Summary
The human 32kDa stress protein is synthesised following cellular redox imbalance and has been identified as a specific marker of oxidative stress; 32kDa stress protein-inducing agents include heavy metals, oxidising species and sulphydryl reactive compounds. As well as inducing the 32kDa protein, the oxidant H2O2 has been shown to induce transcription of the immediate-early genes and this activation is serum dependent. Our evidence that hypoxia/ reperfusion events occur in mobile inflamed joints prompted us to examine the vasculature. Therefore, human umbilical vein endothelial cells (HUVEC) were challenged with cadmium chloride, hydrogen peroxide (H2O2) and disodium aurothiomalate in the presence and absence of serum. The results show that a 32kDa protein can be induced in HUVEC, that the response to H2O2 is serum dependent and that it occurs at the level of transcription. Thus, two mechanisms of induction are possible: oxidants (eg H2O2) require serum while heavy metals and sulphydryl-reactive compounds may use a different pathway.
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Winrow, V.R., Watson, A., Harley, S.L., Blake, D.R. (1994). Hydrogen peroxide-induced synthesis of the 32kDa stress protein (HO-1) in endothelial cells is serum dependent. In: Pasquier, C., Olivier, R.Y., Auclair, C., Packer, L. (eds) Oxidative Stress, Cell Activation and Viral Infection. Molecular and Cell Biology Updates. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7424-3_10
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DOI: https://doi.org/10.1007/978-3-0348-7424-3_10
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