Arachidonic acid-dependent gene regulation during preadipocyte differentiation controls adipocyte potential.
J Lipid Res
; 55(12): 2479-90, 2014 Dec.
Article
en En
| MEDLINE
| ID: mdl-25325755
ABSTRACT
Arachidonic acid (AA) is a major PUFA that has been implicated in the regulation of adipogenesis. We examined the effect of a short exposure to AA at different stages of 3T3-L1 adipocyte differentiation. AA caused the upregulation of fatty acid binding protein 4 (FABP4/aP2) following 24 h of differentiation. This was mediated by the prostaglandin F(2α) (PGF(2α)), as inhibition of cyclooxygenases or PGF(2α) receptor signaling counteracted the AA-mediated aP2 induction. In addition, calcium, protein kinase C, and ERK are all key elements of the pathway through which AA induces the expression of aP2. We also show that treatment with AA during the first 24 h of differentiation upregulates the expression of the transcription factor Fos-related antigen 1 (Fra-1) via the same pathway. Finally, treatment with AA for 24 h at the beginning of the adipocyte differentiation is sufficient to inhibit the late stages of adipogenesis through a Fra-1-dependent pathway, as Fra-1 knockdown rescued adipogenesis. Our data show that AA is able to program the differentiation potential of preadipocytes by regulating gene expression at the early stages of adipogenesis.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Receptores de Prostaglandina
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Proteínas Proto-Oncogénicas c-fos
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Ácido Araquidónico
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Regulación del Desarrollo de la Expresión Génica
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Proteínas de Unión a Ácidos Grasos
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Adipogénesis
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Adipocitos Blancos
Límite:
Animals
Idioma:
En
Año:
2014
Tipo del documento:
Article