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Tartrate‐resistant acid phosphatase type 5/ ACP5 promotes cell cycle entry of 3T3‐L1 preadipocytes by increasing IGF‐1/Akt signaling
Author(s) -
Lång Pernilla,
Patlaka Christina,
Andersson Göran
Publication year - 2021
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 - 10.1002/1873-3468.14184
Subject(s) - protein kinase b , signal transduction , tartrate resistant acid phosphatase , endocrinology , medicine , stimulation , microbiology and biotechnology , phosphatase , insulin receptor , insulin like growth factor , receptor , growth factor , chemistry , irs1 , biology , phosphorylation , insulin , biochemistry , insulin resistance , osteoclast
Tartrate‐resistant acid phosphatase (TRAP, encoded by ACP5 )‐overexpressing mice exhibit hyperplastic obesity. As the molecular mechanism remains elusive, the aims were to characterize the effect of TRAP on preadipocyte proliferation. We investigated cell cycle entry and signal transduction, that is, insulin‐like growth factor 1 (IGF‐1)/ insulin receptor substrate 1 (IRS‐1) and the Akt signaling pathways, in 3T3‐L1 preadipocytes treated with the TRAP 5a isoform. Results show that TRAP 5a increases S‐phase entry. TRAP 5a stimulation increases IGF‐1 mRNA and IRS‐1 activation, indicative of insulin‐like growth factor 1 receptor (IGF1R) activation. Furthermore, TRAP 5a stimulation resulted in Akt signaling pathway activation and subsequent increased nuclear translocation of β‐catenin. In conclusion, TRAP 5a increases proliferation of preadipocytes in a dose‐dependent fashion by promoting entry into S‐phase. Part of this effect is likely due to increased IGF‐1 signaling through the Akt signaling pathway.