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Condition: Heart Attack

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Total 280 results found since Jan 2013.

Silencing collapsin response mediator protein-2 reprograms macrophage phenotype and improves infarct healing in experimental myocardial infarction model
Conclusion: CRMP2 is highly expressed in M1 macrophages and silencing CRMP2 reprograms macrophage phenotype and improves infarct healing in atherosclerotic mice.
Source: Journal of Inflammation - February 10, 2015 Category: Allergy & Immunology Authors: Long-Shu ZhouGuo-Long ZhaoQiang LiuShu-Cai JiangYun WangDong-Mei Zhang Source Type: research

Activation of NADPH oxidase mediates increased endoplasmic reticulum stress and left ventricular remodeling after myocardial infarction in rabbits.
In this study, we proposed to test whether activation of NADPH oxidase in the remote non-infarcted myocardium mediates ER stress and left ventricular (LV) remodeling after MI. Rabbits with MI or sham operation were randomly assigned to orally receive an NADPH oxidase inhibitor apocynin or placebo for 30days. The agents were administered beginning at 1week after surgery. MI rabbits exhibited decreases in LV fractional shortening, LV ejection fraction and the first derivative of the LV pressure rise, which were abolished by apocynin treatment. NADPH oxidase Nox2 protein and mRNA expression was increased in the remote non-inf...
Source: Biochimica et Biophysica Acta - January 20, 2015 Category: Biochemistry Authors: Li B, Tian J, Sun Y, Xu TR, Chi RF, Zhang XL, Hu XL, Zhang YA, Qin FZ, Zhang WF Tags: Biochim Biophys Acta Source Type: research

Deoxycholic acid-modified polyethylenimine based nanocarriers for RAGE siRNA therapy in acute myocardial infarction.
Abstract The activation of receptor for advanced glycation end products (RAGE) signaling is mainly associated with myocardial ischemia/reperfusion injury. Thus the blockade of RAGE-ligands axis can be considered as a potential therapeutic strategy to protect myocardial infarction after ischemia/reperfusion injury. Herein, we strengthened the cardioprotective effect with combinatorial treatment of soluble RAGE (sRAGE) and RAGE siRNA (siRAGE) causing more effective suppression of RAGE-mediated signaling transduction. For pharmacological blockade of RAGE, sRAGE, the extracellular ligand binding domain of RAGE, acts a...
Source: Archives of Pharmacal Research - January 6, 2015 Category: Drugs & Pharmacology Authors: Ku SH, Hong J, Moon H, Jeong JH, Mok H, Park S, Choi D, Kim SH Tags: Arch Pharm Res Source Type: research

Microglial P2X7 receptor in the hypothalamic paraventricular nuclei contributes to sympathoexcitatory responses in acute myocardial infarction rat
Publication date: 5 February 2015 Source:Neuroscience Letters, Volume 587 Author(s): Dongshu Du , Meiyan Jiang , Min Liu , Jin Wang , Chunmei Xia , Ruijuan Guan , Linlin Shen , Yonghua Ji , Danian Zhu Several pieces of evidence indicate that the microglial P2X7 receptor (P2X7R) regulate cardiovascular activities. We explored the possible roles of microglial P2X7R in the PVN mediated sympathoexcitatory responses in acute myocardial infarction (AMI) rat. Sprague–Dawley rats underwent coronary artery ligation to induce AMI. The rats received intraperitoneal administration of the P2X7R antagonist Brilliant Blue-G (BBG, 25 ...
Source: Neuroscience Letters - December 29, 2014 Category: Neuroscience Source Type: research

Anti-Inflammatory Peptides From Cardiac Progenitors Ameliorate Dysfunction After Myocardial Infarction Heart Failure
Conclusions Soluble JAM-A secreted from cardiac progenitor cells reduces infiltration of neutrophils after myocardial infarction and ameliorates tissue damage through prevention of excess inflammation. Our finding may lead to a new therapy for cardiovascular disease by using the anti-inflammatory effect of JAM-A.
Source: JAHA:Journal of the American Heart Association - December 2, 2014 Category: Cardiology Authors: Liu, M.-L., Nagai, T., Tokunaga, M., Iwanaga, K., Matsuura, K., Takahashi, T., Kanda, M., Kondo, N., Naito, A. T., Komuro, I., Kobayashi, Y. Tags: Heart Failure Source Type: research

Exendin-4 protects adipose-derived mesenchymal stem cells from apoptosis induced by hydrogen peroxide through the PI3K/Akt-Sfrp2 pathways.
Abstract Adipose-derived mesenchymal stem cells (ADMSCs)-based therapy is a promising modality for the treatment of myocardial infarction in the future. However, the majority of transplanted cells are readily lost after transplantation because of hypoxia and oxidative stress. An efficient means to enhance the ability of ADMSCs to survive under pathologic conditions is required. In our study, we explored the effects of exendin-4 (Ex-4) on ADMSCs apoptosis in vitro induced by hydrogen peroxide, focusing in particular on mitochondrial apoptotic pathways and PI3K/Akt-secreted frizzled-related protein 2 (Sfrp2) surviva...
Source: Free Radical Biology and Medicine - October 16, 2014 Category: Biology Authors: Zhou H, Yang J, Xin T, Li D, Guo J, Hu S, Zhou S, Zhang T, Zhang Y, Han T, Chen Y Tags: Free Radic Biol Med Source Type: research

Expression of fibulin-6 in failing hearts and its role for cardiac fibroblast migration
Conclusion Fibulin-6, a fibroblast-released ECM protein, may play an important role during MR by imparting an effect on CF migration in close and complementary interplay with TGF-β1 signalling.
Source: Cardiovascular Research - August 26, 2014 Category: Cardiology Authors: Chowdhury, A., Herzog, C., Hasselbach, L., Khouzani, H. L., Zhang, J., Hammerschmidt, M., Rudat, C., Kispert, A., Gaestel, M., Menon, M. B., Tudorache, I., Hilfiker-Kleiner, D., Muhlfeld, C., Schmitto, J. D., Muller, M., Theilmeier, G. Tags: Cardiac biology and remodelling Source Type: research

Specific inhibition of HDAC4 in cardiac progenitor cells enhances myocardial repairs
We have recently shown that in vivo inhibition of histone deacetylase (HDAC) stimulates endogenous myocardial regeneration in infarcted hearts (Zhang L et al. J Pharmacol Exp Ther 341: 285–293, 2012). Furthermore, our observation demonstrates that HDAC inhibition promotes cardiogenesis, which is associated with HDAC4 reduction. However, it remains unknown as to whether specific inhibition of HDAC4 modulates cardiac stem cells (CSCs) to facilitate myocardial repair and to preserve cardiac performance. c-kit+ CSCs were isolated from adult mouse hearts and were transfected with HDAC4 siRNA to knockdown HDAC4 of c-kit+ C...
Source: AJP: Cell Physiology - August 15, 2014 Category: Cytology Authors: Zhang, L. X., DeNicola, M., Qin, X., Du, J., Ma, J., Tina Zhao, Y., Zhuang, S., Liu, P. Y., Wei, L., Qin, G., Tang, Y., Zhao, T. C. Tags: ARTICLES Source Type: research

Mineralocorticoid and angiotensin II type 1 receptors in the paraventricular nucleus contribute to sympathetic hyperactivity and cardiac dysfunction in rats post myocardial infarction.
This article is protected by copyright. All rights reserved. PMID: 24951624 [PubMed - as supplied by publisher]
Source: The Journal of Physiology - June 20, 2014 Category: Physiology Authors: Huang BS, Chen A, Ahmad M, Wang HW, Leenen FH Tags: J Physiol Source Type: research

Specific Inhibition of HDAC4 in Cardiac Progenitor Cells Enhances Myocardial Repairs.
Abstract We have recently shown that in vivo inhibition of histone deacetylase (HDAC) stimulates endogenous myocardial regeneration in infarcted hearts. Furthermore, our observation demonstrates that HDAC inhibition promotes cardiogenesis, which is associated with HDAC4 reduction. However, it remains unknown as to whether specific inhibition of HDAC4 modulates cardiac stem cells (CSCs) to facilitate myocardial repair and to preserve cardiac performance. c-kit(+)CSCs were isolated from adult mouse hearts and were transfected with HDAC4siRNA to knockdown HDAC4 of c-kit(+)CSCs. The transfection of HDAC4siRNA caused a...
Source: Am J Physiol Cell Ph... - June 18, 2014 Category: Cytology Authors: Zhang LX, DeNicola M, Qin X, Du J, Ma J, Zhao TY, Zhuang S, Liu PY, Wei L, Qin G, Tang Y, Zhao TC Tags: Am J Physiol Cell Physiol Source Type: research

p27-Regulated Cardiac Autophagy Cell Biology
p27Kip1 (p27), a key regulator of cell division, has been implicated in autophagy of cancer cells. However, its role in autophagy, the evolutionarily conserved catabolic process that enables cells to remove unwanted proteins and damaged organelles, had not been examined in the heart. Here we report that ectopic delivery of a p27 fusion protein (TAT-p27) was sufficient to induce autophagy in neonatal rat ventricular cardiomyocytes in vitro, under basal conditions and after glucose deprivation. Conversely, lentivirus-delivered shRNA against p27 successfully reduced p27 levels and suppressed basal and glucose-deprived levels ...
Source: Journal of Biological Chemistry - June 12, 2014 Category: Chemistry Authors: Sun, X., Momen, A., Wu, J., Noyan, H., Li, R., von Harsdorf, R., Husain, M. Tags: Molecular Bases of Disease Source Type: research

Cardiac RNAi therapy using RAGE siRNA/deoxycholic acid-modified polyethylenimine complexes for myocardial infarction.
Abstract Inflammatory response in myocardial ischemia-reperfusion injury plays a critical role in ventricular remodeling. To avoid deleterious effects of overwhelming inflammation, we blocked the expression of receptor for advanced glycation end-products (RAGE), a key mediator of the local and systemic inflammatory responses, via RNAi mechanism. Herein, a facial amphipathic deoxycholic acid-modified low molecular weight polyethylenimine (DA-PEI) was used as a siRNA delivery carrier to myocardium. The DA-PEI conjugate formed a stable complex with siRNA via electrostatic and hydrophobic interactions. The siRAGE/DA-P...
Source: Biomaterials - June 7, 2014 Category: Materials Science Authors: Hong J, Ku SH, Lee MS, Jeong JH, Mok H, Choi D, Kim SH Tags: Biomaterials Source Type: research

Bone Morphogenetic Protein‐10 induces cardiomyocyte proliferation and improves cardiac function after myocardial infarction
Heart disease is among the leading causes of death worldwide, and the limited proliferation of mammalian cardiomyocytes prevents heart regeneration in response to injury. Bone morphogenetic protein‐10 (BMP10) exerts multiple roles in various developmental events; however, the effect of BMP10 and the underlying mechanism involved in cardiac repair remains unclear. After stimulation with the recombinant BMP10, an obvious dose‐dependent cardiomyocyte proliferation and reentry of differentiated mammalian cardiomyocytes into the cell cycle was observed. Furthermore, BMP10 stimulation strikingly enhanced Tbx20 expression. Fu...
Source: Journal of Cellular Biochemistry - June 6, 2014 Category: Biochemistry Authors: Lijun Sun, Jing Yu, Shun Qi, Yuewen Hao, Ying Liu, Zhenwu Li Tags: Article Source Type: research

Inhibition of MMP-2 expression affects metabolic enzyme expression levels: Proteomic analysis of rat cardiomyocytes.
In this study we examined the effect of inhibition of MMP-2 expression, using siRNA, on the cardiomyocyte proteome. Isolated cardiomyocytes were transfected with MMP-2 siRNA and incubated for 24 hours. Control cardiomyocytes from the same heart were transfected with scrambled siRNA following the same protocol. Comparison of control cardiomyocyte proteomes with proteomes from MMP-2 suppressed cardiomyocytes revealed 13 protein spots of interest (9 protein spots increased; 4 decreased). Seven protein spots were identified as mitochondrial enzymes involved in energy production and represent: ATP synthase beta subunit, dihydro...
Source: Journal of Proteomics - April 23, 2014 Category: Biochemistry Authors: Lin HB, Sharma K, Bialy D, Wawrzynska M, Purves R, Cayabyab FS, Wozniak M, Sawicki G Tags: J Proteomics Source Type: research

In Vivo Silencing of the Transcription Factor IRF5 Reprograms the Macrophage Phenotype and Improves Infarct Healing
ObjectivesThe aim of this study was to test whether silencing of the transcription factor interferon regulatory factor 5 (IRF5) in cardiac macrophages improves infarct healing and attenuates post–myocardial infarction (MI) remodeling.BackgroundIn healing wounds, the M1 toward M2 macrophage phenotype transition supports resolution of inflammation and tissue repair. Persistence of inflammatory M1 macrophages may derail healing and compromise organ functions. The transcription factor IRF5 up-regulates genes associated with M1 macrophages.MethodsHere we used nanoparticle-delivered small interfering ribonucleic acid (siRNA) ...
Source: Journal of the American College of Cardiology: Cardiovascular Imaging - April 14, 2014 Category: Radiology Source Type: research