2. Academic Validation
  3. ADAR1 inhibits adipogenesis and obesity by interacting with Dicer to promote the maturation of miR-155-5P

ADAR1 inhibits adipogenesis and obesity by interacting with Dicer to promote the maturation of miR-155-5P

  • J Cell Sci. 2022 Mar 1;135(5):jcs259333. doi: 10.1242/jcs.259333.
Zuying Yu 1 2,  Ruijie Luo 1 2,  Yutian Li 3,  Xiaoguang Li 2,  Zhengrui Yang 4,  Jiangtong Peng 1 4,  Kai Huang 1 2
Affiliations

Affiliations

  • 1 Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
  • 2 Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
  • 3 Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH 45221, USA.
  • 4 Department of Cardiology, The Second People's Hospital of Lincang City, Lincang 677099, China.
PMID: 35067718 DOI: 10.1242/jcs.259333
Abstract

Adipogenesis is closely related to various metabolic diseases, such as obesity, type 2 diabetes, cardiovascular diseases and Cancer. This cellular process is highly dependent on the expression and sequential activation of a diverse group of transcription factors. Here, we report that ADAR1 (also known as ADAR) could inhibit adipogenesis through binding with Dicer (also known as DICER1), resulting in enhanced production of miR-155-5p, which downregulates the adipogenic early transcription factor C/EBPβ. Consequently, the expression levels of late-stage adipogenic transcription factors (C/EBPα and PPARγ) are reduced and adipogenesis is inhibited. More importantly, in vivo studies reveal that overexpression of ADAR1 suppresses white adipose tissue expansion in high fat diet-induced obese mice, leading to improved metabolic phenotypes, such as Insulin sensitivity and glucose tolerance.

Keywords

ADAR1; Adipogenic differentiation; Obesity; miR-155-5P.

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