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Caca, J.* ; Bartelt, A. ; Egea, V.*

Hypoxia regulates brown adipocyte differentiation and stimulates miR-210 by HIF-1α.

Int. J. Mol. Sci. 26:117 (2025)
Verlagsversion DOI PMC
Free journal
Creative Commons Lizenzvertrag
MicroRNAs (miRNAs) are short sequences of single-stranded non-coding RNAs that target messenger RNAs, leading to their repression or decay. Interestingly, miRNAs play a role in the cellular response to low oxygen levels, known as hypoxia, which is associated with reactive oxygen species and oxidative stress. However, the physiological implications of hypoxia-induced miRNAs ("hypoxamiRs") remain largely unclear. Here, we investigate the role of miR-210 in brown adipocyte differentiation and thermogenesis. We treated the cells under sympathetic stimulation with hypoxia, CoCl2, or IOX2. To manipulate miR-210, we performed reverse transfection with antagomiRs. Adipocyte markers expression, lipid accumulation, lipolysis, and oxygen consumption were measured. Hypoxia hindered BAT differentiation and suppressed sympathetic stimulation. Hypoxia-induced HIF-1α stabilization increased miR-210 in brown adipocytes. Interestingly, miR-210-5p enhanced differentiation under normoxic conditions but was insufficient to rescue the inhibition of brown adipocyte differentiation under hypoxic conditions. Although adrenergic stimulation activated HIF-1α signaling and upregulated miR-210 expression, inhibition of miR-210-5p did not significantly influence UCP1 expression or oxygen consumption. In summary, hypoxia and adrenergic stimulation upregulated miR-210, which impacted brown adipocyte differentiation and thermogenesis. These findings offer new insights for the physiological role of hypoxamiRs in brown adipose tissue, which could aid in understanding oxidative stress and treatment of metabolic disorders.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Brown Adipocytes ; Hypoxamirs ; Hypoxia ; Mir-210 ; Mirnas ; Thermogenesis; Adipose-tissue; Microrna; Fat
ISSN (print) / ISBN 1422-0067
e-ISSN 1661-6596
Quellenangaben Band: 26, Heft: 1, Seiten: , Artikelnummer: 117 Supplement: ,
Verlag MDPI
Verlagsort Basel
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Förderungen Forderprogramm fur Forschung und Lehre (FoFoLe) scholarship of the LMU Faculty of Medicine
Deutsche Forschungsgemeinschaft S
Deutsches Zentrum fur Herz-Kreislauf-Forschung Junior Research Group Grant
European Research Council Starting Grant PROTEOFIT
Deutsche Forschungsgemeinschaft