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: Induction of transforming growth factor beta 1 by insulin-like growth factor-1 in dermal fibroblasts.
    Author: Ghahary A, Shen Q, Shen YJ, Scott PG, Tredget EE.
    Journal: J Cell Physiol; 1998 Mar; 174(3):301-9. PubMed ID: 9462692.
    Abstract:
    Transforming growth factor beta1 (TGF-beta1) belongs to a family of multifunctional modulatory proteins involved in cell growth, differentiation, development, and wound healing. Although the biological activities of TGF-beta1 have been extensively studied, its regulation remains obscure. Here we report the effects of insulin-like growth factor-1 (IGF-1) on the expression of TGF-beta1 by dermal fibroblasts and suggest a possible mechanism. An enzyme-linked immunosorbent assay (ELISA) specific for TGF-beta revealed a greater than twofold increase (12.3 +/- 1.6 vs. 4.8 +/- 0.8 pg/10(4) cells, n = 7, P < 0.05) in the protein in conditioned medium obtained from IGF-1-treated cells compared to that from untreated controls. Similar results were obtained by the mink lung epithelial cell growth inhibition assay. The results of Northern analysis revealed a dose-dependent increase in TGF-beta1 mRNA in response to IGF-1 treatment. Using the optimum concentration of IGF-1 (100 ng/ml), a greater than twofold increase (25.43 +/- 5.7 vs. 12.13 +/- 4.5, P < 0.05) in TGF-beta1 mRNA was observed. This effect persisted for at least 48 h after IGF-1 was removed from the culture medium. Nuclear run-on assay showed that this stimulation was due, at least in part, to an increase in the rate of transcription of the TGF-beta1 gene. Treatment of human dermal fibroblasts with IGF-1 caused a substantial increase in c-fos and c-jun mRNA expression within 30 and 60 min, respectively. In contrast to c-jun mRNA which was constitutively expressed by dermal fibroblasts, the expression of c-fos mRNA was transient and only detectable between 15 and 60 min. Greater than 58% of the increase in TGF-beta1 caused by IGF-1 could be blocked by the addition of anti-TGF-beta1 neutralizing antibody to the culture medium, suggesting that autoinduction of TGF-beta1 may be involved. An increase in IGF-1-induced TGF-beta1 should be important in many different physiological processes such as cellular proliferation, differentiation, and wound healing. These findings also suggest that induction of TGF-beta1 mRNA and protein by IGF-1 may be a mechanism by which this cytokine is regulated in physiological and/or pathological conditions.
    [Abstract] [Full Text] [Related] [New Search]