Authors
Marcella E O’Reilly, Sebastian Ho, Johana Coronel, Lucie Zhu, Wen Liu, Chenyi Xue, Eunyoung Kim, Esther Cynn, Caio V Matias, Rajesh Kumar Soni, Chen Wang, Iuliana Ionita-Laza, Robert C Bauer, Leila Ross, Yiying Zhang, Silvia Corvera, Susan K Fried, Muredach P Reilly
Publication date
2024/5/28
Journal
Cell Reports
Volume
43
Issue
5
Publisher
Elsevier
Description
Adipose tissue remodeling and dysfunction, characterized by elevated inflammation and insulin resistance, play a central role in obesity-related development of type 2 diabetes (T2D) and cardiovascular diseases. Long intergenic non-coding RNAs (lincRNAs) are important regulators of cellular functions. Here, we describe the functions of linc-ADAIN (adipose anti-inflammatory), an adipose lincRNA that is downregulated in white adipose tissue of obese humans. We demonstrate that linc-ADAIN knockdown (KD) increases KLF5 and interleukin-8 (IL-8) mRNA stability and translation by interacting with IGF2BP2. Upregulation of KLF5 and IL-8, via linc-ADAIN KD, leads to an enhanced adipogenic program and adipose tissue inflammation, mirroring the obese state, in vitro and in vivo. KD of linc-ADAIN in human adipose stromal cell (ASC) hTERT adipocytes implanted into mice increases adipocyte size and …
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