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Expression of PTEN and Akt phosphorylation in lipopolysaccharide‐treated NIH3T3 cells
Author(s) -
Okamura Hirohiko,
Yoshida Kaya,
Sasaki Eiko,
Qiu Lihong,
Amorim Bruna Rabelo,
Morimoto Hiroyuki,
Haneji Tatsuji
Publication year - 2007
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2006.09.014
Subject(s) - pten , protein kinase b , tensin , phosphorylation , pi3k/akt/mtor pathway , cancer research , phosphatase , microbiology and biotechnology , biology , kinase , rna interference , chemistry , signal transduction , rna , gene , biochemistry
PTEN is a tumor suppressor gene encoding a phosphatase, and it negatively regulates cell survival mediated by the phosphoinositol 3‐kinase (PI3‐Kinase)‐Akt pathway. To elucidate PTEN expression and its effect on the PI3‐kinase‐Akt pathway in fibroblasts and macrophages, we investigated the expression of PTEN and the phosphorylation status of Akt in NIH3T3 and RAW264.7 cells treated with LPS. Phosphorylation of Akt was induced by LPS treatment in a dose‐dependent manner in RAW264.7 cells, but not in NIH3T3 cells. LPS induced the expression of PTEN in a dose and time‐dependent manner in NIH3T3 cells (0–1 μg/ml, 0–6 h). However, LPS did not stimulate PTEN expression in RAW264.7 cells. These data indicate the existence of diverse mechanisms for PTEN expression and Akt activation in fibroblasts and macrophages. RNA interference using double‐stranded RNA specific for the PTEN gene reduced both mRNA and protein levels of PTEN in NIH3T3 cells treated or not with LPS. The phosphorylation status of Akt in NIH3T3 cells stimulated with LPS did not change when the PTEN expression had been inhibited by RNA interference. The present results suggest that the up‐regulation of PTEN expression by LPS is not involved in the activation of Akt in NIH3T3 cells. PTEN expression might be involved in the diverse inflammatory responses to LPS in fibroblasts and macrophages.