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DOI

10.1016/j.jds.2024.10.029

First Page

989

Last Page

994

Abstract

Abstract Background/purpose Periodontitis has been documented to increase the risk of diabetic nephropathy. However, the specific mechanisms through which periodontitis affects renal function remain unclear. This study aimed to investigate the mechanism by which an inflammatory reaction stimulated by periodontal pathogens affects mesangial cell fibrosis under hyperglycemic conditions in vitro. Materials and methods Murine mesangial cells were stimulated with 1,000 ng/mL of Porphyromonas gingivalis -derived lipopolysaccharide ( Pg LPS) in a control or high glucose (HG) medium. Activation of the extracellular signal-regulated kinase (ERK1/2) and expression of alpha-smooth muscle actin (α-SMA) and collagen type 1a2 ( Col1a2 ) were analyzed for fibrosis and transformation via the transforming growth factor (TGF)-β1/Smad signaling pathway. Results Pg LPS stimulation significantly upregulated TGF-β1 expression and Smad3 phosphorylation in the HG group compared to the control group. Additionally, activation of ERK1/2 and expression of Col1a2 and α-SMA were significantly elevated in the HG group compared to the control following Pg LPS stimulation. The TGF-β1 inhibitor significantly suppressed Smad3 phosphorylation and mRNA expression of Col1a2 in the HG group. Conclusion Under HG conditions, Pg LPS may aggravate fibrosis in mesangial cells via the TGF-β1/Smad signaling pathway, leading to nephrosclerotic modifications. The presented study may support the association between periodontitis and chronic kidney disease, mediated by hyperglycemia.

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