Abstract
Skeletal cells secrete insulin-like growth factors (IGFs) I and II and six known IGF binding proteins (IGFBPs). IGFBP-5 stimulates bone formation, and its synthesis correlates with changes in osteoblast cell growth. We tested the effects of basic fibroblast growth factor (bFGF), transforming growth factor beta 1 (TGF beta 1), and platelet-derived growth factor (PDGF) BB on IGFBP-5 expression in cultures of osteoblast-enriched cells from 22-day-old fetal rat calvariae (Ob cells). Treatment of Ob cells with bFGF, TGF beta 1, and PDGF BB caused a time- and dose-dependent decrease in IGFBP-5 mRNA levels and inhibited IGFBP-5 polypeptide levels in the extracellular matrix. The effects of bFGF, TGF beta 1, and PDGF BB on IGFBP-5 transcripts were independent of cell division and were observed in the presence and absence of hydroxyurea. bFGF, TGF beta 1, and PDGF BB did not modify the decay of IGFBP-5 mRNA in transcriptionally arrested Ob cells, and they inhibited IGFBP-5 heterogeneous nuclear RNA and the rate of IGFBP-5 transcription. In conclusion, bFGF, TGF beta 1, and PDGF BB inhibit IGFBP-5 expression in Ob cells independently of their mitogenic activity and through mechanisms that involve decreased transcription.
Highlights
Skeletal cells secrete insulin-like growth factors (IGFs) I and II and six known IGF binding proteins
The present studies were undertaken to examine the effects of basic fibroblast growth factor, transforming growth factor /31 (TGF /31), and platelet-derived growth factor (PDGF) BB on IGFBP-5 synthesis in cultures of osteoblast-enriched cells from fetal rat parietal bone (Ob cells) and to determine possible mechanisms involved
Because the growth factors te sted increase (3-actin and glyceralde hy de -3-phos phate dehydrogenase mRNA, IGFBP-5 mRNA levels were not corrected for changes in (3-actin or glyceralde hy de-3-phos phate deh ydrogena se mRNA, a nd uniform ity of RNA loading of t he gels was estimated by et hi dium bromi de staini ng of ribosom al RNA [9]
Summary
Skeletal cells secrete insulin-like growth factors (IGFs) I and II and six known IGF binding proteins (lGFBPs). Agents that regulate the synthesis and activity of IGFBP-5 in bone cells are critical to our understanding of its role in bone physiology Investigations from this and other laboratories have revealed that skeletal growth factors inhibit the synthesis of IGFs I and II in cells of the osteoblastic lineage and that the synthesis of IGF I and IGFBP-5 is coordinated [9, 10, 16, 17]. The present studies were undertaken to examine the effects of basic fibroblast growth factor (bFGF), transforming growth factor /31 (TGF /31), and platelet-derived growth factor (PDGF) BB on IGFBP-5 synthesis in cultures of osteoblast-enriched cells from fetal rat parietal bone (Ob cells) and to determine possible mechanisms involved
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