Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling.

Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling. Research Abstract Details 

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Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling. Abstract Text:

Meijing Wang,Wenjun Zhang,Paul Crisostomo,Troy Markel,Kirstan K Meldrum,Xin Y Fu,Daniel R Meldrum,Meijing Wang,Wenjun Zhang,Paul Crisostomo,Troy Markel,Kirstan K Meldrum,Xin Y Fu,Daniel R Meldrum,

Signal transducer and activator of transcription (STAT) 3 is involved in mediating a broad range of biological processes, including cell survival, proliferation, and immune response. Recent evidence has indicated that STAT3 in cardiomyocytes can be activated by ischemic-oxidative stress and exerts cardioprotection in the ischemic heart. There is no information, however, regarding the effect of endothelial cell-derived STAT3 on the myocardial response to ischemiareperfusion (I/R) injury. We hypothesized that the ablation of the STAT3 gene in endothelial cells would worsen postischemic myocardial function by affecting capillary network integrity, suppressing antiapoptotic signaling. Isolated hearts from wild-type and endothelial cell STAT3 knockout (STAT3KO) mice were subjected to 20 min of global ischemia followed by 60 min of reperfusion. Endothelial cell STAT3 deficiency decreased recovery of myocardial function in response to I/R, which was associated with higher levels of LDH release, decreased activation of myocardial STAT3, and elevated p38 MAPK activation in STAT3 endothelial knockout (KO) hearts. In addition, although no significant apoptosis was observed in wild-type and KO hearts, our results showed more expression of myocardial caspase-8 and more apoptosis in the myocardium around the capillary in STAT3KO mice subjected to I/R. Furthermore, endothelial cell STAT3 ablation resulted in increased myocardial expression of IL-6 and suppressor of cytokine signal 3. This study demonstrates that endothelial cell-derived STAT3 plays an important role in postischemic myocardial function.

Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling. Publishing Authors By Initials

M Wang,W Zhang,P Crisostomo,T Markel,KK Meldrum,XY Fu,DR Meldrum,M Wang,W Zhang,P Crisostomo,T Markel,KK Meldrum,XY Fu,DR Meldrum,

For similar enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research abstracts see: enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research

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Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Heart and circulat

VOLUME: 293

Page Numbers: H2101-8

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 3

MONTH: 08

YEAR: 2007

Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901228

Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling. Keywords Mesh Terms:

KEYWORDS: p38 Mitogen-Activated Protein Kinases

MESH TERMS: metabolism

Chemical & Substance for Abstract: Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling. Information

Substance Name: Caspase 8

Registry Number: EC 3.4.22.-

Grant and Affiliation Information for Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling.

AFFILIATION: Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Country: United States

AGENCY: United States NIGMS

GRANT: R01-GM-070628

ACRONYM: GM

MEDLINETA: Am J Physiol Heart Circ Physio

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