Quantitative Proteomics Reveals the Development of HBV-Associated Glomerulonephritis Triggered by the Downregulation of SLC7A7.
2020
As
a hepadnavirus, hepatitis B virus (HBV) can cause damage to
extrahepatic organs. The kidney is one of the organs that is more
susceptible to damage. Research studies on HBV-associated glomerulonephritis
(HBV-GN) have been going on for decades. However, the underlying molecular
mechanism remains obscure. Here, we applied a tandem mass tag (TMT)
isobaric labeling-based method to quantitatively profile the kidney
proteome of HBV transgenic mice to illustrate the pathological mechanisms
of HBV-GN. Weighted correlation network analysis, a clustering method
for gene expression, is used to cluster proteins. Totally, we identified
127 proteins that were highly associated with HBV expression out of
a total of 5169 quantified proteins. Among them, the downregulated
solute carrier (SLC) family proteins are involved in the process of
HBV-GN. We also found that IL1B was upregulated in the kidney tissue
of HBV transgenic mice. These findings suggest that HBV disrupts the
small molecule transport network of the kidney, which contributes
to the occurrence of HBV-GN. The transporter, particularly SLC family
7 member 7 (SLC7A7), is involved in this process, which might serve
as an intervention target for HBV-GN. All MS data have been deposited
to the ProteomeXchange Consortium via the iProX partner repository
with the data set identifier PXD016450.
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