Caveolin‐2 in association with nuclear lamina controls adipocyte hypertrophy

Here, we identify that Caveolin‐2 (Cav‐2), an integral membrane protein, controls adipocyte hypertrophy in association with nuclear lamina. In the hypertrophy stage of adipogenesis, pY19‐Cav‐2 association with lamin A/C facilitated the disengagement of CCAAT/enhancer‐binding protein α (C/EBPα) and p...

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Published in:The FASEB journal 2023-02, Vol.37 (2), p.e22745-n/a
Main Authors: Choi, Moonjeong, Kwon, Hayeong, Pak, Yunbae
Format: Article
Language:English
Subjects:
3T3-L1 Cells
adipocyte hypertrophy
Adipocytes - metabolism
Adipogenesis - genetics
Animals
C/EBPα
Caveolin 2 - genetics
Caveolin 2 - metabolism
Caveolin‐2
CCAAT-Enhancer-Binding Protein-alpha - metabolism
Cell Differentiation
Humans
Hypertrophy - metabolism
lamin A/C
Lamin Type A - metabolism
Mice
Nuclear Lamina - metabolism
obesity
PPAR gamma - genetics
PPAR gamma - metabolism
PPARγ
PTP1B
Uchl5
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Summary:Here, we identify that Caveolin‐2 (Cav‐2), an integral membrane protein, controls adipocyte hypertrophy in association with nuclear lamina. In the hypertrophy stage of adipogenesis, pY19‐Cav‐2 association with lamin A/C facilitated the disengagement of CCAAT/enhancer‐binding protein α (C/EBPα) and peroxisome proliferator‐activated receptor γ (PPARγ) from lamin A/C and repressed Cav‐2 promoter at the nuclear periphery for epigenetic activation of Cav‐2, and thereby promoted C/EBPα and PPARγ‐induced adipocyte hypertrophy. Stable expression of Cav‐2 was required and retained by phosphorylation, deubiquitination, and association with lamin A/C for the adipocyte hypertrophy. However, obese adipocytes exhibited augmented Cav‐2 stability resulting from the up‐regulation of lamin A/C over lamin B1, protein tyrosine phosphatase 1B (PTP1B), and nuclear deubiquitinating enzyme (DUB), Uchl5. Our findings show a novel epigenetic regulatory mechanism of adipocyte hypertrophy by Cav‐2 at the nuclear periphery.
ISSN:0892-6638
1530-6860
DOI:10.1096/fj.202201028RR