Erythropoietin prevents the acute myocardial inflammatory response induced by ischemia/reperfusion via induction of AP-1

Tao, Rui; Feng, Qingping; Lei, Ming; Peng, Tianqing; Zhang, Jianhua; Xu, Ming; Abel, E. Dale; Xenocostas, Anargyros; Kvietys, Peter R.

doi:10.1016/j.cardiores.2004.11.019

Cited by 136 publications

(97 citation statements)

References 43 publications

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“…As mentioned above EPO in various studies has been reported to exert number of important actions like anti-oxidative (Genc et al, 2004;Signore et al, 2006;Xue et al, 2007;Wang et al, 2009), neuroprotective (Morishita et al, 1997;Lewczuk et al, 2000;Siren et al, 2001b), neurotrophic (Viviani et al, 2005) effects and a vital role in hippocampal LTP (Adamcio et al, 2008;El-Kordi et al, 2009). EPO has also shown to exert potential anti-inflammatory actions (Rui et al, 2005;Liu et al, 2006) and role of inflammation in the pathobiology of AD is well documented (Granic et al, 2009;Salminen et al, 2009). Therefore, with support from literature and data in hand it may be proposed that EPO mediated beneficial effect in STZ (i.c.v.…”

Section: Discussionmentioning

confidence: 96%

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Kumar

Jaggi

Singh

2010

Korean J Physiol Pharmacol

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The present study was undertaken to explore the potential of erythropoietin in memory deficits of mice. Memory impairment was produced by scopolamine (0.5 mg/kg, i.p.) and intracerebroventricular streptozotocin (i.c.v STZ, 3 mg/kg, 10 μl, 1 st and 3 rd day) in separate groups of animals. Morris watermaze test was employed to assess learning and memory. The levels of brain thio-barbituric acid reactive species (TBARS) and reduced glutathione (GSH) were estimated to assess degree of oxidative stress. Brain acetylcholinesterase enzyme (AChE) activity was also measured. Scopolamine/streptozotocin administration induced significant impairment of learning and memory in mice as indicated by marked decrease in Morris water-maze performance. Scopolamine/streptozotocin administration also produced a significant enhancement of brain AChE activity and brain oxidative stress (an increase in TBARS and a decrease in GSH) levels. Treatment of erythropoietin (500 and 1,000 IU/Kg i.p.) significantly reversed scopolamine-as well as streptozotocin-induced learning and memory deficits along with attenuation of those-induced rise in brain AChE activity and brain oxidative stress levels. It may be concluded that erythropoietin exerts a beneficial effect in memory deficits of mice possibly through its multiple actions including potential anti-oxidative effect.

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Section: Discussionmentioning

confidence: 96%

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Kumar

Jaggi

Singh

2010

Korean J Physiol Pharmacol

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“…Myocardial Inflammation-As an index of polymorphonuclear neutrophil infiltration, myeloperoxidase activity in the myocardium was determined by measuring hydrogen peroxide-dependent oxidation of 3,3Ј, 5,5Ј-tetramethylbenzidine as described previously (33). To quantify the mast cells in the heart, cardiac tissue sections were stained with 0.02% toluidine blue in 0.25% acetic acid (pH 2.0 -2.5).…”

Section: Capn4mentioning

confidence: 99%

Deficiency of Capn4 Gene Inhibits Nuclear Factor-κB (NF-κB) Protein Signaling/Inflammation and Reduces Remodeling after Myocardial Infarction

Wei²,

Wang

et al. 2012

Journal of Biological Chemistry

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Background:The causal role of calpain in myocardial remodeling after infarction has not been addressed. Results: Deficiency of Capn4 inhibited NF-B signaling and inflammation and reduced myocardial remodeling, dysfunction, and mortality after infarction. Conclusion: Calpain contributes to myocardial inflammation and remodeling after infarction. Significance: This study provides a significant insight into the function of calpain in post-myocardial infarction remodeling.

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“…Western blot. Phosphorylated and total protein of interest in endothelial cells was assessed by Western blot as previously described (39,40). In brief, after challenge, the cells were harvested in lysis buffer, sonicated, and 5 g of cell protein was resolved by 10% SDS-PAGE.…”

Section: Assaysmentioning

confidence: 99%

Alveolar Macrophages from Septic Mice Promote Polymorphonuclear Leukocyte Transendothelial Migration via an Endothelial Cell Src Kinase/NADPH Oxidase Pathway

Wang

Tao

Yang

et al. 2008

The Journal of Immunology

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Alveolar macrophages (AMφ) have been implicated in the polymorphonuclear leukocyte (PMN) recruitment to the lungs during sepsis. Using an in vivo murine model of sepsis (feces in the peritoneum), we show that peritonitis leads to increased activation of AMφ and PMN migration into pulmonary alveoli. To assess cellular mechanisms, an in vitro construct of the pulmonary vascular-interstitial interface (murine AMφ, pulmonary endothelial cells, and PMN) and a chimera approach were used. Using immunologic (Abs) and genetic blockade (CXCR2-deficient AMφ), we show that CXC chemokines in septic plasma are responsible for the activation of AMφ. The activated AMφ can promote PMN transendothelial migration, even against a concentration gradient of septic plasma, by generating platelet-activating factor and H2O2. Platelet-activating factor/H2O2 induce an oxidant stress in the adjacent endothelial cells, an event that appears to be a prerequisite for PMN transendothelial migration, since PMN migration is abrogated across Cu/Zn-superoxide dismutase overexpressing endothelial cells. Using gp91-deficient endothelial cells, we show that NADPH oxidase plays an important role in the AMφ-induced PMN transendothelial migration. Pharmacologic/small interfering RNA blockade of Src kinase inhibits AMφ-induced endothelial NADPH oxidase activation and PMN migration. Collectively, our findings indicate that the PMN transendothelial migration induced by septic AMφ is dependent on the generation of superoxide in endothelial cells via the Src kinase/NADPH oxidase signaling pathway.

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Erythropoietin prevents the acute myocardial inflammatory response induced by ischemia/reperfusion via induction of AP-1

Abstract: Collectively, these findings indicate that EPO can ameliorate the myocardial inflammatory response in both in vitro and in vivo models of I/R. This beneficial effect of EPO is mediated by eNOS-derived NO via a PI3-kinase-dependent activation of AP-1.

Cited by 136 publications

References 43 publications

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Deficiency of Capn4 Gene Inhibits Nuclear Factor-κB (NF-κB) Protein Signaling/Inflammation and Reduces Remodeling after Myocardial Infarction

Alveolar Macrophages from Septic Mice Promote Polymorphonuclear Leukocyte Transendothelial Migration via an Endothelial Cell Src Kinase/NADPH Oxidase Pathway

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