MicroRNA‐188 regulates aging‐associated metabolic phenotype. Issue 1 (25th November 2019)

• Record Type: Journal Article
• Authors: Huang, Yan; Xiao, Ye; Liu, Ya; Guo, Min; Guo, Qi; Zhou, Fangliang; Liu, Ting; Su, Tian; Xiao, Yuzhong; Luo, Xiang‐Hang
• Is Part Of: Aging cell. Volume 19:Issue 1(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-11-25
• Subjects: aging‐associated metabolic phenotype -- brown adipose tissue -- energy expenditure -- inguinal white adipose tissue -- MicroRNA‐188 -- PRDM16; Cells -- Aging -- Periodicals; 571.8783605
• DOI: 10.1111/acel.13077
• Languages: English
• ISSNs: 1474-9718

Abstract

Abstract: With the increasing aging population, aging‐associated diseases are becoming epidemic worldwide, including aging‐associated metabolic dysfunction. However, the underlying mechanisms are poorly understood. In the present study, we aimed to investigate the role of microRNA miR‐188 in the aging‐associated metabolic phenotype. The results showed that the expression of miR‐188 increased gradually in brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT) of mice during aging. MiR‐188 knockout mice were resistant to the aging‐associated metabolic phenotype and had higher energy expenditure. Meanwhile, adipose tissue‐specific miR‐188 transgenic mice displayed the opposite phenotype. Mechanistically, we identified the thermogenic‐related gene Prdm16 (encoding PR domain containing 16) as the direct target of miR‐188. Notably, inhibition of miR‐188 expression in BAT and iWAT of aged mice by tail vein injection of antagomiR‐188 ameliorated aging‐associated metabolic dysfunction significantly. Taken together, our findings suggested that miR‐188 plays an important role in the regulation of the aging‐associated metabolic phenotype, and targeting miR‐188 could be an effective strategy to prevent aging‐associated metabolic dysfunction. Abstract : 1) MiR‐188 expression increased gradually in the BAT and iWAT of mice during aging. 2) MiR‐188 knockout mice were resistant to aging‐associated metabolic phenotype and had higher energy expenditure, whereas adipose tissue‐specific miR‐188 transgenic mice had the opposite effects. 3) Inhibiting miR‐188 expression in BAT and iWAT of aged mice by tail vein injection of antagomiR‐188 significantly ameliorated the aging‐associated metabolic phenotype, and targeting miR‐188 might be an effective way to prevent aging‐associated metabolic dysfunction.