Heat-shock response and limitation of tissue necrosis during occlusion/reperfusion in rabbit hearts.

Currie, R. William; Rm, Tanguay; Kingma, Jr Jg

doi:10.1161/01.cir.87.3.963

Cited by 257 publications

(123 citation statements)

References 34 publications

Supporting

Mentioning

115

Contrasting

Unclassified

Order By: Relevance

“…They showed a strong relationship between the acquisition and decay of the postischemic ventricular recovery of the heart and the induction of HSP70. 30 In contrast, Currie et al 31 demonstrated that in spite of easily detectable expression of HSP70, hyperthermia-induced myocardial protection was observed only transiently at 24 hours and dissipated by 40 hours. These studies show that the protective effect of stress preconditioning does not always correlate with HSP70 induction.…”

Section: Resultsmentioning

confidence: 96%

Impact of hyperthermic preconditioning on postischemic hepatic microcirculatory disturbances in an isolated perfusion model of the rat liver

et al. 2000

View full text Add to dashboard Cite

Sublethal hyperthermia and the following recovery from this heat exposure, referred to as hyperthermic preconditioning, elicits a transient state of tolerance to oxidative insults through an intracellular protective response: stress response. The impact of hyperthermic preconditioning on hepatic microcirculatory disturbance, which is one of the determinants of ischemia/reperfusion-induced injury of the liver, was investigated by using intravital fluorescence microscopy. Thirty minutes of ischemia and a subsequent 120 minutes of reperfusion was induced in an in situ isolated perfusion model of Sprague-Dawley rats. Heat stress was given by whole-body hyperthermia, and a subsequent recovery was allowed for 18 or 48 hours, respectively. Postischemic decrease in sinusoidal perfusion rate and sinusoidal diameter, leukocyte stagnation in sinusoids, and leukocyte adhesion in postsinusoidal venules were significantly attenuated in both hyperthermia-pretreated groups. A recovery of bile production, a reduction of liver enzyme release, and an attenuation of tissue edema and histological damage were also observed. A marked expression of heat shock protein (HSP) 70 and heme oxygenase (HO-1)/HSP32 was correlatively observed in the liver tissue coincident with the induction of these protective effects. Hyperthermic preconditioning provides a continuous long-term and constant inhibitory effect (up to 48 hours after heat exposure) on postischemic injury of the liver through the attenuation of microcirculatory disturbances. These beneficial effects might be associated with a concomitant increase in HSP70 and HO-1/HSP32 expression. (HEPATOLOGY 2000;31:407-415.)Ischemia/reperfusion-induced injury is one of the major perioperative complications in liver surgery and liver transplantation. The administration of specific protective agents has been attempted to reduce postischemic hepatic injury. [1][2][3] To the contrary, preconditioning therapies based on an endogenous protection response against stressful events, referred to as heat stress response, have been studied as another therapeutic strategy. Hyperthermic preconditioning, the exposure to a transient sublethal hyperthermia, and the following appropriate recovery develops protection not only to subsequent thermal stress, but also to oxidative stress such as ischemia/reperfusion. [4][5][6][7][8] Heat stress response has been reported to be associated with the induction of specific heat shock proteins (HSPs). In particular, HSP70 is generally considered to contribute to the protective mechanism of hyperthermic preconditioning, based on the finding that overexpression of HSP70 in a transgenic mouse increases the resistance of the heart to ischemic injury. 9,10 Heme oxygenase (HO)-1/HSP32 is another HSP playing a role in the modulation of the inflammatory response. HO catabolizes intracellular heme to biliverdin, which is converted to bilirubin by bilirubin reductase. During this degradation process, carbon monoxide (CO) is released. 11 HO consists of HO-1 (inducible isoenzyme) and ...

show abstract

Section: Resultsmentioning

confidence: 96%

Impact of hyperthermic preconditioning on postischemic hepatic microcirculatory disturbances in an isolated perfusion model of the rat liver

et al. 2000

View full text Add to dashboard Cite

show abstract

“…For example, transgenic overexpression of HSP70 in the myocardium confers protection against both myocar- dial stunning and infarction following ischemia (14,21,28,30,42), whereas pharmacological induction of HSP70 in the myocardium also imparts resistance to ischemia (15,20,29,46). Furthermore, heat stress induction of HSP70 in the myocardium is associated with the development of "cross tolerance" to subsequent prolonged ischemia (4,43). Thus numerous studies substantiate the conclusion that cellular expression of HSP70 can confer protection against I/R injury in the myocardium.…”

Section: Discussionmentioning

confidence: 96%

“…Although IP of the myocardium has been shown to increase the expression of inducible HSP70 in the myocardium and is associated with cardioprotection (4,16,22,27,44), no direct evidence has been reported to support the conclusion that HSP70 mediates the late cardioprotection induced by IP. Moreover, two previous studies suggest that expression of inducible HSP70 following IP does not provide protection against ischemia, as assessed by a reduction in infarct size.…”

Section: Discussionmentioning

confidence: 99%

HSP70.1 and -70.3 are required for late-phase protection induced by ischemic preconditioning of mouse hearts

Hampton

Shimamoto

Rothnie

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…More than 10 differentially expressed genes were found in total 588 genes, most of these were digestive enzyme related genes, one of the overexpression gene was inducible heat shock protein 70 gene [20] . A variety of chemicals, viruses, and noxious stimuli such as trauma, hypoxia, or ischemia trigger the heat shock response and the subsequent synthesis of heat shock proteins [35][36][37][38][39][40][41][42][43] . The results of our experiment indicated that sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats, which was confirmed by RT-PCR, Western blotting and immunostaining.…”

Section: Discussionmentioning

confidence: 99%

Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa

Shen¹

2001

WJG

View full text Add to dashboard Cite

AIM To investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense.METHODS Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7d sleep deprivation. RT-PCR, immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70. Ethanol (500mL·L -1 , i.g.) was used to induce gastric mucosa damage.RESULTS RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL·L -1 ethanol challenge, the ulcer area found in the rats with 7d sleep deprivation (19.15±4.2)mm 2 was significantly lower (P<0.01) than the corresponding control (53.7± 8.1) mm 2 .CONCLUSION Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection. Subject headingssleep deprivation; heat shock proteins 70/biosynthesis; gastric mucosa; rats Shen XZ, Koo MWL, Cho CH. Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa. World J Gastroenterol, 2001;7(4):496-499

show abstract

Heat-shock response and limitation of tissue necrosis during occlusion/reperfusion in rabbit hearts.

Cited by 257 publications

References 34 publications

Impact of hyperthermic preconditioning on postischemic hepatic microcirculatory disturbances in an isolated perfusion model of the rat liver

Impact of hyperthermic preconditioning on postischemic hepatic microcirculatory disturbances in an isolated perfusion model of the rat liver

HSP70.1 and -70.3 are required for late-phase protection induced by ischemic preconditioning of mouse hearts

Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa

Contact Info

Product

Resources

About