Rapamycin Improves Palmitate-Induced ER StressNFκB Pathways Associated with Stimulating Autophagy in Adipocytes
Joint Authors
Yin, Jiajing
Gu, Liping
Wang, Yufan
Fan, Nengguang
Ma, Yuhang
Peng, Yongde
Source
Issue
Vol. 2015, Issue 2015 (31 Dec. 2015), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2015-01-14
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Obesity-induced endoplasmic reticulum (ER) stress and inflammation lead to adipocytes dysfunction.
Autophagy helps to adapt to cellular stress and involves in regulating innate inflammatory response.
In present study, we examined the activity of rapamycin, a mTOR kinase inhibitor, against endoplasmic reticulum stress and inflammation in adipocytes.
An in vitro model was used in which 3T3-L1 adipocytes were preloaded with palmitate (PA) to generate artificial hypertrophy mature adipocytes.
Elevated autophagy flux and increased number of autophagosomes were observed in response to PA and rapamycin treatment.
Rapamycin attenuated PA-induced PERK and IRE1-associated UPR pathways, evidenced by decreased protein levels of eIF2α phosphorylation, ATF4, CHOP, and JNK phosphorylation.
Inhibiting autophagy with chloroquine (CQ) exacerbated these ER stress markers, indicating the role of autophagy in ameliorating ER stress.
In addition, cotreatment of CQ abolished the anti-ER stress effects of rapamycin, which confirms the effect of rapamycin on ERs is autophagy-dependent.
Furthermore, rapamycin decreased PA-induced nuclear translocation of NFκB P65 subunit, thereby NFκB-dependent inflammatory cytokines MCP-1 and IL-6 expression and secretion.
In conclusion, rapamycin attenuated PA-induced ER stress/NFκB pathways to counterbalance adipocytes stress and inflammation.
The beneficial of rapamycin in this context partly depends on autophagy.
Stimulating autophagy may become a way to attenuate adipocytes dysfunction.
American Psychological Association (APA)
Yin, Jiajing& Gu, Liping& Wang, Yufan& Fan, Nengguang& Ma, Yuhang& Peng, Yongde. 2015. Rapamycin Improves Palmitate-Induced ER StressNFκB Pathways Associated with Stimulating Autophagy in Adipocytes. Mediators of Inflammation،Vol. 2015, no. 2015, pp.1-12.
https://search.emarefa.net/detail/BIM-1072220
Modern Language Association (MLA)
Yin, Jiajing…[et al.]. Rapamycin Improves Palmitate-Induced ER StressNFκB Pathways Associated with Stimulating Autophagy in Adipocytes. Mediators of Inflammation No. 2015 (2015), pp.1-12.
https://search.emarefa.net/detail/BIM-1072220
American Medical Association (AMA)
Yin, Jiajing& Gu, Liping& Wang, Yufan& Fan, Nengguang& Ma, Yuhang& Peng, Yongde. Rapamycin Improves Palmitate-Induced ER StressNFκB Pathways Associated with Stimulating Autophagy in Adipocytes. Mediators of Inflammation. 2015. Vol. 2015, no. 2015, pp.1-12.
https://search.emarefa.net/detail/BIM-1072220
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1072220