scholarly journals Ischemic preconditioning increases adenosine release and 5'-nucleotidase activity during myocardial ischemia and reperfusion in dogs. Implications for myocardial salvage.

Circulation ◽  
1993 ◽  
Vol 87 (1) ◽  
pp. 208-215 ◽  
Author(s):  
M Kitakaze ◽  
M Hori ◽  
S Takashima ◽  
H Sato ◽  
M Inoue ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemic Preconditioning ◽  
Myocardial Salvage ◽  
Ischemia And Reperfusion ◽  
Nucleotidase Activity ◽  
Myocardial Ischemia And Reperfusion ◽  
Adenosine Release

STAT signaling in ischemic heart: a role of STAT5A in ischemic preconditioning

2003 ◽  
Vol 285 (2) ◽  
pp. H476-H482 ◽  
Author(s):  
Genbu Yamaura ◽  
Tibor Turoczi ◽  
Fumio Yamamoto ◽  
M. A. Q. Siddqui ◽  
Nilanjana Maulik ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemic Preconditioning ◽  
Knockout Mice ◽  
Knockout Mouse ◽  
Src Kinase ◽  
Janus Kinase ◽  
Myocardial Infarct Size ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

We recently demonstrated that ischemic preconditioning (PC) induced by cyclic episodes of short duration of ischemia and reperfusion potentiates a signal transduction cascade involving Janus kinase (JAK) 2 and signal transducer and activator of transcription 3 (STAT3). A rapid activation of JAK and several STATs, including STAT3, STAT5A, and STAT6 also occurred during myocardial ischemia and reperfusion. This study sought to examine whether STAT5A and STAT6 were also involved in PC. Two different animal models were used: isolated perfused working rat hearts and STAT5A and STAT6 knockout mouse hearts. The results of our study indicated phosphorylation of STAT 5A and STAT6 in the preconditioned myocardium. Tyrphostin AG490, a JAK2 inhibitor, or 4-amino-5-(4-methylphenyl)-7-( t-butyl)-pyrazolo-3,4-d-pyrimidine (PPI), a Src kinase blocker, blocked STAT5A phosphorylation, whereas STAT6 phosphorylation was blocked only with tyrphostin. As expected, significant cardioprotection was achieved in the preconditioned heart as evidenced by reduced myocardial infarct size and decreased number of apoptotic cardiomyocytes. PC-mediated cardioprotection was partially abolished when hearts were pretreated with tyrphostin, PPI, or LY-294002, a phosphatidylinositol (PI)-3 kinase inhibitor. Studies with STAT5A and STAT6 knockout mouse hearts revealed that STAT6 knockout mouse hearts, and not STAT5A knockout mouse hearts, were resistant to myocardial ischemia-reperfusion injury. The hearts from STAT5A knockout mice could not be preconditioned, whereas those from STAT6 knockout mice were easily preconditioned. The results of the present study demonstrate that STAT5A, and not STAT6, plays a role in ischemic PC. For the first time, the results also indicated a role of Src kinase pathway in STAT5A PC and PI-3 kinase-Akt pathways appear to be the downstream regulator for STAT5A-STAT6 signaling pathway.

In Vivo MRI Visualization of Acute Myocardial Ischemia and Reperfusion in Ferrets by the Persistent Action of the Contrast Agent Gd(BME-DTTA)

Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3549-3559 ◽  
Author(s):  
Tamás Simor ◽  
Wen-Jang Chu ◽  
Lynne Johnson ◽  
Andras Safranko ◽  
Mark Doyle ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Contrast Agent ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

scholarly journals Activation of signaling pathways and regulatory mechanisms of mRNA translation following myocardial ischemia-reperfusion

2006 ◽  
Vol 101 (2) ◽  
pp. 576-582 ◽  
Author(s):  
Stephen J. Crozier ◽  
Xueqian Zhang ◽  
Jufang Wang ◽  
Joseph Cheung ◽  
Scot R. Kimball ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Myocardial Ischemia ◽  
Protein Expression ◽  
Signaling Pathways ◽  
Mrna Translation ◽  
Mitogen Activated Protein Kinase ◽  
Regulatory Mechanisms ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion ◽  
Mitogen Activated Protein

Protein expression in the heart is altered following periods of myocardial ischemia. The changes in protein expression are associated with increased cell size that can be maladaptive. There is little information regarding the regulation of protein expression through the process of mRNA translation during ischemia and reperfusion in the heart. Therefore, the purpose of this study was to identify changes in signaling pathways and downstream regulatory mechanisms of mRNA translation in an in vivo model of myocardial ischemia and reperfusion. Hearts were collected from rats whose left main coronary arteries had either been occluded for 25 min or reversibly occluded for 25 min and subsequently reperfused for 15 min. Following reperfusion, both the phosphoinositide 3-kinase and mitogen-activated protein kinase pathways were activated, as evidenced by increased phosphorylation of Akt (PKB), extracellular signal-regulated kinase 1/2, and p38 mitogen-activated protein kinase. Activation of Akt stimulated signaling through the protein kinase mammalian target of rapamycin, as evidenced by increased phosphorylation of two of its effectors, the ribosomal protein S6 kinase and the eukaryotic initiation factor eIF4E binding protein 1. Ischemia and reperfusion also resulted in increased phosphorylation of eIF2 and eIF2B. These changes in protein phosphorylation suggest that control of mRNA translation following ischemia and reperfusion is modulated through a number of signaling pathways and regulatory mechanisms.

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