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

08:00 EDT 10th March 2020 | BioPortfolio

Summary of "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.


Journal Details

This article was published in the following journal.

Name: Journal of proteome research
ISSN: 1535-3907


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