Chapter category: Heat Shock Proteins
Stress Proteins in Myocardial Protection: Culture Shock Protein, Heme Oxygenase–1 (Hsp32), Induced by Sublethal Stresses Protects the Heart Against Oxidative Stress
Heat Shock Proteins in Myocardial Protection
Edited by: Rakesh C. KukrejaISBN: 1-58706-021-3
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Chapter authors:
Shiro Hoshida
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The formation of a stress protein comprises a mechanism of cell protection highly conserved in evolution. As the induction of stress proteins makes cells more tolerant towards a second, more toxic, and otherwise lethal stress, the stress protein response might be involved in cardioprotective mechanisms.1,2 The term 'culture shock' is used under some circumstances triggered on exposure to serum–free conditions, during proliferation from subconfluent densities, or during isolation from whole tissue.3,4 The preferential synthesis of stress proteins by means of procedures for establishing primary cell cultures (culture shock) has been proposed; stress proteins (90, 70, 30 kD) are synthesized in Xenopus hepatocytes during the stepping up of primary cultures.3 In cultured myocardial cells, heavy metals such as cadmium chloride and cytokines such as interleukin–1 also induce the synthesis of stress proteins (70 and 30 kD).5,6 Although several reports showed a significant role of the 70 kD stress protein (Hsp70) in protection against oxidative stress of cardiac tissue,7,8 no reports have shown the role of the 30 kD stress protein in cardioprotection against oxidative stress.
Heme oxygenase (HO), which constitutes the rate–limiting enzyme in the degradation of heme, cleaves heme to form biliverdin, with the concomitant formation of carbon monoxide. The biliverdin is subsequently reduced to form the antioxidant, bilirubin.9–11 On the other hand, carbon monoxide, like nitric oxide, has the ability to bind to the iron atom of hemoproteins, and has been shown to activate guanylyl cyclase, resulting in an elevated cGMP content. The inducible type of HO (HO–1) is known to be Hsp32.12 HO–1 is inducible in various tissues with a large number of agents, including heme compounds, heavy metals, sulfhydryl reagents and hydrogen peroxide.13,14 The heart is rich in cytochromes and a site of heme synthesis. Myocardial cells are sensitive to changes in environment and can be considerably modified from their native in vivo state to a different state in culture. Considering with the functional properties of HO–related products, HO–1 could be involved in a mechanism of cellular adaptation.
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Heat Shock Proteins in Myocardial Protection, edited by Rakesh C. Kukreja
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In all organisms examined heat stress results in the synthesis of a specific group of proteins known as the heat shock or stress proteins (Hsps). Cells that accumulate these proteins adapt ...
