Effects of 1,25(OH)2D3 in experimental mesangial proliferative nephritis in rats

Panichi, Vincenzo; Migliori, Massimiliano; Taccola, D; Filippi, C.; Nisco, L. De; Giovannini, Luca; Palla, Roberto; Tetta, Ciro; Camussi, Giovanni

doi:10.1046/j.1523-1755.2001.00775.x

Cited by 96 publications

(90 citation statements)

References 25 publications

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“…7,23 Animal studies have shown that elevated levels of active vitamin D contribute to factors that are hypothesized to be associated with a reduction of kidney disease progression, including reduction in proteinuria, decrease in TGF-b, inhibition of mesangial cell proliferation, and preservation of the structural integrity of glomerular podocytes. [24][25][26][27] Finally, FGF-23 might directly contribute to kidney injury, similar to the direct effect of FGF-23 on cardiac myocytes. 9 Previous studies suggest that FGF-23 elevation precedes abnormalities in other mineral metabolism markers, which supports the potential role of FGF-23 as an early indicator of renal pathology.…”

Section: Discussionmentioning

confidence: 94%

Serum Fibroblast Growth Factor-23 Is Associated with Incident Kidney Disease

Rebholz

Grams

Coresh

et al. 2015

Journal of the American Society of Nephrology

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Fibroblast growth factor-23 is a bone-derived hormone that increases urinary phosphate excretion and inhibits hydroxylation of 25-hydroxyvitamin D. Recent studies suggest that fibroblast growth factor-23 may be an early biomarker of CKD progression. However, its role in kidney function decline in the general population is unknown. We assessed the relationship between baseline (1990-1992) serum levels of intact fibroblast growth factor-23 and incident ESRD in 13,448 Atherosclerosis Risk in Communities study participants (56.1% women, 74.7% white) followed until December 31, 2010. At baseline, the mean age of participants was 56.9 years and the mean eGFR was 97 ml/min per 1.73 m 2 . During a median follow-up of 19 years, 267 participants (2.0%) developed ESRD. After adjustment for demographic characteristics, baseline eGFR, traditional CKD risk factors, and markers of mineral metabolism, the highest fibroblast growth factor-23 quintile (.54.6 pg/ml) compared with the lowest quintile (,32.0 pg/ml) was associated with risk of developing ESRD (hazard ratio, 2.10; 95% confidence interval, 1.31 to 3.36; trend P,0.001). In a large, community-based study comprising a broad range of kidney function, higher baseline fibroblast growth factor-23 levels were associated with increased risk of incident ESRD independent of the baseline level of kidney function and a number of other risk factors.

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Section: Discussionmentioning

confidence: 94%

Serum Fibroblast Growth Factor-23 Is Associated with Incident Kidney Disease

Rebholz

Grams

Coresh

et al. 2015

Journal of the American Society of Nephrology

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“…6,18 In animal models of primary glomerular diseases, administration of vitamin D reduces glomerular infiltration of inflammatory cells. 6,9 Consistently, a decreased inflammation is associated with higher serum vitamin D level in patients with CKD. 19 Vitamin D may exert its immunomodulatory action through regulating the activity of many types of immune cells such as macrophages, dendritic cells, and T cells.…”

mentioning

confidence: 87%

“…[3][4][5] Evidence is also mounting that vitamin D analogue is renoprotective in different experimental nephropathies. 6 Although early studies largely focused on primary glomerular diseases, [7][8][9] active vitamin D was shown to display beneficial effects in obstructive nephropathy, 10 a model characterized by inflammatory infiltration, tubular atrophy, and interstitial fibrosis. The therapeutic effects of active vitamin D in obstructive nephropathy are thought to be mediated by its ability to preserve tubular epithelial integrity via inhibiting epithelial-to-mesenchymal transition (EMT) 10 ; however, in view of its pleiotropic property, it is conceivable that vitamin D could elicit its renoprotection by a multitude of actions.…”

mentioning

confidence: 99%

Paricalcitol Inhibits Renal Inflammation by Promoting Vitamin D Receptor–Mediated Sequestration of NF-κB Signaling

Tan

Wen

Liu

2008

Journal of the American Society of Nephrology

243

194

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Inflammation is a pathologic feature of a variety of chronic kidney diseases. Several lines of evidence suggest a potential anti-inflammatory role for vitamin D in chronic kidney disease, but the underlying mechanism remains unknown. Here, the effect of the synthetic vitamin D analogue paricalcitol on renal inflammation was investigated in a mouse model of obstructive nephropathy. Paricalcitol reduced infiltration of T cells and macrophages in the obstructed kidney. This inhibition of inflammatory cell infiltration was accompanied by a decreased expression of RANTES and TNF-␣. Induction of RANTES was localized primarily to the tubular epithelium, underscoring a role for tubular cells in renal inflammation. In a human proximal tubular cell line (HKC-8), paricalcitol inhibited RANTES mRNA and protein expression and abolished the ability of tubular cells to recruit lymphocytes and monocytes after TNF-␣ stimulation. Although RANTES induction depended on NF-B signaling, paricalcitol affected neither TNF-␣-mediated IB␣ phosphorylation and degradation nor p65 NF-B activation and nuclear translocation. Instead, chromatin immunoprecipitation assay showed that paricalcitol abolished the binding of p65 to its cognate cis-acting element in the RANTES promoter. The vitamin D receptor (VDR) and p65 formed a complex in tubular cells after paricalcitol treatment, which inhibited the ability of p65 to trans-activate gene transcription. In vivo, paricalcitol did not block NF-B nuclear translocation after obstructive injury but did increase the expression and nuclear distribution of VDR. These results suggest that paricalcitol inhibits renal inflammatory infiltration and RANTES expression by promoting VDRmediated sequestration of NF-B signaling.

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“…Panichi et al [19] investigated the role of 1,25-(OH) 2 D 3 in a rat model with mesangial nephritis, and found that 1,25-(OH) 2 D 3 treatment reduced IL-6 cytokine, macrophage infiltration, apoptosis. They also demonstrated its antiproliferative effect by attenuating immunolabeling to proliferating cell nuclear antigen (PCNA), as well as its anti-inflammatory activities and effects on cell differentiation, proliferation and apoptosis [19].…”

Section: Vitamin D In Inflammationmentioning

confidence: 99%

“…They also demonstrated its antiproliferative effect by attenuating immunolabeling to proliferating cell nuclear antigen (PCNA), as well as its anti-inflammatory activities and effects on cell differentiation, proliferation and apoptosis [19].…”

Section: Vitamin D In Inflammationmentioning

confidence: 99%

Vitamin D Actions on Cell Differentiation, Proliferation and Inflammation

Almeida¹,

Coimbra²

2017

IJCAM

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The most well-known function of vitamin D (1,25-(OH) 2 D 3 ) is to maintain calcium and phosphate homeostasis and promote bone mineralization. However, apart from these traditional calcium-related actions, 1,25-(OH) 2 D 3 is being increasingly recognized for its potent antiproliferative, pro-differentiation, and immunomodulatory roles. Along with these non-calcemic or non-classic actions of 1,25-(OH) 2 D 3 , new therapeutic actions of 1,25-(OH) 2 D 3 have been discovered in recent years.

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Effects of 1,25(OH)2D3 in experimental mesangial proliferative nephritis in rats

Abstract: 1,25(OH)2D3 can reduce glomerular hypercellularity, inflammatory infiltration in anti-Thy-1.1 nephritis, preserving the apoptotic response of the reparative phase.

Cited by 96 publications

References 25 publications

Serum Fibroblast Growth Factor-23 Is Associated with Incident Kidney Disease

Serum Fibroblast Growth Factor-23 Is Associated with Incident Kidney Disease

Paricalcitol Inhibits Renal Inflammation by Promoting Vitamin D Receptor–Mediated Sequestration of NF-κB Signaling

Vitamin D Actions on Cell Differentiation, Proliferation and Inflammation

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