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Quantitative Proteomics Reveals the Development of HBV-associated Glomerulonephritis Triggered by the Down-regulation of SLC7A7.

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. Researches on HBV-associated glomerulonephritis (HBV-GN) have been going on for decades. But the underlying molecular mechanism remains obscure. Here, we applied tandem mass tag (TMT) isobaric labelling-based method to quantitatively profile the kidney proteome of HBV transgenic mice to illustrate the pathological mechanisms of HBV-GN. Weighted correlation network analysis (WGCNA), 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 5,169 quantified proteins. Among them, the down-regulated solute carrier (SLC) family proteins are involved in the process of HBV-GN. We also found IL1B was up-regulated 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. Transporter, particularly solute carrier 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 dataset identifier PXD016450.