

Cell Stress and Chaperones

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Previous hypertension studies have shown that low levels of vitamin D are linked to elevated renin-angiotensin system. The heat shock protein 70 regulates signaling pathways for cellular oxidative stress responses. Hsp70 has been shown to protect against angiotensin II-induced hypertension and exert a cytoprotective effect. Here, we wanted to evaluate whether the vitamin D receptor (VDR) associated with Hsp70/ AT 1 expression may be involved in the mechanism by which paricalcitol provides renal protection in spontaneously hypertensive rats (SHRs). One-month-old female SHRs were treated for 4 months with vehicle, paricalcitol, enalapril, or a combination of both paricalcitol and enalapril. The following were determined: blood pressure; biochemical parameters; fibrosis; apoptosis; mitochondrial morphology; and VDR, AT 1 receptor, and Hsp70 expression in the renal cortex. Blood pressure was markedly reduced by enalapril or the combination but not by paricalcitol alone. However, VDR activation, enalapril or combination, prevented fibrosis, the number of TUNEL-positive apoptotic cells, mitochondrial damage, and NADPH oxidase activity in SHRs. Additionally, high AT 1 receptor expression, like low Hsp70 expression (immunohistochemical/immunofluorescence studies), was reversed in the renal cortices of paricalcitol-and/or enalapriltreated animals (SHRs), and these changes were most marked in the combination therapy group. Finally, all of the recovery parameters were consistent with an improvement in VDR expression. Data suggest that Hsp70/AT 1 modulated by VDR is involved in the mechanism by which paricalcitol provides renal protection in SHRs. We propose that low AT 1 expression through VDR induction could be a consequence of the heat shock response Hsp70-mediated cell protection.

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“…We showed that VDR activation attenuated oxidative stress in both in vivo MI/R and in vitro H/R experiments. Although the anti-oxidative action of VDR has been increasingly recognized in various types of cells (13,49,53,55), little is known on the molecular mechanism by which VDR decreases oxidative stress. Recently, it has been suggested that G6PD and MT were the direct target genes of VDR and might be involved in the anti-oxidative and cytoprotective effects of VDR (5,17).…”

Section: Vdr Attenuates Mi/r Injurymentioning

confidence: 99%

Vitamin D Receptor Activation Protects Against Myocardial Reperfusion Injury Through Inhibition of Apoptosis and Modulation of Autophagy

Yao

Ying

Zhao

et al. 2015

Antioxidants & Redox Signaling

143

100

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Aims: To determine the roles of vitamin D receptor (VDR) in ischemia/reperfusion-induced myocardial injury and to investigate the underlying mechanisms involved. Results: The endogenous VDR expression was detected in the mouse heart, and myocardial ischemia/reperfusion (MI/R) upregulated VDR expression. Activation of VDR by natural and synthetic agonists reduced myocardial infarct size and improved cardiac function. Mechanistically, VDR activation inhibited endoplasmic reticulum (ER) stress (determined by the reduction of CCAAT/enhancer-binding protein homologous protein expression and caspase-12 activation), attenuated mitochondrial impairment (determined by the decrease of mitochondrial cytochrome c release and caspase-9 activation), and reduced cardiomyocyte apoptosis. Furthermore, VDR activation significantly inhibited MI/Rinduced autophagy dysfunction (determined by the inhibition of Beclin 1 over-activation, the reduction of autophagosomes, the LC3-II/LC3-I ratio, p62 protein abundance, and the restoration of autophagy flux). Moreover, VDR activation inhibited MI/R-induced oxidative stress through a metallothionein-dependent mechanism. The cardioprotective effects of VDR agonists mentioned earlier were impaired in the setting of cardiac-specific VDR silencing. In contrast, adenovirus-mediated cardiac VDR overexpression decreased myocardial infarct size and improved cardiac function through attenuating oxidative stress, and inhibiting apoptosis and autophagy dysfunction. Innovation and Conclusion: Our data demonstrate that VDR is a novel endogenous self-defensive and cardioprotective receptor against MI/R injury, via mechanisms (at least in part) reducing oxidative stress, and inhibiting apoptosis and autophagy dysfunction-mediated cell death. Antioxid. Redox Signal. 22,[633][634][635][636][637][638][639][640][641][642][643][644][645][646][647][648][649][650]

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Ethanol and Vitamin D Receptor in T Cell Apoptosis

Cited by 14 publications

References 58 publications

1,25(OH)2D3 inhibits high glucose-induced apoptosis and ROS production in human peritoneal mesothelial cells via the MAPK/P38 pathway

1,25(OH)2D3 inhibits high glucose-induced apoptosis and ROS production in human peritoneal mesothelial cells via the MAPK/P38 pathway

Vitamin D receptor-modulated Hsp70/AT1 expression may protect the kidneys of SHRs at the structural and functional levels

Vitamin D Receptor Activation Protects Against Myocardial Reperfusion Injury Through Inhibition of Apoptosis and Modulation of Autophagy

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