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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
MiR-183-5p modulates inflammatory response and apoptosis in diabetic nephropathy by targeting the TTP
1Department of Geriatric Medicine, Nantong First People's Hospital Nantong 226000, Jiangsu, China.
Objective:
To clarify the involvement of miR-183-5p, tristetraprolin (TTP), and inflammatory cytokines in Diabetic nephropathy (DN).
Methods:
This retrospective study included 10 patients with DN, 10 patients with type 2 diabetes (T2DM) and 10 controls. Expression levels of miR-183-5p and TTP in T2DM patients and DN patients were detected, and the correlation between miR-183-5p, TTP, and inflammatory cytokines were analyzed. Renal tubular epithelial cells (HK-2) served as the cell model. The expression of TTP and cytokines in the cell cultures was detected using qRT-PCR or ELISA.
Results:
miR-183-5p promoted inflammation and apoptosis in the context of hyperglycemia. TTP was identified as the direct target of miR-183-5p. Elevated miR-183-5p expression in HK-2 cells resulted in increased inflammatory cytokine release and enhanced apoptosis. miR-183-5p inhibitors significantly reduced the levels of inflammatory cytokines in HK-2 cells.
Conclusions:
MiR-183-5p accelerates DN development through its action on TTP, thereby presenting a new therapeutic avenue for DN.
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