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Human Antigen R (HuR) Regulates Structure and Function of Brown Adipose Tissue
Author(s) -
Lanzillotta Lindsey,
Anthony Sarah R.,
Yamamoto Kaila,
Jones Shan,
Taylor Zachary,
Yoshida George,
Owens A. Phillip,
Tranter Michael
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.826.12
Subject(s) - brown adipose tissue , mitochondrial biogenesis , endocrinology , medicine , thermogenesis , biology , thermogenin , downregulation and upregulation , uncoupling protein , white adipose tissue , adipose tissue , coactivator , receptor , knockout mouse , peroxisome proliferator activated receptor , mitochondrion , microbiology and biotechnology , gene , biochemistry , transcription factor
Human antigen R (HuR) is an RNA binding protein widely expressed throughout the body, including in both white (WAT) and brown (BAT) adipose tissue. Recent work from our lab has shown that adipocyte‐specific HuR knockout (adipo‐HuR −/− ) mice gain less weight following a high fat diet (HFD) compared to wild type (WT) controls. In this study, we focused on the role of HuR deletion on the function of BAT, which mediates non‐shivering thermogenesis. Histological analysis revealed that, while the BAT of the chow fed adipo‐HuR −/− mice appeared normal, the BAT of the HFD fed adipo‐HuR −/− mice appears less dense with a cell size that more closely resembles WAT. Upon further examination of BAT function, our results show that, when subjected to cold stress (4°C), adipo‐HuR −/− mice are less cold tolerant compared to their WT counterparts. We also show that, compared to the WT mice, adipo‐HuR −/− mice have decreased mitochondrial density and expression of uncoupling protein‐1 (UCP‐1) in their BAT. This may be caused by a HuR‐dependent decrease in expression of peroxisome proliferator‐activated receptor gamma coactivator 1 alpha (PGC‐1a), which plays a key role in mitochondrial biogenesis and is upregulated during exposure to cold (4°C). In conclusion, our results indicate that HuR regulates both the structure and function of BAT, at least in part through modulation of PGC‐1a mRNA expression. Support or Funding Information This work was supported by a University of Cincinnati Heart, Lung, and Vascular Institute Near Horizons Grant (MT, APO). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .