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Loss of ability to synthesize collagen in fibroblasts transformed by rous sarcoma virus
Abstract:
Transformation of chick embryo fibroblasts by Rous sarcoma virus inhibited their ability to synthesize collagen. Kinetic experiments showed that 72 hours after infection, collagen synthesis was reduced by 90%. Nontransforming Rous-associated viruses did not inhibit collagen synthesis. The inhibition resulted from the failure of the cells to synthesize collagen polypeptides rather than from a decrease in the activity of prolyl hydroxylase; the levels of prolyl hydroxylase were fourfold those in uninfected cells. The addition of dibutyryl cyclic AMP and theophylline, alone or together, did not restore collagen synthesis.
Insights
Rous sarcoma virus significantly reduces collagen synthesis in chick cells by 90%. This inhibition stems from a failure in collagen polypeptide production, not prolyl hydroxylase activity, and is not reversed by cyclic AMP.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Rous sarcoma virus (RSV) is a retrovirus known to transform cells.
- Collagen is a crucial structural protein in connective tissues.
- Understanding viral effects on cellular matrix production is vital for disease research.
Purpose of the Study:
- To investigate the impact of Rous sarcoma virus transformation on collagen synthesis in chick embryo fibroblasts.
- To determine the mechanism behind RSV-induced inhibition of collagen production.
Main Methods:
- Infection of chick embryo fibroblasts with Rous sarcoma virus and Rous-associated viruses.
- Kinetic analysis of collagen synthesis over 72 hours post-infection.
- Measurement of prolyl hydroxylase activity and collagen polypeptide levels.
Main Results:
- RSV infection reduced collagen synthesis by 90% within 72 hours.
- Nontransforming Rous-associated viruses did not affect collagen synthesis.
- Inhibition was due to decreased collagen polypeptide synthesis, not reduced prolyl hydroxylase activity (which was elevated).
Conclusions:
- Viral transformation by RSV directly inhibits cellular collagen production.
- The mechanism involves a block in collagen polypeptide synthesis, independent of prolyl hydroxylase levels.
- Therapeutic interventions like cyclic AMP did not restore collagen synthesis.