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- W2146314322 abstract "Wnt/β-catenin signaling mediates renal fibrosis in several model systems including diabetic nephropathy. Dickkopf-1 (DKK-1) is an endogenous inhibitor of Wnt/β-catenin signaling, but whether DKK-1 modulates diabetic nephropathy is unknown. Here, we studied whether DKK-1 participates in high glucose (HG)-induced expression of profibrotic factors and renal damage. In vitro, HG increased expression of DKK1, receptor Kremen-2, TGF-β1, and fibronectin in mesangial cells. Loss and gain of DKK1 function modulated HG-mediated c-Jun, TGF-β1, and fibronectin expression. DKK1 mediated HG-induced phosphorylation of Ser45-β-catenin and reduction of nuclear β-catenin levels, but not phosphorylation of ERK kinase. Wnt3a protein and the β-catenin (Δ45) mutation increased nuclear β-catenin but abrogated HG-induced DKK1 and fibronectin expression. Exogenous DKK1 antisense oligonucleotide attenuated the increase in both serum DKK1 and urinary protein excretion in streptozotocin-induced diabetic rats. Knocking down DKK1 inhibited mesangial expression of TGF-β1 and fibronectin and reduced both the glomerular volume and deposition of mesangial matrix in diabetic kidneys. Taken together, DKK1 mediates HG-induced destabilization of β-catenin and matrix accumulation in mesangial cells. Knocking down DKK1 prevents diabetes-induced renal dysfunction and microstructure deterioration, suggesting that inhibition of DKK1offers therapeutic potential for diabetic nephropathy." @default.
- W2146314322 created "2016-06-24" @default.
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- W2146314322 date "2010-01-01" @default.
- W2146314322 modified "2023-10-16" @default.
- W2146314322 title "Dickkopf-1 Promotes Hyperglycemia–Induced Accumulation of Mesangial Matrix and Renal Dysfunction" @default.
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- W2146314322 doi "https://doi.org/10.1681/asn.2008101059" @default.
- W2146314322 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2799277" @default.
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