Abstract
Background
Thyroid-stimulating hormone (TSH) plays an important role in the regulation of lipid metabolism. However, little is known about the role that exosomes play in the process of TSH-induced lipotoxicity in non-alcoholic fatty liver disease (NAFLD). As a preliminary step, the present study set out to investigate alterations in protein expression in exosomes derived from TSH-stimulated HepG2 cells.
Methods
HepG2 cells were treated with TSH, exosomes were collected, and proteins were identified by mass spectrometry (MS). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analysis were performed to analyze the identified proteins.
Results
TSH treatment significantly increased exosomal production and changed the exosomal proteomic profile in HepG2 cells. Among the 1728 proteins, 140 identified proteins were upregulated and seven proteins were downregulated. GO analysis and KEGG analysis revealed that these proteins were involved in multiple processes including metabolism, apoptosis, and inflammation.
Conclusion
Our preliminary study demonstrated that exosomes derived from TSH-stimulated hepatocytes were increased and showed a specific altered spectrum of proteins, many of which were involved in metabolism, signal transduction, apoptosis, and inflammation. This study offers new insights into the pathogenesis of TSH-induced lipotoxicity in NAFLD.
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Acknowledgements
This work was supported by the Natural Science Foundation of China (nos. 81230018, 81430020, 81500595, 81600604, 81900716), the Special Funds of Taishan Scholars Project of Shandong Province, Shandong Provincial Natural Science Foundation (ZR2019BH023), and the Medical and Health Technology Development Program in Shandong Province (2016WS0427).
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Ma, S., Shao, S., Yang, C. et al. A preliminary study: proteomic analysis of exosomes derived from thyroid-stimulating hormone-stimulated HepG2 cells. J Endocrinol Invest 43, 1229–1238 (2020). https://doi.org/10.1007/s40618-020-01210-y
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DOI: https://doi.org/10.1007/s40618-020-01210-y