Abstract
This study aimed to investigate the regulatory function of lncRNA RMRP in non-alcoholic fatty liver disease (NAFLD). In vitro and in vivo NAFLD models were constructed. Hematoxylin & Eosin (H&E) and Oil-Red O staining assays were conducted to observe the morphology and lipid accumulation in liver tissues. Triglycine (TG) secretion was detected by ELISA assay. The expression levels of RMRP, microRNA-206, PTPN1 (protein tyrosine phosphatase, non-receptor type 1), and their downstream genes were assessed by qRT-PCR and Western blot. The regulatory relationship among these molecules was determined by luciferase reporter and RNA pull-down assays. RMRP and PTPN1 were up-regulated, while miR-206 was down-regulated in the liver tissues of NAFLD patients and rat model. RMRP inhibition improved the pathological state and liver function-related indexes of liver lipid deposition in the liver tissues of NAFLD rats. RMRP inhibition alleviated steatosis and TG secretion in free fatty acids (FFA)-treated AML-12 cells. RMRP could bind to miR-206 and downregulate its expression. Meanwhile, RMRP inhibition attenuated lipid accumulation by downregulating the PTPN1-PP2ASP1-SREBP1C pathway. Furthermore, RMRP inhibited the miR-206/PTPN1-SREBP1C signaling pathway in NAFLD rats and FFA-treated AML-12 cells. RMRP inhibition prevented NAFLD progression in rats via targeting the miR-206/PTPN1 axis.
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The datasets generated and/or analyzed during the current study are not publicly available due research design but are available from the corresponding author on reasonable request.
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MZ and JJY: study concepts, study design, literature research, experimental studies, manuscript preparation and editing; XFC and FZ: definition of intellectual content, literature research experimental studies, manuscript preparation and editing; all authors read and approved the final manuscript.
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Yin, J., Chen, X., Zhang, F. et al. RMRP inhibition prevents NAFLD progression in rats via regulating miR-206/PTPN1 axis. Mamm Genome 33, 480–489 (2022). https://doi.org/10.1007/s00335-022-09945-0
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DOI: https://doi.org/10.1007/s00335-022-09945-0