miR-1934, downregulated in obesity, protects against low-grade inflammation in adipocytes

Abstract

It has been previously demonstrated that miR-1934 was specially regulated by adiponectin, an anti-inflammatory adipokine, in adipose tissue (AT) in vivo. Herein we investigated the role of miR1934 in the regulation of inflammatory response. Compared with chow-diet fed mice, miR1934 expression was down-regulated in epididymal AT of high-fat diet-induced obese mice. miR1934 expression was down-regulated as well in omental AT of obese subjects in comparison with lean subjects. The circulating miR-1934 was also lower in obese subjects and its levels were correlated negatively with body mass index (BMI), waist circumference (WC), low-density lipoprotein cholesterol (LDL-c), insulin resistance and high-sensitivity C-reactive protein (hs-CRP). The down-regulation of miR1934 in obesity was mimicked by TNF-α treatment of 3T3-L1 adipocytes. Moreover, overexpression of miR1934 suppressed the TNF-α-induced gene expression of interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) in 3T3-L1 adipocytes. De novo formed AT in nude mice transplanted with 3T3-L1 preadipocytes overexpressing miR1934 displayed a reduction in IL-6, TNF-α, IL-1β and an enhancement in IL-10 gene expression when compared with transplant with 3T3-L1 preadipocytes overexpressing miR1934 scrambled control sequence. These results suggest that miR1934 is an important anti-inflammatory factor and may represent a novel mechanism for controlling AT inflammation.

MicroRNA expression profiling of porcine mammary epithelial cells after challenge with Escherichia coli in vitro

“…Interaction of signaling molecules that are involved in these pathways seems to be important to balance pro- and anti-inflammatory processes and to ensure immune homeostasis as well as host protection [ 55 ]. This is confirmed by our results, as some miRNAs that were DE in PMECs after pathogen challenge play crucial roles in innate and adaptive immune responses (miR-101, miR-125-star, miR-423-5p, miR-10a, miR-23a-star, miR-1934-star, miR-29a, miR-29b, miR-24-star, let-7 g-star, miR-320, miR-17-3p, miR-324-5p, and miR-8-star) [ 20 , 25 , 27 , 31 , 42 , 46 , 56 – 64 ] as well as negative feedback regulation of inflammation (miR-210 and miR-17-3p) [ 22 , 62 ].…”

Utilization of adipocyte-derived lipids and enhanced intracellular trafficking of fatty acids contribute to breast cancer progression

“…Murine 3 T3-L1 preadipocytes (generously provided by the Laboratory of Glucose and Lipid Metabolism, The First Affiliated Hospital of Chongqing Medical University, Chongqing) were cultivated and induced to differentiation as described by Liu et al [ 17 ]. Immortalized normal breast epithelium MCF-10A cells (provided by the Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Kunming) were cultured in Dulbecco’s modified Eagle’s medium (DMEM)/F12 medium (Gibco, Carlsbad, CA) supplemented with 5% horse serum (Gibco), 10 μg/ml insulin (Sigma–Aldrich, St. Louis, MO), 20 ng/ml EGF (Invitrogen, Carlsbad, CA), 100 ng/ml cholera toxin (Sigma–Aldrich) and 0.5 μg/ml hydrocortisone (Sigma–Aldrich).…”

Epigenetic signatures underlying inflammation: an interplay of nutrition, physical activity, metabolic diseases, and environmental factors for personalized nutrition

“…miR-126 and miR-193b were further identified as important regulators of adipose inflammation in human obesity through effects on CCL2 production [102]. In contrast, the anti-inflammatory miR-1934, miR532-5p, and miR-146a were down-regulated in obesity, which promoted inflammation in adipose tissues [103][104][105]. Moreover, down-regulation of miR-706 played a role in increasing adipose tissue inflammation in the offspring during maternal obesity in mice [106].…”