Caveolin-2 controls preadipocyte survival in the mitotic clonal expansion for adipogenesis.
Biochim Biophys Acta Mol Cell Res
; 1871(7): 119793, 2024 Oct.
Article
em En
| MEDLINE
| ID: mdl-39038612
ABSTRACT
Here, we report that Caveolin-2 (Cav-2) is a cell cycle regulator in the mitotic clonal expansion (MCE) for adipogenesis. For the G2/M phase transition and re-entry into the G1 phase, dephosphorylated Cav-2 by protein tyrosine phosphatase 1B (PTP1B) controlled epigenetic activation of Ccnb1, Cdk1, and p21 in a lamin A/C-dependent manner, thereby ensuring the survival of preadipocytes. Cav-2, associated with lamin A/C, recruited the repressed promoters of Ccnb1 and Cdk1 for activation, and disengaged the active promoter of p21 from lamin A/C for inactivation through histone H3 modifications at the nuclear periphery. Cav-2 deficiency abrogated the histone H3 modifications and impeded the transactivation of Ccnb1, Cdk1, and p21, leading to a delay in mitotic entry, retardation of re-entry into G1 phase, and the apoptotic cell death of preadipocytes. Re-expression of Cav-2 restored the G2/M phase transition and G1 phase re-entry, preadipocyte survival, and adipogenesis in Cav-2-deficient preadipocytes. Our study uncovers a novel mechanism by which cell cycle transition and apoptotic cell death are controlled for adipocyte hyperplasia.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteína Quinase CDC2
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Adipócitos
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Caveolina 2
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Inibidor de Quinase Dependente de Ciclina p21
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Adipogenia
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Mitose
Limite:
Animals
Idioma:
En
Revista:
Biochim Biophys Acta Mol Cell Res
Ano de publicação:
2024
Tipo de documento:
Article