We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
IGF-1 Combined with OPN Promotes Neuronal Axon Growth in Vitro Through the IGF-1R/Akt/mTOR Signaling Pathway in Lipid Rafts.
- Authors
Zhao, Qin; Su, Hong; Jiang, Wei; Luo, Haodong; Pan, Lu; Liu, Yuan; Yang, Ce; Yin, Ying; Yu, Lehua; Tan, Botao
- Abstract
This study aims to investigate the effect of insulin-like growth factor 1 (IGF-1) combined with osteopontin (OPN) on the protein expression levels and growth of neuronal axons and its possible mechanism. In this study, IGF-1 combined with OPN promoted neuronal axon growth through the IGF-1R/Akt/mTOR signaling pathway in lipid rafts, and the effect was better than that of either agent alone. This effect was suppressed when given the mTOR inhibitor rapamycin or the lipid raft cholesterol extraction agent methyl-β-cyclodextrin (M-β-CD). Rapamycin could inhibit the expression of phosphorylated ribosomal S6 protein (p-S6) and phosphorylated protein kinase B (p-Akt) and limit axon growth. In addition to the above effects, M-β-CD significantly downregulated the expression of phosphorylated insulin-like growth factor 1 receptor (p-IR). To further investigate the changes in lipid rafts when stimulated by different recombinant proteins, membrane lipid rafts were isolated to observe the changes by western blot. The expression levels of insulin-like growth factor 1 receptor (IR) and P-IR in the IGF-1 combined with OPN group were the highest. When M-β-CD was administered to the lipid rafts of neurons, the enrichment of IR by IGF-1 combined with OPN was weakened, and the p-IR was decreased. Our study found that IGF-1 combined with OPN could promote axon growth by activating the IGF-1R/Akt/mTOR signaling pathway in neuronal lipid rafts.
- Subjects
LIPID rafts; SOMATOMEDIN C; CELLULAR signal transduction; PROTEIN kinase B; MEMBRANE lipids; AXONS; INSULIN-like growth factor receptors
- Publication
Neurochemical Research, 2023, Vol 48, Issue 10, p3190
- ISSN
0364-3190
- Publication type
Article
- DOI
10.1007/s11064-023-03971-3