The expression of heat shock protein 60 in myocardium of patients with chronic atrial fibrillation

Schafler, A. E.; Kirmanoglou, Kiriakos; Balbach, Jochen; Pecher, P.; Hannekum, A; Schumacher, B.

doi:10.1007/s003950200019

Cited by 45 publications

(34 citation statements)

References 13 publications

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“…The abundance of IGF-1 receptor in myocardium is reduced in animal models of diabetes, as shown in the present study. This is different from ischemic cardiomyopathy and hypertrophic cardiomyopathy, which are associated with increased IGF-1 receptor expression and increased Hsp60 expression in myocardium (20 -22), probably representing a myocardial selfdefense mechanism (8). Because IGF-1 has cardiac protective action, reduced IGF-1 receptor and its signaling can potentially lead to decreased myocardial protection during myocardial ischemia and thus may play a fundamental role during the development of diabetic cardiomyopathy.…”

Section: Discussionmentioning

confidence: 96%

Insulin Deficiency Downregulated Heat Shock Protein 60 and IGF-1 Receptor Signaling in Diabetic Myocardium

et al. 2005

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Heat shock protein (Hsp)60 and IGF-1 receptor signaling protect cardiac muscle against injury. The abundance of cardiac IGF-1 receptor can be upregulated by Hsp60, but how diabetes modulates cardiac muscle Hsp60 has not yet been defined. We investigated the changes of Hsp60 and IGF-1 receptor signaling in the diabetic myocardium and studied how diabetes modulates Hsp60 and IGF-1 receptor in diabetic myocardium. In the streptozotocin (STZ)-induced diabetic rat, downregulation of Hsp60 and IGF-1 receptor occurred 4 days after induction of diabetes. IGF-1 activation of IGF-1 receptor, Mek, and Akt were reduced accordingly in the diabetic myocardium. The independent effect of insulin and hyperglycemia on Hsp60 was investigated in primary cardiomyocytes. Incubating cardiomyocytes with insulin was associated with dose-dependent increase of Hsp60 protein. In contrast, the abundance of Hsp60 was not affected by high concentration of glucose in these cells. To further determine the independent effects of hyperglycemia and insulin deficiency on the changes of myocardial Hsp60 and IGF-1 receptor, we used phlorizin to normalize blood glucose in diabetic rats. In the phlorizin-treated diabetic rats, myocardial Hsp60 was lower than that of the normal controls. In contrast, insulin treatment normalized myocardial Hsp60 in the diabetic rats. Because phlorizin does not alter insulin secretion, Hsp60 expression was modulated by insulin and not by hyperglycemia. Similar changes of Hsp60 and IGF-1 receptor were observed in the skeletal muscle of STZ-induced diabetic rats. These findings suggest that insulin deficiency is a novel mechanism that leads to downregulation of Hsp60 in diabetic muscle tissues. The development of diabetic cardiomyopathy might have involved downregulation of Hsp60 and subsequent reduction of IGF-1 receptor signaling. Diabetes 54: 175-181, 2005

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Section: Discussionmentioning

confidence: 96%

Insulin Deficiency Downregulated Heat Shock Protein 60 and IGF-1 Receptor Signaling in Diabetic Myocardium

et al. 2005

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“…HSP60 protein was found to be increased in atrial myocardial samples of patients with chronic AF compared with patients in sinus rhythm [47,48]. HSP10 was also found to be increased [48].…”

Section: Hsp60 Increase In Atrial Fibrillation: Cause or Consequence?mentioning

confidence: 88%

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

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Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecular chaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60, the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotective but a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examples of specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicate a pathogenic role for HSP60 but also its potential as a biomarker with applications for diagnosis, assessing prognosis and response to treatment, as well as for preventing and treating CVD.

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“…As discussed earlier, HSPD1 expression is increased in ischemic and hypertrophic cardiomyopathies (Li et al 1998, Schafler et al 2002, Sakai et al 2003, and decreased in the diabetic myocardium (Chen et al 2005). The present study shows that in fructose-fed rats, administration of amlodipine normalizes both BP and HSPD1 levels despite elevated insulin levels, suggesting that only hyperinsulinemia does not up-regulate myocardial HSPD1 levels.…”

Section: Nomentioning

confidence: 80%

“…Heat shock proteins play cardio-protective roles during myocardial injury and their expression typically increases upon myocardial stress (Latchman 2001, Lepore et al 2001, Delogu et al 2002, Cornelussen et al 2003. Several studies have shown the potentially important function of heat shock protein 60 (HSPD1) in the heart (Lau et al 1997, Latchman 2001, Snoeckx et al 2001, Kirchhoff et al 2002, Schafler et al 2002, Shamaei-Tousi et al 2007). Its expression is increased under ischemic distress (Snoeckx et al 2001), while its over-expression leads to the inhibition of apoptosis in cardiomyocytes that have undergone ischemic and reperfusion injuries (Izaki et al 2001).…”

Section: Introductionmentioning

confidence: 99%

“…Increased HSPD1 expression during ischemic and reperfusion injuries (Latchman 2001, Kirchhoff et al 2002 and in ischemic and hypertrophic cardiomyopathies (Li et al 1998, Sakai et al 2003 probably represent a myocardial self-defense mechanism (Schafler et al 2002). However, HSPD1 expression has been found to be reduced in diabetic myocardium (Chen et al 2005).…”

Section: Introductionmentioning

confidence: 99%

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Myocardial heat shock protein 60 expression in insulin-resistant and diabetic rats

Chen¹,

Wu²,

Juan³

et al. 2008

Journal of Endocrinology

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Heat shock protein 60 (HSPD1) plays a critical role in myocardial protection. Its reduced expression may lower myocardial protection against ischemic injury in the diabetic state. This study was conducted to investigate the natural course of fructose-fed insulin-resistant rats, define changes in myocardial HSPD1 expression, and determine the effects of thiazolidinedione or anti-hypertensive treatment. Results showed that insulin resistance with hyperinsulinemia and hypertension developed after 6 weeks of fructose feeding. This time-course study also showed that myocardial HSPD1 expression was mildly increased in week 6 (PZ0 . 05) and significantly increased in week 8. Rosiglitazone-treated rats had restored systolic blood pressure (BP) and normalized plasma insulin level during oral glucose tolerance tests, whereas amlodipine-treated rats restored only systolic BP. Both amlodipine and rosiglitazone treatments normalized the abundance of myocardial HSPD1 expression in fructose-fed rats. When these rats received streptozotocin injection and diabetes developed, myocardial HSPD1 expression decreased despite persistent hypertension. In conclusion, this is the first study to report that myocardial HSPD1 expression is increased in high-fructose-fed rats, which may be due to increased BP. Once the high-fructose-fed rats developed diabetes with insulin deficiency, the myocardial HSPD1 expression decreased in spite of persistent hypertension.

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The expression of heat shock protein 60 in myocardium of patients with chronic atrial fibrillation

Abstract: This result indicates an up regulation of HSP60 in response to chronic atrial fibrillation.

Cited by 45 publications

References 13 publications

Insulin Deficiency Downregulated Heat Shock Protein 60 and IGF-1 Receptor Signaling in Diabetic Myocardium

Insulin Deficiency Downregulated Heat Shock Protein 60 and IGF-1 Receptor Signaling in Diabetic Myocardium

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Myocardial heat shock protein 60 expression in insulin-resistant and diabetic rats

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