Abstract
A previous study has demonstrated that adiponectin (APN) could promote preadipocyte differentiation, and the present study further explored its mechanism. 3T3-L1 cells were infected with adenovirus holding human adiponectin gene apM1 and mouse neuronatin (Nnat) shRNA and initiated differentiation while coculturing with mature adipocytes stimulated with LPS. After 8 days, preadipocyte differentiation was observed by Oil Red O staining. Real-time quantitative PCR was used to evaluate mRNA expression levels of monocyte chemoattractant protein-1 (MCP-1), interleukin- (IL-) 6, IL-8, and tumor necrosis factor α (TNF-α). The levels of reactive oxygen species (ROS), total antioxidant capacity (T-AOC), malondialdehyde (MDA), and superoxide dismutase (SOD) in 3T3-L1 cells were detected. Western blotting was done to quantify the protein expression levels of Nnat, peroxisome proliferator-activated receptor (PPAR) γ, p65, and inhibitor of nuclear factor κB (IκB) α. Results demonstrated that APN overexpression markedly increased preadipocyte differentiation; inhibited gene expression of MCP-1, IL-6, IL-8, and TNF-α; reduced ROS and MDA release; increased T-AOC and SOD levels; upregulated Nnat, PPAR γ, and IκB α protein expressions; and downregulated p65 protein expression under LPS stimulation. However, the effects of APN were markedly attenuated when Nnat expression was knocked down. Taken together, the present study provided evidences that the effects of APN on promoting preadipocyte differentiation under inflammatory conditions via anti-inflammation and antioxidative stress may be regulated by the PPAR γ/Nnat/NF-κB signaling pathway.
Highlights
Epicardial adipose tissue (EAT) is an adipose tissue located between the myocardium and the pericardium, surrounding and contacting directly the blood vessels of the heart
The paracrine and vascular effects resulting from the close contacting between the EAT and coronary artery make a great contribution to the occurrence and development of atherosclerosis [1, 2]
Disorder of cytokines secreted by EAT would induce inflammation and especially atherosclerosis [7], and APN has a protective effect on atherosclerosis [8, 9]
Summary
Epicardial adipose tissue (EAT) is an adipose tissue located between the myocardium and the pericardium, surrounding and contacting directly the blood vessels of the heart. The paracrine and vascular effects resulting from the close contacting between the EAT and coronary artery make a great contribution to the occurrence and development of atherosclerosis [1, 2]. Imaging studies have treated EAT as a quantifiable risk marker of cerebrovascular diseases (CVDs) [3, 4]. Adipose tissue is a nonnegligible endocrine organ, which secretes various sorts of cytokines, called “adipocytokines,” such as tumor necrosis factor- (TNF-) α, interleukin-6 (IL6), and adiponectin (APN) [5]. Studies showed that EAT could express inflammatory cytokines and chemokines as other adipose tissues [6]. Disorder of cytokines secreted by EAT would induce inflammation and especially atherosclerosis [7], and APN has a protective effect on atherosclerosis [8, 9]. The regulation mechanism of APN on atherosclerosis still needs to be further discussed
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