Vitamin D receptor activation reduces inflammatory cytokines and plasma MicroRNAs in moderate chronic kidney disease – a randomized trial

Mansouri, Ladan; Lundwall, Kristina; Moshfegh, Ali; Jacobson, Stefan H.; Lundahl, Joachim; Spaak, Jonas

doi:10.1186/s12882-017-0576-8

Cited by 33 publications

(26 citation statements)

References 39 publications

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“…The protective effect of vitamin D/VDR in kidney diseases has been validated by a lot of research works including ours 10,21 . While most of those work mainly focused on chronic kidney diseases like diabetic kidney disease.…”

Section: Discussionmentioning

confidence: 81%

“…Numerous studies including our previous work have shown that 1,25(OH)2D3 or its active analogs, through VDR activation, are protective against proteinuria, renal fibrosis, and inflammation in patients with chronic kidney disease and in animal models of diabetic nephropathy or end-stage renal disease [10][11][12][13] . However, few attentions were focused on the role of VDR in AKI.…”

Section: Introductionmentioning

confidence: 98%

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VDR activation attenuate cisplatin induced AKI by inhibiting ferroptosis

et al. 2020

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Our preliminary work has revealed that vitamin D receptor (VDR) activation is protective against cisplatin induced acute kidney injury (AKI). Ferroptosis was recently reported to be involved in AKI. Here in this study, we investigated the internal relation between ferroptosis and the protective effect of VDR in cisplatin induced AKI. By using ferroptosis inhibitor ferrostatin-1 and measurement of ferroptotic cell death phenotype in both in vivo and in vitro cisplatin induced AKI model, we observed the decreased blood urea nitrogen, creatinine, and tissue injury by ferrostatin-1, hence validated the essential involvement of ferroptosis in cisplatin induced AKI. VDR agonist paricalcitol could both functionally and histologically attenuate cisplatin induced AKI by decreasing lipid peroxidation (featured phenotype of ferroptosis), biomarker 4-hydroxynonenal (4HNE), and malondialdehyde (MDA), while reversing glutathione peroxidase 4 (GPX4, key regulator of ferroptosis) downregulation. VDR knockout mouse exhibited much more ferroptotic cell death and worsen kidney injury than wild type mice. And VDR deficiency remarkably decreased the expression of GPX4 under cisplatin stress in both in vivo and in vitro, further luciferase reporter gene assay showed that GPX4 were target gene of transcription factor VDR. In addition, in vitro study showed that GPX4 inhibition by siRNA largely abolished the protective effect of paricalcitol against cisplatin induced tubular cell injury. Besides, pretreatment of paricalcitol could also alleviated Erastin (an inducer of ferroptosis) induced cell death in HK-2 cell. These data suggested that ferroptosis plays an important role in cisplatin induced AKI. VDR activation can protect against cisplatin induced renal injury by inhibiting ferroptosis partly via trans-regulation of GPX4.

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 98%

VDR activation attenuate cisplatin induced AKI by inhibiting ferroptosis

et al. 2020

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“…Vitamin D supplementation has been proven to modulate some of the miRNAs posing a risk towards MS, such as miR-146a, miR-150, miR-155, miR-30c, miR-23a, miR-181b, miR-449c, miR-125b, miR-7, and miR-432-5p. 120,[182][183][184][185][186] It was also linked to EAE amelioration. 120 The EBV drug, ACV, was related to a significant downregulation of MS-associated miR-146a.…”

Section: Resultsmentioning

confidence: 99%

“…Notably, miR-7 was observed to be increased in EAE lymph nodes (P = 1.2E-03, fold change = 1.4) ( Table 2). 153 In an article by Mansouri et al, 186 daily supplementation of 2 μg paricalcitol in 12 patients with chronic kidney disease (CKD) significantly reduced the levels of miR-432-5p, miR-495-3p, and miR-576-5p compared with those in the placebo group (n = 12). miR-432-5p was reported to be a significantly dysregulated miRNA that could distinguish between healthy controls and progressive MS and between progressive MS and RRMS (P = .002, 0.051, fold-change = 2.2, 0.5; respectively).…”

Section: Table 5 (Continued)mentioning

confidence: 99%

Environmental Influencers, MicroRNA, and Multiple Sclerosis

Mohammed

2020

J Cent Nerv Syst Dis

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Multiple sclerosis (MS) is a complex neurological disorder characterized by an aberrant immune system that affects patients’ quality of life. Several environmental factors have previously been proposed to associate with MS pathophysiology, including vitamin D deficiency, Epstein-Barr virus (EBV) infection, and cigarette smoking. These factors may influence cellular molecularity, interfering with cellular proliferation, differentiation, and apoptosis. This review argues that small noncoding RNA named microRNA (miRNA) influences these factors’ mode of action. Dysregulation in the miRNAs network may deeply impact cellular hemostasis, thereby possibly resulting in MS pathogenicity. This article represents a literature review and an author’s theory of how environmental factors may induce dysregulations in the miRNAs network, which could ultimately affect MS pathogenicity.

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“…Activation of the transcription nuclear factor-κB (NF-κB) and the intrarenal renin-angiotensin system, in ltration of macrophages, and tubulointerstitial in ammation may also be involved [10,35]. On the contrary, vitamin D has been shown to reduce levels of reactive oxygen species, suppress renin-angiotensin system and decrease circulating angiotensin II levels, inhibit in ammatory responses, and prevent podocyte loss and glomerulosclerosis [13,36,37], thereby potentially protect kidney from damage induced by lead exposure. A recent study in rats revealed that vitamin D alleviated lead induced kidney injury (i.e.…”

Section: Discussionmentioning

confidence: 99%

The effects of vitamin D on albuminuria relative to blood lead in patients with type 2 diabetes

Wang

Wan

Cheng

et al. 2020

Preprint

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Background: Environmental lead exposure has been linked with reduced kidney function. However, evidence about its role in diabetic kidney damage, especially when considering the nutritional status of vitamin D, is sparse. Methods: This observational study comprised 4,033 diabetic patients from seven communities in Shanghai, China. The associations of blood lead with urinary albumin-to-creatinine ratio (UACR) and albuminuria, defined as UACR ≥30 mg/g, according to serum 25-hydroxyvitamin D [25(OH)D] levels were analyzed using linear and Poisson regression models, respectively. Results: A doubling of blood lead level was associated with a 10.7% higher UACR (95% CI, 6.19% to 15.5%) in diabetic patients with 25(OH)D <50 nmol/L, whereas the estimate declined to 2.03% (95% CI, −5.18% to 9.78%) in those with 25(OH)D ≥50 nmol/L. The difference in the association for albuminuria prevalence was also observed between the two groups, with risk ratios of 1.09 (95% CI, 1.03–1.15) and 0.99 (95% CI, 0.86–1.14) per doubling of blood lead level, respectively. Furthermore, the increment of UACR in relation to blood lead appeared to be two times higher in patients with 25(OH)D <50 nmol/L and estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 than those with eGFR ≥60 mL/min/1.73 m2. While in patients with 25(OH)D ≥50 nmol/L, there was no association between blood lead and UACR regardless of eGFR category. Conclusions: Higher blood lead levels were associated with increased urinary albumin excretion in diabetic patients with vitamin D deficiency, which became more pronounced in the presence of reduced eGFR. Further prospective studies are needed to validate our findings and to determine whether vitamin D supplementation yields a benefit.

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Vitamin D receptor activation reduces inflammatory cytokines and plasma MicroRNAs in moderate chronic kidney disease – a randomized trial

Cited by 33 publications

References 39 publications

VDR activation attenuate cisplatin induced AKI by inhibiting ferroptosis

VDR activation attenuate cisplatin induced AKI by inhibiting ferroptosis

Environmental Influencers, MicroRNA, and Multiple Sclerosis

The effects of vitamin D on albuminuria relative to blood lead in patients with type 2 diabetes

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