LncRNA HEM2ATM improves obesity-associated adipose tissues meta-inflammation and insulin resistance by interacting with heterogeneous nuclear ribonucleoprotein U.
Clin Immunol
; 247: 109234, 2023 02.
Article
em En
| MEDLINE
| ID: mdl-36649749
ABSTRACT
Obesity is a complicated metabolic disease characterized by meta-inflammation in adipose tissues. In this study, we explored the roles of a new long non-coding RNA (lncRNA), HEM2ATM, which is highly expressed in adipose tissue M2 macrophages, in modulating obesity-associated meta-inflammation and insulin resistance. HEM2ATM expression decreased significantly in adipose tissue macrophages (ATMs) obtained from epididymal adipose tissues of high-fat diet (HFD)-induced obese mice. Overexpression of macrophage HEM2ATM improved meta-inflammation and insulin resistance in the adipose tissues of HFD-fed mice. Functionally, HEM2ATM negatively regulated the production of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in macrophages. Mechanistically, HEM2ATM bound to heterogeneous nuclear ribonucleoprotein U (hnRNP U), suppressed hnRNP U translocation from the nucleus to the cytoplasm, hindered the function of cytoplasmic hnRNP U on TNF-α and IL-6 mRNA stabilization, and decreased the secretion of TNF-α and IL-6. Collectively, HEM2ATM is a novel suppressor of obesity-associated meta-inflammation and insulin resistance.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Resistência à Insulina
/
RNA Longo não Codificante
Tipo de estudo:
Risk_factors_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article