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: Synthesis and regulation of insulin-like growth factor binding protein-5 in FRTL-5 cells.
    Author: Backeljauw PF, Dai Z, Clemmons DR, D'Ercole AJ.
    Journal: Endocrinology; 1993 Apr; 132(4):1677-81. PubMed ID: 7681763.
    Abstract:
    FRTL-5 cells, a diploid nontransformed line of rat thyroid follicular cells, exhibit a marked mitogenic response to insulin-like growth factors (IGFs) when they are exposed to TSH. Because IGF binding proteins (IGFBPs) are important modulators of IGF actions, we investigated the capacity of FRTL-5 cells to synthesize IGFBPs. We found that FRTL-5 cell conditioned media contained a single band of approximately 31 kilodaltons on ligand blot analysis. This band represents IGFBP-5 because: 1) it can be immunostained with a specific antibody raised against human IGFBP-5; 2) by Northern analysis, total RNA from FRTL-5 cells contains a major 6-kilobase transcript when hybridized with a cDNA for rat IGFBP-5; and 3) no transcripts were observed when Northern blots of FRTL-5 cells were hybridized with complementary DNAs for rat IGFBP-1, -2, -3, -4 or -6. Conditioned media IGFBP-5 increased in response to IGF-I, IGF-II, and insulin in a dose-dependent fashion, compared with unstimulated FRTL-5 cells. At maximally effective concentrations IGF-I was 3.5- and 6-fold more potent than IGF-II and insulin, respectively. The addition of a monoclonal antibody (Sm 1.2) to IGF-I completely inhibited IGF-I stimulation of the IGFBP-5 6-kilobase transcript and the appearance of IGFBP-5 in FRTL-5 conditioned media. Stimulation of IGFBP-5 synthesis by the IGFs and insulin appeared to be regulated at the messenger RNA (mRNA) level, because each stimulated similar increases in both IGFBP-5 mRNA and media protein at maximally effective concentrations. TSH, on the other hand, inhibited basal levels of IGFBP-5 mRNA and attenuated the increase in IGFBP-5 mRNA stimulated by IGF-I. FRTL-5 cells provide a relatively uncomplicated model to study the regulation and action of IGFBP-5 and the mechanisms by which IGFs interact with this binding protein.
    [Abstract] [Full Text] [Related] [New Search]