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3 "Heat shock protein"
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Effect of Heat Shock on the Vascular Reactivity and Expression of Heat Shock Protein in an Animal Model of Type 2 Diabetes Mellitus (OLETF rat).
Soon Hee Lee, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 2003;27(3):199-212.   Published online June 1, 2003
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BACKGROUND
Heat shock proteins (HSPs) are highly expressed in cardiovascular tissues, with heat shock possibly modulating the vascular reactivity to vasoactive agents. An abnormal vascular reactivity has been shown in diabetes, and may be closely associated to diabetic vascular complications. The aim of this study was to investigate the effects of heat shock on the vascular reactivity and the expression of HSP70 in the isolated aortae of OLETF rats, a commonly used animal model for type 2 diabetes mellitus, and LETO rats, as age matched controls. METHODS: In 4 ring segments of the thoracic aorta isolated from each rat, the endothelium was denuded in 2 (EC-) and reserved in the other 2 (EC+). To induce heat shock, the aortic rings were exposed to 42 degrees C for 45 minutes. The vascular reactivity responses to various vasoactive agents were measured by organ chamber studies, and by changes in the HSP expression, using Western blotting of the aortic rings in the OLETF rats and controls. RESULTS: The contractile responses to KCl became apparent 4 hours after the end of the heat shock induction. After heat shock, the phenylnephrine-induced contractile responses were similarly increased in the OLETF rats and the controls, but the increase was more significant in the EC(-) than the EC(+) rings, in both the OLETF rats and the controls. The relaxative responses to either acetylcholine (ACh) in the EC(+) aortic rings, or to sodium nitroprusside in the EC(-) rings, were not significantly affected by the heat shock treatment in either the OLETF rats or the controls, although the maximal relaxative response to ACh before the induction of the heat shock was lower in the aortic rings of the OLETF rats than in the controls. The HSP70 levels before the heat shock were higher in the aortic rings of the OLETF rats than in the controls, whereas those after heat shock were higher than those before in both the OLETF rats and the controls. The increase in the expression of HSP70 following the heat shock was higher in rings of the controls than in those of the OLETF rats. The HSP70 levels following the heat shock were increased to a greater extent in the EC(+) than the EC(-) rings of both the OLETF rats and the controls. CONCLUSION: These results suggest that the vascular reactivity to heat shock was decreased to a greater extent in the aortae of OLETF rats than in those of the controls, and that HSP70 seems to play an important role in the vascular response to heat shock through interaction of the endothelium and the smooth muscle.
Effect of Heat Shock on the Vascular Reactivity in Diabetic Rat Aorta.
Seong Mo Koo, Soon Hee Lee, Jung Hun Han, Gi Young Jeong, In Kyum Kim, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 2001;25(5):343-353.   Published online October 1, 2001
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AbstractAbstract PDF
BACKGROUND
Heat shock has been known to change cellular response to noxious stimuli by inducing heat shock proteins (HSP). HSP are expressed in many tissues, and increased expression of some HSP enhances the survival of cells exposed to oxidative stress. Recently, Some HSP are known to associate with vascular reactivity. Under diabetic conditions, there is abnormal vascular reactivity to relaxing or contracting factors. Abnormal vascular response to some stimuli is an important role in the development of diabetic complications. However, the effects of heat shock on the vascular reactivity in diabetic condition is unclear. Therefore, we investigated effects of heat shock on the vascular reactivity in isolated aorta of streptozotocin-induced diabetic rats. METHODS: After mounced in organ bath, aortic ring preparations were exposed to 42 for 45 minutes followed by being subjected to contraction and relaxation in 4 hours. Tissues were frozen for measurement of HSP 70 and phosphorylation of myosin light chain after functional study. RESULTS: Heat shock not only increased expression of HSP70 in rat aorta but also augmented contraction to KCl and phenylephrine in the aorta of control and diabetic rats (p<0.05). Relaxation responses to acetylcholine (ACh) were not changed in the aorta of control rats with and without heat shock for 45 minutes. However, heat shock for 45 minutes decreased relaxative responses to ACh in the aorta of diabetic rats compared to those in the aorta of control rats. CONCLUSION: This result suggests that heat shock increases vascular contractility in the aorta of diabetic and control rats through the induction of HSP70 while heat shock seems to decrease relaxative response in the aorta of diabetic ratscompared to control rats (p<0.05). Whether heat shock impaired relaxative response in the aorta of diabetic rats deserves additional studies.
Effects of Aminoguanidine on Nitric Oxide Production, Insulin Release and Hsp 70 Expression in Cultured Rat Islets Exposed to IL-1betabeta.
Kyu Chang Won, Mi Jung Eun, Jae Hong Kim, Jung Hyun Oh, Sang Yub Nam, Ji Sung Yoon, Hyun Dae Yoon, In Ho Cho, Hyoung Woo Lee
Korean Diabetes J. 2001;25(4):273-285.   Published online August 1, 2001
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BACKGROUND
IL-1beta has been implicated to play an important role in the autoimmune beta cell lesion of type 1 diabetes because of its inhibition of insulin secretion and direct islet cytotoxicity. Thus, this study evaluated the effect of aminoguanidine on No production, insulin release and hsp 70 expression in cultured rat islets exposed to IL-1beta. METHOD: Islets isolated from Sprague-Dawley rats were cultured with IL-1beta , aminoguanidine AG and GSNO, individually and in combination for 24hours. Accumulated nitrite production, insulin release and islet expression of hsp 70 were measured. RESULTS: IL-1beta increased nitrite production, inhibited insulin release, and increased hsp 70 expression. AG alone had no effect on nitrite production, insulin release and hsp 70 expression. In combination, AG completely blocked IL-1beta but increased nitrite production, reversed IL-1beta inhibited insulin release and reversed IL-1beta increased hsp 70 expression. Moreover, nitric oxide NO donor, GSNO stimulated hsp 70 expression. CONCLUSION: Findings from this study suggest that hsp 70 may be one potential protein that is expressed in response to NO and that participates in islet recovery from NO mediated islet damage.

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