Effects of acupuncture pretreatment on ischemic cardiac muscle cell apoptosis and gene expression in ischemia-reperfusion rats

2009 ◽  
Vol 7 (2) ◽  
pp. 71-74
Author(s):  
Yu-hui Zhao ◽  
Zhong-ren Sun
Keyword(s):  
Gene Expression ◽  
Cardiac Muscle ◽  
Muscle Cell ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion ◽  
Cardiac Muscle Cell ◽  
Muscle Cell Apoptosis

Cardiotrophin-1 phosphoaylates akt and bad, and inhibits cardiac muscle cell apoptosis via PI3-kinase-dependent pathway

1999 ◽  
Vol 5 (3) ◽  
pp. 37
Author(s):  
Koichiro Kuwahara ◽  
Yoshihiko Saito ◽  
Ichiro Kishimoto ◽  
Masaki Harada ◽  
Ichiro Hamanaka ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Muscle Cell ◽  
Cell Apoptosis ◽  
Pi3 Kinase ◽  
Cardiac Muscle Cell ◽  
Muscle Cell Apoptosis ◽  
Dependent Pathway

The protective effect of AT1-antibody against myocardial ischemia-reperfusion injury through inhibition of inflammation and apoptosis

2015 ◽  
Vol 3 (4) ◽  
pp. 295-305
Author(s):  
Najah R. Hadi ◽  
Fadhil G. Al-Amran
Keyword(s):  
Myocardial Ischemia ◽  
Protective Effect ◽  
Cardiac Muscle ◽  
Muscle Cell ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Muscle Cell ◽  
Myocardial Ischemia And Reperfusion ◽  
Myocardial Ischemia Reperfusion ◽  
Underlying Mechanisms

Myocardial ischemia and reperfusion (I/R) injury is known to occur on restoration of coronary flow after a period of myocardial ischemia. Angiotensin II (Ang II) is the most important bioactive substance of the renin-angioensin system (RAS), and exerts its physiological actions through AT1 receptors by regulating vascular tension and blood flow, and promoting cell growth and proliferation. The aim of the present study is to investigate the effects and its possible underlying mechanisms of AT1-AB on myocardial ischemia/reperfusion (I/R) injury. To test this hypothesis, we randomly assigned four groups (six mice per group) for experiment. To produce myocardial injury, the left anterior coronary artery (LAD) was occluded for 30 min, followed by 120 min of reperfusion in anesthetized mice. In the mice heart subjected to I/R injury, pretreatment AT1-AB (1mcg/gm) decreased the pathological scores of myocardium, and significantly attenuated I/R-induced increases of myocardial TNFα, IL-1β, IL-6. Further, 1mcg/gm AT1-AB significantly attenuated cTn-I and reduced apoptosis index of cardiac muscle cell of mice subjected to I/R injury. Therefore, these results demonstrate that AT1-AB exhibits significant protective effect against myocardial I/R injury which is related to inhibition of the release of inflammatory cytokines and the apoptosis of cardiac muscle cell.

scholarly journals Marginal dietary zinc deficiency in vivo induces vascular smooth muscle cell apoptosis in large arteries

2013 ◽  
Vol 99 (3) ◽  
pp. 525-534 ◽  
Author(s):  
Keith Allen-Redpath ◽  
Ou Ou ◽  
John H. Beattie ◽  
In-Sook Kwun ◽  
Jorg Feldmann ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Zinc Deficiency ◽  
Vascular Smooth Muscle Cell ◽  
Cell Apoptosis ◽  
Large Arteries ◽  
Muscle Cell Apoptosis

Mast cell chymase induces smooth muscle cell apoptosis by disrupting NF-κB-mediated survival signaling☆

2006 ◽  
Vol 312 (8) ◽  
pp. 1289-1298 ◽  
Author(s):  
M LESKINEN ◽  
H HEIKKILA ◽  
M SPEER ◽  
J HAKALA ◽  
M LAINE ◽  
...  
Keyword(s):  
Mast Cell ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cell Apoptosis ◽  
Survival Signaling ◽  
Muscle Cell Apoptosis ◽  
Mast Cell Chymase

scholarly journals Vascular smooth muscle cell apoptosis in aneurysmal, occlusive, and normal human aortas

2000 ◽  
Vol 31 (3) ◽  
pp. 567-576 ◽  
Author(s):  
Vincent L. Rowe ◽  
Scott L. Stevens ◽  
Tonya T. Reddick ◽  
Michael B. Freeman ◽  
Robert Donnell ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Apoptosis ◽  
Normal Human ◽  
Muscle Cell Apoptosis

scholarly journals Dialysis Accelerates Medial Vascular Calcification in Part by Triggering Smooth Muscle Cell Apoptosis

Circulation ◽  
2008 ◽  
Vol 118 (17) ◽  
pp. 1748-1757 ◽  
Author(s):  
Rukshana C. Shroff ◽  
Rosamund McNair ◽  
Nichola Figg ◽  
Jeremy N. Skepper ◽  
Leon Schurgers ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Vascular Calcification ◽  
Muscle Cell ◽  
Cell Apoptosis ◽  
Muscle Cell Apoptosis

scholarly journals Mechanisms for the adverse effects of late gestational increases in maternal cortisol on the heart revealed by transcriptomic analyses of the fetal septum

2014 ◽  
Vol 46 (15) ◽  
pp. 547-559 ◽  
Author(s):  
Elaine M. Richards ◽  
Charles E. Wood ◽  
Maria Belen Rabaglino ◽  
Andrew Antolic ◽  
Maureen Keller-Wood
Keyword(s):  
Gene Expression ◽  
Gene Ontology ◽  
Cell Apoptosis ◽  
Metabolic Pathways ◽  
Fetal Heart ◽  
Pathway Inference ◽  
Apoptosis Pathways ◽  
Altered Metabolism ◽  
Mitochondrial Number ◽  
Muscle Cell Apoptosis

We have previously shown in sheep that 10 days of modest chronic increase in maternal cortisol resulting from maternal infusion of cortisol (1 mg/kg/day) caused fetal heart enlargement and Purkinje cell apoptosis. In subsequent studies we extended the cortisol infusion to term, finding a dramatic incidence of stillbirth in the pregnancies with chronically increased cortisol. To investigate effects of maternal cortisol on the heart, we performed transcriptomic analyses on the septa using ovine microarrays and Webgestalt and Cytoscape programs for pathway inference. Analyses of the transcriptomic effects of maternal cortisol infusion for 10 days (130 day cortisol vs 130 day control), or ∼25 days (140 day cortisol vs 140 day control) and of normal maturation (140 day control vs 130 day control) were performed. Gene ontology terms related to immune function and cytokine actions were significantly overrepresented as genes altered by both cortisol and maturation in the septa. After 10 days of cortisol, growth factor and muscle cell apoptosis pathways were significantly overrepresented, consistent with our previous histologic findings. In the term fetuses (∼25 days of cortisol) nutrient pathways were significantly overrepresented, consistent with altered metabolism and reduced mitochondria. Analysis of mitochondrial number by mitochondrial DNA expression confirmed a significant decrease in mitochondria. The metabolic pathways modeled as altered by cortisol treatment to term were different from those modeled during maturation of the heart to term, and thus changes in gene expression in these metabolic pathways may be indicative of the fetal heart pathophysiologies seen in pregnancies complicated by stillbirth, including gestational diabetes, Cushing's disease and chronic stress.

Sign in / Sign up

Export Citation Format

Share Document