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TNF‐α inhibits UCP‐1 expression in brown adipocytes via ERKs
Author(s) -
Valladares Amparo,
Roncero Cesar,
Benito Manuel,
Porras Almudena
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02264-5
Subject(s) - adipogenesis , p38 mitogen activated protein kinases , tumor necrosis factor alpha , transcription factor , protein kinase a , adipocyte , kinase , microbiology and biotechnology , biology , endocrinology , medicine , chemistry , gene , biochemistry , adipose tissue
Tumor necrosis factor‐α (TNF‐α) activates extracellular‐regulated kinases (ERKs) and p38 mitogen‐activated protein kinase (p38MAPK), and inhibits the expression of uncoupling protein‐1 (UCP‐1) and adipocyte‐specific genes in rat fetal brown adipocytes. MEK inhibition with PD98059 abolished the inhibitory effect of TNF‐α on UCP‐1, but not on adipogenic genes. In contrast, inhibition of p38MAPK with SB203580 potentiated the negative effect of TNF‐α on UCP‐1 and adipogenic genes. The inhibitory action of TNF‐α was partially correlated with changes in C/EBPα and β protein levels and in their DNA binding activity, suggesting a role for these transcription factors. However, other transcription factors might explain the different regulation of UCP‐1 and adipogenic genes by ERKs.