| Autor: |
D, Kothapalli, K S, Frazier, A, Welply, P R, Segarini, G R, Grotendorst |
| Rok vydání: |
1997 |
| Předmět: |
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| Zdroj: |
Cell growthdifferentiation : the molecular biology journal of the American Association for Cancer Research. 8(1) |
| ISSN: |
1044-9523 |
| Popis: |
Connective tissue growth factor (CTGF) is a M(r)38,000 cysteine-rich peptide, the synthesis and secretion of which are selectively induced by transforming growth factor beta (TGF-beta). The relationship of CTGF to TGF-beta action on fibroblastic cells is not well understood. TGF-beta has the unique ability to stimulate the growth of normal fibroblasts in soft agar, a property of transformed cells. We have investigated whether CTGF can substitute for TGF-beta or whether CTGF action is essential for TGF-beta to stimulate anchorage-independent growth (AIG) of NRK fibroblasts. Our studies demonstrate that CTGF cannot induce AIG of NRK fibroblasts. However, CTGF synthesis and action are essential for the TGF-beta-induced AIG of NRK fibroblasts. Anti-CTGF antibodies specifically block TGF-beta-induced AIG but have no effect on platelet-derived growth factor or epidermal growth factor-induced growth in monolayer cultures and do not cross-react with platelet-derived growth factor or TGF-beta. Clones of NRK fibroblasts that express an antisense CTGF gene (NRK-ASCTGF), which blocks the expression of the endogenous CTGF gene, do not respond to TGF-beta in the AIG assay. The growth and morphology of the cells (NRK-ASCTGF) in monolayer culture are unaltered from the parent NRK cell line. The addition of recombinant CTGF to the NRK-ASCTGF clones in the presence of TGF-beta restores the AIG response of the cells. These studies demonstrate that the TGF-beta stimulation of NRK fibroblast AIG is dependent on events induced via the synergistic action of CTGF-dependent and CTGF-independent signaling pathways. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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