These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Modulation of insulin-like growth factor I mitogenic signaling in 3T3-L1 preadipocyte differentiation.
    Author: Boney CM, Smith RM, Gruppuso PA.
    Journal: Endocrinology; 1998 Apr; 139(4):1638-44. PubMed ID: 9528944.
    Abstract:
    Insulin-like growth factor I (IGF-I) stimulates mitogenesis in proliferating 3T3-L1 preadipocytes. However, IGF-I functions to stimulate differentiation once growth arrest occurs at confluence. Epidermal growth factor (EGF) is also a potent mitogen in these cells, but inhibits differentiation of preadipocytes. We compared mitogenic signaling via the mitogen-activated protein kinase (MAPK) pathway in response to IGF-I or EGF in proliferating, growth-arrested, and differentiating 3T3-L1 cells. IGF-I stimulation of MAPK was rapid and maximal in proliferating 3T3-L1 preadipocytes, but decreased greatly in differentiating cells. EGF was more potent than IGF-I in stimulating MAPK activity in 3T3-L1 cells, and activation of MAPK was maintained in differentiating cells. These results suggest an uncoupling of MAPK activation specific to IGF-I-mediated 3T3-L1 preadipocyte differentiation. Studies of proximal signaling revealed Shc phosphorylation and Shc/Grb2 complex formation in IGF-I-treated proliferating, but not differentiating, cells. Insulin receptor substrate-1 phosphorylation after IGF-I treatment was present in proliferating, quiescent, and differentiating preadipocytes. Shc phosphorylation and Grb2 association after EGF treatment were present throughout all phases of growth. The change in IGF-I signaling via Shc phosphorylation and MAPK activity during 3T3-L1 differentiation indicates that loss of IGF-I mitogenic signaling via the MAPK pathway is part of the differentiation process.
    [Abstract] [Full Text] [Related] [New Search]