Why the study?
Does homocysteine alter proliferation, apoptosis, and collagen production in human arterial smooth muscle cells?
Does homocysteine alter proliferation, apoptosis, and collagen production in human arterial smooth muscle cells?
Homocysteine promotes human aortic smooth muscle cell proliferation and alters collagen production, suggesting a cellular mechanism for accelerated atherosclerotic plaque fibrosis.
Hypothesis-generating for homocysteine in vascular fibrosis; leaves open clinical relevance without in vivo confirmation.
Homocysteine (H(e)) is an important and independent risk factor for atherosclerosis. We showed that human aortic smooth muscles in cultures proliferated significantly at a concentration of 25 micromol/L H(e) without the presence of serum. There was no effect of H(e) on apoptosis as determined by TUNEL-assay and gene expression of proapoptotic protein bax, caspases and TNFalpha families. However, collagen types I, III and IV increased significantly in a dose-dependent manner at elevated concentrations of H(e) and the amount of type VI collagen was significantly reduced in a dose-dependent manner. H(e) induced increased cell replication with an unaffected apoptosis rate. The present observations suggest that H(e) may contribute to accelerated progression of atherosclerotic lesions with collagen alterations which transform the injury into fibrotic plaques.
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Rasmussen et al. (2004) studied this question.
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