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Condition: Heart Attack

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Total 280 results found since Jan 2013.

Inhibition of MiR-92a May Protect Endothelial Cells After Acute Myocardial Infarction in Rats: Role of KLF2/4.
CONCLUSIONS MiR-92a was involved in the endothelial injury process after AMI and was able to suppress KLF2 and KLF4 expression. PMID: 27411964 [PubMed - in process]
Source: Medical Science Monitor - July 16, 2016 Category: Research Tags: Med Sci Monit Source Type: research

Suppressive effect of epigallocatechin ‐3‐O‐gallate on endoglin molecular regulation in myocardial fibrosis in vitro and in vivo
In conclusion, epigallocatechin‐3‐O‐gallate (EGCG) attenuated the endoglin expression and myocardial fibrosis by anti‐inflammatory effect in vitro and in vivo, the novel suppressive effect was mediated through JNK/AP‐1 pathway.
Source: Journal of Cellular and Molecular Medicine - June 15, 2016 Category: Molecular Biology Authors: Chiu ‐Mei Lin, Hang Chang, Bao‐Wei Wang, Kou‐Gi Shyu Tags: Original Article Source Type: research

Suppressive effect of epigallocatechin‐3‐O‐gallate on endoglin molecular regulation in myocardial fibrosis in vitro and in vivo
In conclusion, epigallocatechin‐3‐O‐gallate (EGCG) attenuated the endoglin expression and myocardial fibrosis by anti‐inflammatory effect in vitro and in vivo, the novel suppressive effect was mediated through JNK/AP‐1 pathway.
Source: Journal of Cellular and Molecular Medicine - June 15, 2016 Category: Molecular Biology Authors: Chiu‐Mei Lin, Hang Chang, Bao‐Wei Wang, Kou‐Gi Shyu Tags: Original Article Source Type: research

Suppressive effect of epigallocatechin-3-O-gallate on endoglin molecular regulation in myocardial fibrosis in vitro and in vivo.
In conclusion, epigallocatechin-3-O-gallate (EGCG) attenuated the endoglin expression and myocardial fibrosis by anti-inflammatory effect in vitro and in vivo, the novel suppressive effect was mediated through JNK/AP-1 pathway. PMID: 27306149 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - June 15, 2016 Category: Molecular Biology Authors: Lin CM, Chang H, Wang BW, Shyu KG Tags: J Cell Mol Med Source Type: research

siRNA nanoparticles reduce post-heart attack inflammation
Technique could help reduce the risk of dangerous complications.
Source: Nanotechweb.org News - June 13, 2016 Category: Nanotechnology Source Type: news

Research Articles RNAi targeting multiple cell adhesion molecules reduces immune cell recruitment and vascular inflammation after myocardial infarction
Myocardial infarction (MI) leads to a systemic surge of vascular inflammation in mice and humans, resulting in secondary ischemic complications and high mortality. We show that, in ApoE–/– mice with coronary ligation, increased sympathetic tone up-regulates not only hematopoietic leukocyte production but also plaque endothelial expression of adhesion molecules. To counteract the resulting arterial leukocyte recruitment, we developed nanoparticle-based RNA interference (RNAi) that effectively silences five key adhesion molecules. Simultaneously encapsulating small interfering RNA (siRNA)–targeting intercel...
Source: Science Translational Medicine - June 7, 2016 Category: Biomedical Science Authors: Sager, H. B., Dutta, P., Dahlman, J. E., Hulsmans, M., Courties, G., Sun, Y., Heidt, T., Vinegoni, C., Borodovsky, A., Fitzgerald, K., Wojtkiewicz, G. R., Iwamoto, Y., Tricot, B., Khan, O. F., Kauffman, K. J., Xing, Y., Shaw, T. E., Libby, P., Langer, R., Tags: Research Articles Source Type: research

MicroRNA-150 Inhibits the Activation of Cardiac Fibroblasts by Regulating c-Myb
Conclusion: These findings reveal that miR-150 acts as a pivotal regulator of pressure overload-induced cardiac fibrosis by regulating c-Myb.Cell Physiol Biochem 2016;38:2103-2122
Source: Cellular Physiology and Biochemistry - May 17, 2016 Category: Cytology Source Type: research

Gallic acid-l-leucine (GAL) conjugate enhances macrophage phagocytosis via inducing leukotriene B4 12-hydroxydehydrogenase (LTB4DH) expression
Publication date: June 2016 Source:Molecular Immunology, Volume 74 Author(s): Yuanyuan Cheng, Hung-Fat Tse, Xuechen Li, Yifan Han, Jianhui Rong Timely clearance of apoptotic cells is an important step in the resolution of ongoing inflammation and the restoration of tissue integrity and function after acute myocardial infarction. Natural products gallic acid and l-leucine are well-documented for anti-inflammatory and anabolic effects. We synthesized gallic acid-l-leucine (GAL) conjugate via direct coupling gallic acid and l-leucine. The aim of the present study was to investigate the effect of GAL conjugate on the ph...
Source: Molecular Immunology - May 1, 2016 Category: Allergy & Immunology Source Type: research

Macrophage migration inhibitory factor promotes cardiac stem cell proliferation and endothelial differentiation through the activation of the PI3K/Akt/mTOR and AMPK pathways.
In conclusion, our results suggest that MIF promotes mCSC survival, proliferation and endothelial differentiation through the activation of the PI3K/Akt/mTOR and AMPK signaling pathways. Thus, MIF may prove to be a potential therapeutic factor in the treatment of heart failure and myocardial infarction by activating CSCs. PMID: 27035848 [PubMed - as supplied by publisher]
Source: International Journal of Molecular Medicine - March 28, 2016 Category: Molecular Biology Authors: Cui J, Zhang F, Wang Y, Liu J, Ming X, Hou J, Lv B, Fang S, Yu B Tags: Int J Mol Med Source Type: research

Tripartite Motif Protein 72 Regulates the Proliferation and Migration of Rat Cardiac Fibroblasts via the Transforming Growth Factor-β Signaling Pathway
Conclusions: We have demonstrated that Trim72 might play a pivotal role in the proliferation of neonatal rat cardiac fibroblasts, which could be a potential target for the treatment of cardiac fibrosis. However, the involvement of other signaling pathways and factors in the formation of cardiac fibrosis cannot be excluded.Cardiology 2016;134:340-346
Source: Cardiology - March 18, 2016 Category: Cardiology Source Type: research

ERK1/2 MAPK signaling in hypothalamic paraventricular nucleus contributes to sympathetic excitation in rats with heart failure after myocardial infarction
Brain MAPK signaling pathways are activated in heart failure (HF) induced by myocardial infarction and contribute to augmented sympathetic nerve activity. We tested whether decreasing ERK1/2 (also known as p44/42 MAPK) signaling in the hypothalamic paraventricular nucleus (PVN), a forebrain source of presympathetic neurons, would reduce the upregulation of sympathoexcitatory mediators in the PVN and augmented sympathetic nerve activity in rats with HF. Sprague-Dawley rats underwent left anterior descending coronary artery ligation to induce HF, with left ventricular dysfunction confirmed by echocardiography. One week after...
Source: AJP: Heart and Circulatory Physiology - March 15, 2016 Category: Cardiology Authors: Yu, Y., Wei, S.-G., Zhang, Z.-H., Weiss, R. M., Felder, R. B. Tags: CARDIOVASCULAR NEUROHORMONAL REGULATION Source Type: research

Exendin-4 protects bone marrow-derived mesenchymal stem cells against oxygen/glucose and serum deprivation-induced apoptosis through the activation of the cAMP/PKA signaling pathway and the attenuation of ER stress.
Abstract Exendin-4 (ex-4) is a long-acting glucagon-like peptide-1 receptor (GLP-1R) agonist which exerts beneficial effects on glycemic control and promotes cell viability. In the present study, we investigated the anti-apoptotic effects of ex-4, as well as the potential mechanisms responsible for these effects in rat bone marrow-derived mesenchymal stem cells (BM-MSCs) under conditions of oxygen, glucose and serum deprivation (OGD). The apoptosis of the MSCs was induced by subjecting the cells to OGD conditions for 4 h and was detected by Annexin V/PI and Hoechst 33258 staining. The MSCs were pre-conditio...
Source: International Journal of Molecular Medicine - February 29, 2016 Category: Molecular Biology Authors: He J, Wang C, Sun Y, Lu B, Cui J, Dong N, Zhang M, Liu Y, Yu B Tags: Int J Mol Med Source Type: research

ERK1/2 MAPK Signaling in Hypothalamic Paraventricular Nucleus Contributes to Sympathetic Excitation in Rats with Heart Failure after Myocardial Infarction.
Abstract Brain mitogen-activated protein kinase (MAPK) signaling pathways are activated in heart failure (HF) induced by myocardial infarction and contribute to augmented sympathetic nerve activity. We tested whether silencing brain extracellular signal-regulated kinases 1 and 2 (ERK1/2, also known as p44/42 MAPK) in the hypothalamic paraventricular nucleus (PVN), a forebrain source of presympathetic neurons, would reduce the upregulation of sympatho-excitatory mediators in the PVN and the augmented sympathetic nerve activity in rats with HF. Sprague-Dawley rats underwent left anterior descending coronary artery l...
Source: American Journal of Physiology. Heart and Circulatory Physiology - January 22, 2016 Category: Physiology Authors: Yu Y, Wei SG, Zhang ZH, Weiss RM, Felder RB Tags: Am J Physiol Heart Circ Physiol Source Type: research

PEDF and 34-mer inhibit angiogenesis in the heart by inducing tip cells apoptosis via up-regulating PPAR-γ to increase surface FasL
Abstract Pigment epithelial-derived factor (PEDF) is a potent anti-angiogenic factor whose effects are partially mediated through the induction of endothelial cell apoptosis. However, the underlying mechanism for PEDF and the functional PEDF peptides 34-mer and 44-mer to inhibit angiogenesis in the heart has not been fully established. In the present study, by constructing adult Sprague–Dawley rat models of acute myocardial infarction (AMI) and in vitro myocardial angiogenesis, we showed that PEDF and 34-mer markedly inhibits angiogenesis by selectively inducing tip cells apoptosis rather than quiescent cells. ...
Source: Apoptosis - January 1, 2016 Category: Molecular Biology Source Type: research

BDNFVal66met polymorphism: a potential bridge between depression and thrombosis
Conclusion</div>Activation of platelets, alteration in coagulation pathways, and changes in vessel wall protein expression in BDNF<sup>Met/Met</sup> mice recapitulate well the features occurring in the anxiety/depression condition. Furthermore, our data suggest that the BDNFVal66Met polymorphism contribute to the individual propensity for arterial thrombosis related to AMI.</span>
Source: European Heart Journal - December 26, 2015 Category: Cardiology Source Type: research