Role of protein kinase C in geranylgeranylacetone-induced expression of heat-shock protein 72 and cardioprotection in the rat heart

Yamanaka, Kunitoshi; Takahashi, Naohiko; Ooie, Tatsuhiko; Kaneda, Koji; Yoshimatsu, Hironobu; Saikawa, Tetsunori

doi:10.1016/s0022-2828(03)00133-0

Cited by 65 publications

(68 citation statements)

References 26 publications

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“…In the rat heart overexpression of HSP72 induced by geranylgeranylacetone (GGA), an antiulcer drug, confers cardioprotection against ischaemia and reperfusion and is accompanied by increased PKC activity. Blockade of PKC abolishes all the effects of GGA on expression of HSP72 and cardioprotection [23]. The result is evidence of a link between PKC and HSP in cardioprotection.…”

Section: Discussionmentioning

confidence: 80%

Failure to confer cardioprotection and to increase the expression of heat-shock protein 70 by preconditioning with a ?-opioid receptor agonist during ischaemia and reperfusion in streptozotocin-induced diabetic rats

Kam

Chen

et al. 2004

Diabetologia

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Aims/hypothesis. The aim of this study was to determine the effects of preconditioning on injury and expression of heat shock proteins 70 in diabetic rat hearts. Methods. Diabetes was induced by an intraperitoneal injection of 65 mg kg −1 streptozotocin. Daily subcutaneous injection of 4 IU insulin started 2 weeks after streptozotocin treatment for 4 weeks. Rats were preconditioned by intravenous injection of 10 mg kg −1 U50,488H, a selective κ-opioid receptor agonist (U50,488H preconditioning). The effects of U50,488H preconditioning had previously been shown to be blocked by a selective κ-opioid receptor antagonist, nor-binaltorphimine. Twenty-four hours later, rats were subjected to 30 min of regional ischaemia by occlusion of the left coronary artery followed by 4 h of reperfusion. Infarct size was determined at the end of reperfusion. Stress-inducible and constitutive heat shock proteins 70 were analysed at the end of ischaemia and reperfusion by Western blotting.Results. Myocardial infarcts induced by ischaemia and reperfusion were greater in diabetic rats. U50,488H preconditioning significantly reduced the infarct size and increased the expression of stress-inducible heatshock protein 70 in normal rats. The effects of U50,488H preconditioning were abolished in streptozotocin-induced diabetic rats, but restored by insulin replacement. Conclusion/interpretation. In addition to a greater susceptibility to ischaemic insults, the delayed cardioprotection of U50,488H preconditioning was lost, which could at least partly be due to impaired synthesis of stress-inducible heat-shock protein 70 in diabetic rats. [Diabetologia (2004) 47:214-220] Keywords U50,488H preconditioning · κ-opioid receptor · Streptozotocin · Diabetic rats · Ischaemia and reperfusion · Cardioprotection stress inducible heat shock protein 70

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Section: Discussionmentioning

confidence: 80%

Failure to confer cardioprotection and to increase the expression of heat-shock protein 70 by preconditioning with a ?-opioid receptor agonist during ischaemia and reperfusion in streptozotocin-induced diabetic rats

Kam

Chen

et al. 2004

Diabetologia

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“…Oral administration of GGA activates protein kinase C, leading to the phosphorylation and translation of HSF1, and thus promotes the expression of HSP72 protein. 21 Similar mechanisms may underlie the induction of HSP72 with GGA treatment after SAH in the basilar artery.…”

Section: Discussionmentioning

confidence: 96%

Potential Role for Heat Shock Protein 72 in Antagonizing Cerebral Vasospasm After Rat Subarachnoid Hemorrhage

et al. 2004

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Background-Cerebral vasospasm can be defined as delayed-onset narrowing of the cerebral arteries that can occur after a spontaneous aneurysmal subarachnoid hemorrhage (SAH). Despite a large number of experimental and clinical investigations, the exact pathophysiology of vasospasm remains unknown. Using a fluorescence differential-display system, we have identified the gene encoding heat shock protein 72 (HSP72) as being highly upregulated by cerebral vasospasm. We therefore elucidated the role of the HSP72 gene in cerebral vasospasm in a rat experimental SAH model. Methods and Results-By angiography, cerebral vasospasm was detected from day 1, with maximal narrowing detected on day 2. Intracisternal injection of antisense HSP72 oligodeoxynucleotide led to specific inhibition of HSP72 gene expression and significantly aggravated cerebral vasospasm on days 2 and 3 of the angiographic studies. Oral administration of geranylgeranylacetone (GGA), an antiulcer drug, enhanced HSP72 induction and reduced cerebral vasospasm. Conclusions-These results suggest HSP72 plays a novel role in antagonizing delayed cerebral vasospasm after SAH and that GGA provides protective effects against delayed cerebral vasospasm, at least partly via induction of HSP72.

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“…These results indicate that the cardioprotective effect induced by GGA during myocardial I/R injury may be associated with the inhibition of HMGB1 expression. The cardioprotective effect induced by GGA during myocardial I/R injury has been demonstrated in previous studies (8,9), but the mechanism remains unclear. Although our findings were consistent with those of previous studies, our results further indicated that GGA inhibits HMGB1 expression during myocardial I/R.…”

Section: Discussionmentioning

confidence: 87%

“…Geranylgeranylacetone (GGA), a heat shock protein 72 (HSP72) inducer, has been reported to reduce myocardial I/R injury (8,9). However, the cardioprotective mechanism of GGA during myocardial I/R remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Geranylgeranylacetone protects against myocardial ischemia and reperfusion injury by inhibiting high-mobility group box 1 protein in rats

Wang

Min

et al. 2011

Mol Med Report

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Abstract. The high mobility group box 1 (HMGB1) protein plays an important role in myocardial ischemia and reperfusion (I/R) injury. Geranylgeranylacetone (GGA), a heat shock protein 72 inducer, has been reported to reduce myocardial I/R injury. The aim of this study was to investigate the cardioprotective mechanism of GGA during myocardial I/R injury in rats. Anesthetized male rats were treated once with GGA (200 mg/ kg, p.o.) 24 h before ischemia, and subjected to ischemia for 30 min, followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting. The results showed that pre-treatment with GGA (200 mg/kg) significantly reduced the infarct size and the levels of LDH and CK after 4 h of reperfusion (all P<0.05). GGA also significantly inhibited the increase in MDA levels and the decrease in SOD levels (both P<0.05). Meanwhile, GGA considerably suppressed the expression of HMGB1 induced by I/R. The present study suggests that GGA is capable of attenuating myocardial I/R injury by inhibiting HMGB1 expression.

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Role of protein kinase C in geranylgeranylacetone-induced expression of heat-shock protein 72 and cardioprotection in the rat heart

Cited by 65 publications

References 26 publications

Failure to confer cardioprotection and to increase the expression of heat-shock protein 70 by preconditioning with a ?-opioid receptor agonist during ischaemia and reperfusion in streptozotocin-induced diabetic rats

Failure to confer cardioprotection and to increase the expression of heat-shock protein 70 by preconditioning with a ?-opioid receptor agonist during ischaemia and reperfusion in streptozotocin-induced diabetic rats

Potential Role for Heat Shock Protein 72 in Antagonizing Cerebral Vasospasm After Rat Subarachnoid Hemorrhage

Geranylgeranylacetone protects against myocardial ischemia and reperfusion injury by inhibiting high-mobility group box 1 protein in rats

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