1α,25-Dihydroxyvitamin D3 Increases TGF β1 Binding to Human Osteoblasts

Nagel, David; Kumar, Rajiv

doi:10.1006/bbrc.2002.6387

Cited by 11 publications

(10 citation statements)

References 43 publications

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“…Nagel et al . have reported that an increase in TGF‐β receptor expression is important in mediating 1,25(OH) 2 D 3 ‐associated changes in the growth rate of osteoblasts 30 . Subramaniam et al 31 and Yanagisawa et al 29 have indicated that Smad3 may mediate cross‐talk between vitamin D and TGF‐β signalling pathways.…”

Section: Discussionmentioning

confidence: 99%

“…28 Nagel et al have reported that an increase in TGF- receptor expression is important in mediating 1,25(OH) 2 D 3 -associated changes in the growth rate of osteoblasts. 30 Subramaniam et al 31 and Yanagisawa et al 29 have indicated that Smad3 may mediate cross-talk between vitamin D and TGF- signalling pathways. Despite some discrepancies, all these studies indicate that modulation of TGF-1/BMP-7 signalling by 1,25(OH) 2 D 3 may be through an interaction between VDR and Smads.…”

Section: Discussionmentioning

confidence: 99%

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PODOCYTE INJURY IS SUPPRESSED BY 1,25‐DIHYDROXYVITAMIN D₃ VIA MODULATION OF TRANSFORMING GROWTH FACTOR‐β1/BONE MORPHOGENETIC PROTEIN‐7 SIGNALLING IN PUROMYCIN AMINONUCLEOSIDE NEPHROPATHY RATS

Xiao

Shi

Liu

et al. 2009

Clin Exp Pharma Physio

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1. Accumulating evidence suggests that vitamin D and its analogues are renoprotective. However, the precise mechanisms and the molecular targets by which active vitamin D exerts its beneficial effects remain obscure. The objective of the present study was to evaluate the effect of active vitamin D on rats with puromycin aminonucleoside (PAN) nephropathy, a model that is characterized by predominant podocyte injury. 2. The PAN nephropathy rats were created by a single intravenous injection of 100 mg/kg PAN. Changes in renal pathology and podocyte numbers were observed. Real-time polymerase chain reaction (PCR) was performed to examine mRNA expression of nephrin, transforming growth factor (TGF)-beta1 and bone morphogenetic protein (BMP)-7. Protein expression of nephrin, TGF-beta1, BMP-7 and p-Smad2/3 and p-Smad1/5/8 was examined by immunofluorescence, immunohistochemistry and western blotting, respectively. Rats were treated with 1,25(OH)(2)D(3) by gastric gavage at a dose of 2.5 microg/kg per day, starting 2 days before PAN injection and continuing throughout the experiment. 3. A single injection of PAN induced massive proteinuria and elevated serum creatinine on Day 7, both of which were significantly suppressed by 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)). Immunofluorescence and real-time PCR of the podocyte-associated protein nephrin revealed reduced and discontinuous staining and this change was reversed by 1,25(OH)(2)D(3). In PAN nephropathy rats, TGF-beta1 and p-Smad2/3 expression was upregulated, whereas that of BMP-7 and p-Smad1/5/8 was downregulated. Treatment with 1,25(OH)(2)D(3) significantly restored BMP-7/Smad signalling while suppressing TGF-beta1/Smad signalling. 4. In conclusion, 1,25(OH)(2)D(3) can ameliorate podocyte damage and proteinuria induced by PAN. The beneficial effects of 1,25(OH)(2)D(3) on podocytes may be attributable, in part, to direct modulation of TGF-beta1/BMP-7 signalling.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

PODOCYTE INJURY IS SUPPRESSED BY 1,25‐DIHYDROXYVITAMIN D₃ VIA MODULATION OF TRANSFORMING GROWTH FACTOR‐β1/BONE MORPHOGENETIC PROTEIN‐7 SIGNALLING IN PUROMYCIN AMINONUCLEOSIDE NEPHROPATHY RATS

Xiao

Shi

Liu

et al. 2009

Clin Exp Pharma Physio

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“…Osteocytes were immortalized using an SV40 T antigen viral construct as described earlier [30]. Clonal populations of osteocytes from Sost KO and WT mice were generated via dilution cloning.…”

Section: Methodsmentioning

confidence: 99%

Enhanced prostacyclin formation and Wnt signaling in sclerostin deficient osteocytes and bone

Ryan

Craig

Salisbury

et al. 2014

Biochemical and Biophysical Research Communications

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We show that prostacyclin production is increased in bone and osteocytes from sclerostin (Sost) knockout mice which have greatly increased bone mass. The addition of prostacyclin or a prostacyclin analog to bone forming osteoblasts enhances differentiation and matrix mineralization of osteoblasts. The increase in prostacyclin synthesis is linked to increases in β-catenin concentrations and activity as shown by enhanced binding of lymphoid enhancer factor, Lef1, to promoter elements within the prostacyclin synthase promoter. Blockade of Wnt signaling reduces prostacyclin production in osteocytes. Increased prostacyclin production by osteocytes from sclerostin deficient mice could potentially contribute to the increased bone formation seen in this condition.

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“…VitD 3 can also modulate TGF-␤ production and TGF-␤ receptor expression. In several cell types (osteoblasts, breast cancer cells, prostatic epithelial cells, and human promyelocytic leukemia HL-60 cells), VitD 3 inhibits cellular growth by increasing secretion of TGF-␤ and up-regulating expression of TGF-␤ receptors, type I and II (T␤RI and T␤RII) (21)(22)(23). However, other investigators have reported an absence of increased expression of the T␤RI and T␤RII caused by VitD 3 in particular cell types, such as human myelomonocytic U937 leukemia cells (24).…”

Section: Endritic Cells (Dcs)mentioning

confidence: 99%

“…The complexity of interactions between the TGF-␤ signaling system and VitD 3 is further highlighted by the observation that Smad proteins, downstream mediators of TGF-␤ signaling, can act both as positive and negative modulators of vitamin D receptor (VDR). Moreover, the cooperative actions of VitD 3 and TGF-␤ can be synergistic or antagonistic in a cell-specific manner (23,25,26), or in other contexts, they can act independently (16).…”

Section: Endritic Cells (Dcs)mentioning

confidence: 99%

TGF-β and Vitamin D3 Utilize Distinct Pathways to Suppress IL-12 Production and Modulate Rapid Differentiation of Human Monocytes into CD83+ Dendritic Cells

Lyakh

Sanford

Chekol

et al. 2005

The Journal of Immunology

101

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We previously demonstrated that agents known to signal infection or inflammation can rapidly and directly drive differentiation of human CD14+ monocytes into CD83+ dendritic cells (DCs) when introduced to cells under serum-free conditions. In this study, we evaluated the effects of TGF-β and vitamin D3 (VitD3) on the proportion and function of monocytes that adopt DC characteristics. TGF-β significantly decreased the proportion of cells that rapidly adopted stable DC characteristics in response to LPS, but had little or no effect on calcium ionophore-induced differentiation. In contrast, VitD3 showed no such pathway specificity and dramatically suppressed differentiation of monocytes into DCs in response to these agents. Both TGF-β and VitD3 altered cytokine and chemokine production in LPS-treated monocytes, inhibited IL-12 and IL-10 secretion, and decreased the functional capacity of DCs. Despite the similar effects of TGF-β and VitD3, there are significant differences in the signaling pathways used by these agents, as evidenced by their distinct effects on LPS- and calcium ionophore-induced DC differentiation, on LPS-induced secretion of IL-10, and on two members of the NF-κB family of transcription factors, RelB and cRel. These studies identify TGF-β and VitD3 as potent regulatory factors that use distinct pathways to suppress both the differentiation of DCs as well as their capacity to secrete the Th1-polarizing cytokine IL-12. Because these agents are present in serum and negatively affect DC differentiation at physiological concentrations, our findings are likely to have significance regarding the in vivo role of TGF-β and VitD3 in determining the type of immune responses.

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1α,25-Dihydroxyvitamin D3 Increases TGF β1 Binding to Human Osteoblasts

Cited by 11 publications

References 43 publications

PODOCYTE INJURY IS SUPPRESSED BY 1,25‐DIHYDROXYVITAMIN D₃ VIA MODULATION OF TRANSFORMING GROWTH FACTOR‐β1/BONE MORPHOGENETIC PROTEIN‐7 SIGNALLING IN PUROMYCIN AMINONUCLEOSIDE NEPHROPATHY RATS

PODOCYTE INJURY IS SUPPRESSED BY 1,25‐DIHYDROXYVITAMIN D₃ VIA MODULATION OF TRANSFORMING GROWTH FACTOR‐β1/BONE MORPHOGENETIC PROTEIN‐7 SIGNALLING IN PUROMYCIN AMINONUCLEOSIDE NEPHROPATHY RATS

Enhanced prostacyclin formation and Wnt signaling in sclerostin deficient osteocytes and bone

TGF-β and Vitamin D3 Utilize Distinct Pathways to Suppress IL-12 Production and Modulate Rapid Differentiation of Human Monocytes into CD83+ Dendritic Cells

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1α,25-Dihydroxyvitamin D3 Increases TGF β1 Binding to Human Osteoblasts

Cited by 11 publications

References 43 publications

PODOCYTE INJURY IS SUPPRESSED BY 1,25‐DIHYDROXYVITAMIN D3 VIA MODULATION OF TRANSFORMING GROWTH FACTOR‐β1/BONE MORPHOGENETIC PROTEIN‐7 SIGNALLING IN PUROMYCIN AMINONUCLEOSIDE NEPHROPATHY RATS

PODOCYTE INJURY IS SUPPRESSED BY 1,25‐DIHYDROXYVITAMIN D3 VIA MODULATION OF TRANSFORMING GROWTH FACTOR‐β1/BONE MORPHOGENETIC PROTEIN‐7 SIGNALLING IN PUROMYCIN AMINONUCLEOSIDE NEPHROPATHY RATS

Enhanced prostacyclin formation and Wnt signaling in sclerostin deficient osteocytes and bone

TGF-β and Vitamin D3 Utilize Distinct Pathways to Suppress IL-12 Production and Modulate Rapid Differentiation of Human Monocytes into CD83+ Dendritic Cells

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Product

Resources

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PODOCYTE INJURY IS SUPPRESSED BY 1,25‐DIHYDROXYVITAMIN D₃ VIA MODULATION OF TRANSFORMING GROWTH FACTOR‐β1/BONE MORPHOGENETIC PROTEIN‐7 SIGNALLING IN PUROMYCIN AMINONUCLEOSIDE NEPHROPATHY RATS

PODOCYTE INJURY IS SUPPRESSED BY 1,25‐DIHYDROXYVITAMIN D₃ VIA MODULATION OF TRANSFORMING GROWTH FACTOR‐β1/BONE MORPHOGENETIC PROTEIN‐7 SIGNALLING IN PUROMYCIN AMINONUCLEOSIDE NEPHROPATHY RATS