Tartrate‐resistant acid phosphatase type 5/ACP5 promotes cell cycle entry of 3T3‐L1 preadipocytes by increasing IGF‐1/Akt signaling

Abstract

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 b-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.

Whole-Transcriptome Sequencing of Antler Tissue Reveals That circRNA2829 Regulates Chondrocyte Proliferation and Differentiation via the miR-4286-R+1/FOXO4 Axis

“…Acid phosphatase 5 (ACP5) is an evolutionarily conserved multifunctional protein involved in normal bone development and osteoblast regulation, among other functions [ 26 ]. PTH can be involved in regulating MGP expression through the MAPK pathway [ 27 ]; ACP can interact with p53 to regulate SMAD3 [ 28 ] and ACP5 can activate the IGF-1/Akt pathway to regulate cell cycles [ 29 ]; and FOXO4 has been reported to be activated by PI3K-AKT to promote cell proliferation [ 30 ] and can also protect the viability of senescent cells and inhibit apoptosis by isolating p53 in the nucleosome to protect the viability of senescent cells and inhibit apoptosis [ 31 ]. Collectively, these functional genes in the network interact with each other and together participate in the PI3K/ATK pathway, MAPKt pathway, and p53 pathway, which may be key signaling pathways in antler regeneration.…”