Journal
IMMUNOLOGY LETTERS
Volume 222, Issue -, Pages 40-48Publisher
ELSEVIER
DOI: 10.1016/j.imlet.2020.03.003
Keywords
MiR-149; NAFLD; Endoplasmic reticulum stress; ATF6; ATF6 signaling pathway; Inflammation; Apoptosis
Categories
Funding
- Hunan Provincial People's Hospital RenShu Foundation [RS201805]
Ask authors/readers for more resources
This study aimed to research the effect of miR-149 on endoplasmic reticulum stress (ERS)-induced inflammation and apoptosis in non-alcoholic fatty liver disease (NAFLD). The mouse model with NAFLD was established by feeding with a high-fat diet, and the model establishment was subsequently confirmed by H&E staining and oil red O staining. MiR-149 agomir was injected into NAFLD mice to observe changes in liver tissues. After cell transfection, qRT-PCR and Western blot were performed to measure the expressions of lipid metabolism-related proteins (SCD-1, PPAR alpha, and ABCA1), miR-149 and ATF6. Luciferase reporter gene assay was applied to verify the relationship between miR-149 and ATF6. Inflammatory factors (TNF-alpha, IL-1 beta, IL-6 and NF-kappa B) and apoptotic-related factors (caspase-12 and CHOP) were measured by ELISA and flow cytometry. qRT-PCR and Western blot were applied to detect expressions of ATF6 signaling pathway-related proteins (GRP94 and Akt). NAFLD progression was attenuated in mice injected with miR-149 agomir. The expression of miR-149 was reduced in liver tissues of NAFLD mice, while the expression of ATF6 was increased. Transfection of miR-149 can result in a decrease of ATF6 expression. ATF6 was a target gene of miR-149. MiR-149 could down-regulate the expressions of inflammatory factors and apoptotic-related factors. MiR-149 could down-regulate expressions of ATF6 signaling pathway-related proteins. MiR-149 alleviates ERS-induced inflammation and apoptosis by down-regulating the ATF6 signaling pathway, thus inhibiting the progression of NAFLD.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available