Acyl-CoA thioesterase 13 () attenuates the progression of autosomal dominant polycystic kidney disease via triggering mitochondrial-related cell apoptosis.

Purpose: Autosomal dominant polycystic kidney disease (ADPKD) is the most common cause of end-stage kidney disease. It has been shown that Acyl-CoA thioesterase 13 () level was reduced in renal cystic tissues from ADPKD patients. However, the role of in ADPKD remains largely elusive.

Methods: The data in the GSE7869 dataset were acquired from the GEO database to determine level between normal renal cortical tissues and renal cystic tissues. Next, the potential functions of were explored by gene set enrichment analysis (GSEA). Furthermore, level in ADPKD cells (WT9-12) was verified by RT-qPCR. The effects of on WT9-12 cell growth were evaluated using the EdU staining and flow cytometry assays.

Results: Compared to normal group, mRNA level was obviously reduced in renal cystic tissues and WT9-12 cells. Meanwhile, GSEA results showed that compared to the low expression group, PI3K-Akt and MAPK signaling pathways were inactivated, and PPAR signaling pathway and fatty acid metabolism were activated in high expression group. Furthermore, overexpression of notably reduced WT9-12 cell proliferation and triggered cell cycle arrest. Moreover, overexpression remarkably triggered apoptosis, increased cleaved caspase 3 protein level, reduced ATP production and induced loss of mitochondrial membrane potential in WT9-12 cells, suggesting that overexpression could trigger mitochondrial-related apoptosis in WT9-12 cells.

Conclusions: Collectively, our results showed that overexpression of could suppress WT9-12 cell proliferation and trigger mitochondrial-mediated cell apoptosis, suggesting that may exert a protective role in ADPKD.