Abstract
Objective
To suppress TNF-α-induced lipogenesis in sebocytes (associated with acne development) with microRNA-338-3p (miR-338-3p) and to explore the underlying mechanisms.
Results
TNF-α increased lipid droplet formation in sebocytes which were used as in vitro model of inflammation-induced acne. Flow cytometry and TLC assays validated that miR-338-3p could suppress TNF-α-induced lipid droplet formation, down-regulate the expression of PREX2a, and inactivate AKT signaling in sebocytes. In addition, suppression of AKT activity by the PI3 K and AKT inhibitors diminished TNF-α-induced lipogenesis. PREX2a siRNA mimics the effects of miR-338-3p on AKT phosphorylation and lipogenesis. PREX2a overexpression consistently restored lipogenesis and AKT phosphorylation attenuated by miR-338-3p.
Conclusions
MiR-338-3p suppresses the TNF-α-induced lipogenesis in sebocytes by targeting PREX2a and down-regulating PI3K/AKT signaling.
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Funding
This study was funded by Heilongjiang province scientific research institution innovation Grants (YC2016D002).
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The authors declare that they have no conflict of interest.
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Liu, J., Cao, L., Feng, Y. et al. MiR-338-3p inhibits TNF-α-induced lipogenesis in human sebocytes. Biotechnol Lett 39, 1343–1349 (2017). https://doi.org/10.1007/s10529-017-2369-3
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DOI: https://doi.org/10.1007/s10529-017-2369-3