Apelin-13 impedes foam cell formation by activating Class III PI3K/Beclin-1-mediated autophagic pathway
Authors: Hai-Peng Cheng
Chao-Ke Tang
Yun-Cheng Lv
Feng Yao
Min Zhang
Wei Xie
Yu-Lin Tan
Liang Li
Xiao-Yan Liu
Xi-Long Zheng
Duo Gong
Dan Liu
Journal: Biochemical and Biophysical Research Communications (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Apelin-13; Autophagy; Cholesterol efflux; Class III PI3K/Beclin-1; Macrophage foam cells.
Affiliations: Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang 421001, Hunan, China; Department of Laboratory Animal Science, University of South China, Hengyang 421001, Hunan, China., Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang 421001, Hunan, China., Department of Biochemistry and Molecular Biology, The Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, The University of Calgary, Health Sciences Center, 3330 Hospital Dr NW, Calgary T2N 4N1, Alberta, Canada., Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang 421001, Hunan, China. Electronic address: .

Abstract:  Apelin-13, an adipokine, promotes cholesterol efflux in macrophages with antiatherosclerotic effect. Autophagy, an evolutionarily ancient response to cellular stress, has been involved in atherosclerosis. Therefore, the purpose of this study was to investigate whether apelin-13 regulates macrophage foam cell cholesterol metabolism through autophagy, and also explore the underlying mechanisms. Here, we revealed that apelin-13 decreased lipid accumulation in THP-1 derived macrophages through markedly enhancing cholesterol efflux. Our study further demonstrated that apelin-13 induced autophagy via activation of Class III phosphoinositide 3-kinase (PI3K) and Beclin-1. Inhibition of Class III PI3K and Beclin-1 suppressed the stimulatory effects of apelin-13 on autophagy activity. The present study concluded that apelin-13 reduces lipid accumulation of foam cells by activating autophagy via Class III PI3K/Beclin-1 pathway. Therefore, our results provide brand new insight about apelin-13 inhibiting foam cell formation and highlight autophagy as a promising therapeutic target in atherosclerosis. 

Retracted: No

PubPeer comments:
 Figure 2. * Red arrows: The first two lanes in the b-actin panel representing the time series in Figure 2A look similar to the last two lanes in the b-actin panel representing the concentration series in Figure 2B. ![file] , 
 Corrigendum, October 2021, found here: https: www.sciencedirect.com science article pii S0006291X21011578  In the Fig. 2, the Fig 2B and 2D should be changed as following: [...] The authors would like to apologize for any inconvenience caused. I thank the authors and journal for correcting this duplication. ,