Journal
RENAL FAILURE
Volume 44, Issue 1, Pages 1216-1226Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/0886022X.2022.2079527
Keywords
IgA nephropathy; TNF-alpha; podocyte; apoptosis; death receptor pathway
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Funding
- Ningbo Health Commission Subject [2019Y49]
- Key Disciplines Group Construction Project of Pudong Health Bureau of Shanghai [PWZxq201707, PWZxq2017-07]
- Three Year Action Plan Project of Shanghai Accelerating Development of Traditional Chinese Medicine [ZY(2018-2020)-CCCX-2003-08, ZY(2018-2020)-FWTX-7005]
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TNF-alpha may play an important role in podocyte injury and apoptosis in IgA nephropathy through the apoptotic death receptor pathway.
Background: IgA nephropathy (IgAN) is the most common primary glomerular disease worldwide and it is characterized by mesangial IgA deposits. Proteinuria is a common clinical feature of IgAN, which has a critical connection to podocyte injury and has been used as a clinical prognostic factor for IgAN. Evidence has shown that TNF-alpha released from mesangial cells may lead to podocyte apoptosis. Methods: Forty male BALB/c mouse were randomly divided into the control group and IgAN group. A mice model of IgAN was developed by oral administration of bovine serum albumin (BSA) combined with Staphylococcus Enterotoxin B (SEB) tail vein injection. Urinary protein concentrations, renal function, renal morphological, IgA deposition, apoptosis situation, and the mRNA and protein expression of nephrin, podocin, TNF-alpha, TNFR1, caspase-8 and caspase-3, were detected after 12 weeks. Results: BSA and SEB can successfully establish an IgAN mouse model, and the main pathological changes are the IgA immune complex deposition in the mesangial area. The gene and protein expression levels of nephrin and podocin were found to be downregulated, and death receptor pathway-related indicators were upregulated, and they were involved in TNF-alpha-activated podocyte injury and apoptosis in IgAN mice. Conclusion: INF-alpha may play an important role in the pathogenesis of podocyte apoptosis in IgAN, and its effects may be mediated through the apoptotic death receptor pathway.
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