HuR-dependent expression of RyR2 contributes to calcium-mediated thermogenesis in murine brown adipocytes.
Guarnieri AR., Anthony SR., Wen BY., Seramur ME., Acharya P., Kasprovic DA.
Animal Study, published in Sci Rep (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Sci Rep (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42236825
- DOI
- 10.1038/s41598-026-54659-x
Abstract (original English)
Several thermogenic pathways have been described in adipose tissue, including calcium-mediated thermogenesis in beige adipocytes. We have previously shown that adipocyte-specific deletion of the RNA binding protein human antigen R (HuR; Elavl1) results in thermogenic dysfunction. RNA sequencing revealed the downregulation of several calcium transport genes upon HuR deletion. The goal of this work was to define the HuR-dependent mechanisms of calcium driven thermogenesis in brown adipocytes. Brown adipose tissue (BAT)-specific HuR-deletion (BAT-HuR -/- ) mice have no changes in their body weight, glucose tolerance, adipose tissue weights, or lipid droplet size compared to control, but are cold intolerant following acute thermal challenge at 4 °C. We also found decreased expression of ryanodine receptor 2 (Ryr2) in BAT from BAT-HuR -/- mice. We show that genetic deletion or pharmacological inhibition of HuR blunts both the increase in cytosolic calcium and the β-adrenergic-mediated heat generation in stromal vascular fraction (SVF)-derived primary brown adipocytes. Mechanistically, we show that HuR directly binds and reduces the decay rate of Ryr2 mRNA in brown adipocytes, and stabilization of Ryr2 via S107 rescues the observed changes. In conclusion, our results suggest that HuR-dependent control of Ryr2 expression plays a significant role in the thermogenic function of brown ad
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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