Open AccessOverexpression of Raidd cDNA inhibits differentiation of mouse preadipocytes
Author(s) -
Felmer R.,
Horvat S.,
Clinton M.,
Clark A. J.
Publication year - 2003
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1046/j.1365-2184.2003.00253.x
Subject(s) - transfection , microbiology and biotechnology , complementary dna , biology , cellular differentiation , apoptosis , adipocyte , cell culture , gene , adipose tissue , biochemistry , genetics
. RAIDD (RIP‐associated ICH‐1 homologous protein with a death domain) is an adaptor molecule that mediates the action of cysteine proteases involved in apoptosis. To study the possibility of a novel system of cell ablation mediated by RAIDD, a preadipocyte cell line (3T3L1) was stably transfected with a plasmid containing the murine Raidd cDNA under the control of the adipocyte specific promoter aP2. Instead of the expected apoptosis, a blockage to differentiation upon hormonal induction was observed as judged by an absence of lipid accumulation, a lack of expression of adipocyte‐specific genes and a fibroblastic appearance. Proliferation rate of Raidd ‐transfected clones remained unaffected. Overexpression of Raidd cDNA in 3T3L1 cell therefore inhibited differentiation, suggesting that Raidd plays a role in controlling differentiation of mouse preadipocytes and, perhaps, in other cell types, in addition to its established role in apoptosis.