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Basic Research in Cardiology

Edward D Coverstone, Richard G Bach, LiShiun Chen, Laura J Bierut, Allie Y Li, Petra A Lenzini, Heidi C O'Neill, John A Spertus, Carmen C Sucharov, Jerry A Stitzel, Joel D Schilling, Sharon Cresci
The CHRNA5 gene encodes a neurotransmitter receptor subunit involved in multiple processes, including cholinergic autonomic nerve activity and inflammation. Common variants in CHRNA5 have been linked with atherosclerotic cardiovascular disease. Association of variation in CHRNA5 and specific haplotypes with cardiovascular outcomes has not been described. The aim of this study was to examine the association of CHRNA5 haplotypes with gene expression and mortality among patients with acute myocardial infarction (AMI) and explore potential mechanisms of this association...
August 10, 2018: Basic Research in Cardiology
Heng Zhou, Ning Li, Yuan Yuan, Ya-Ge Jin, Haipeng Guo, Wei Deng, Qi-Zhu Tang
Cardiovascular diseases (CVDs) are the primary causes of death worldwide. Among the numerous signaling molecules involved in CVDs, transcriptional factors directly influence gene expression and play a critical role in regulating cell function and the development of diseases. Activating transcription factor (ATF) 3 is an adaptive-response gene in the ATF/cAMP responsive element-binding (CREB) protein family of transcription factors that acts as either a repressor or an activator of transcription via the formation of homodimers or heterodimers with other ATF/CREB members...
August 9, 2018: Basic Research in Cardiology
Jing Li, Sean XiaoXiao Cai, Quan He, Helena Zhang, Daniel Friedberg, Fangfei Wang, Andrew N Redington
MicroRNA-144 is a cytoprotective miRNA. Our previous study showed that miR-144 provides potent acute cardioprotection in an ischemia/reperfusion injury model. This study was performed to further assess whether miR-144 improves post-MI remodeling in a non-reperfused myocardial infarction (MI) model. C57BL/6 mice were subjected to MI by permanent left anterior descending artery (LAD) ligation. miR-144 was delivered by intravenous injections of 8 mg/kg, 16 mg/kg, or 32 mg/kg at day 0, day 1, day 3, and then a similar dose given once every 3 days, until day 28 after MI...
August 6, 2018: Basic Research in Cardiology
Yonis Abukar, Rohit Ramchandra, Sally G Hood, Michael J McKinley, Lindsea C Booth, Song T Yao, Clive N May
Increased cardiac sympathetic nerve activity (CSNA) is a key feature of heart failure (HF) and is associated with poor outcome. There is evidence that central angiotensinergic mechanisms contribute to the increased CSNA in HF, but the central sites involved are unknown. In an ovine, rapid pacing model of HF, we investigated the contribution of the lamina terminalis and area postrema to the increased CSNA and also the responses to fourth ventricular infusion of the angiotensin type 1 receptor antagonist losartan...
August 3, 2018: Basic Research in Cardiology
Andreas Deussen
No abstract text is available yet for this article.
August 3, 2018: Basic Research in Cardiology
Alexander M Kiel, Adam G Goodwill, Hana E Baker, Gregory M Dick, Johnathan D Tune
The local metabolic hypothesis proposes that myocardial oxygen tension determines the degree of autoregulation by increasing the production of vasodilator metabolites as perfusion pressure is reduced. Thus, normal physiologic levels of coronary venous PO2 , an index of myocardial oxygenation, are proposed to be required for effective autoregulation. The present study challenged this hypothesis through determination of coronary responses to changes in coronary perfusion pressure (CPP 140-40 mmHg) in open-chest swine in the absence (n = 7) and presence of euvolemic hemodilution (~ 50% reduction in hematocrit), with (n = 5) and without (n = 6) infusion of dobutamine to augment MVO2 ...
August 2, 2018: Basic Research in Cardiology
Jonathon P Audia, Xi-Ming Yang, Edward S Crockett, Nicole Housley, Ehtesham Ul Haq, Kristen O'Donnell, Michael V Cohen, James M Downey, Diego F Alvarez
Patients with acute myocardial infarction receive a P2Y12 receptor antagonist prior to reperfusion, a treatment that has reduced, but not eliminated, mortality, or heart failure. We tested whether the caspase-1 inhibitor VX-765 given at reperfusion (a requirement for clinical use) can provide sustained reduction of infarction and long-term preservation of ventricular function in a pre-clinical model of ischemia/reperfusion that had been treated with a P2Y12 receptor antagonist. To address, the hypothesis open-chest rats were subjected to 60-min left coronary artery branch occlusion/120-min reperfusion...
July 10, 2018: Basic Research in Cardiology
Franz Hofmann
The underlying cause of cardiac hypertrophy, fibrosis, and heart failure has been investigated in great detail using different mouse models. These studies indicated that cGMP and cGMP-dependent protein kinase type I (cGKI) may ameliorate these negative phenotypes in the adult heart. Recently, evidence has been published that cardiac mitochondrial BKCa channels are a target for cGKI and that activation of mitoBKCa channels may cause some of the positive effects of conditioning in ischemia/reperfusion injury...
June 22, 2018: Basic Research in Cardiology
C Gebhard, F Maafi, B E Stähli, J Dang, W Nachar, A B de Oliveira Moraes, A E Kernaleguen, V Lavoie, M Mecteau, T Mihalache-Avram, Y Shi, M Chabot-Blanchet, D Busseuil, D Rhainds, E Rhéaume, Jean-Claude Tardif
Aortic valve stenosis (AVS) is the most common valvular heart disease in the Western world. Therapy based on apolipoprotein A-I (apoA-I), the major protein component of high-density lipoproteins, results in AVS regression in experimental models. Nevertheless, apoA-I degradation by proteases might lead to suboptimal efficacy of such therapy. An activatable probe using a quenched fluorescently labeled full-length apoA-I protein was generated to assess apoA-I-degrading protease activity in plasma derived from 44 men and 20 women with severe AVS (age 65...
June 18, 2018: Basic Research in Cardiology
Jan Beckendorf, Maarten M G van den Hoogenhof, Johannes Backs
In the cardiomyocyte, CaMKII has been identified as a nodal influencer of excitation-contraction and also excitation-transcription coupling. Its activity can be regulated in response to changes in intracellular calcium content as well as after several post-translational modifications. Some of the effects mediated by CaMKII may be considered adaptive, while effects of sustained CaMKII activity may turn into the opposite and are detrimental to cardiac integrity and function. As such, CaMKII has long been noted as a promising target for pharmacological inhibition, but the ubiquitous nature of CaMKII has made it difficult to target CaMKII specifically where it is detrimental...
June 15, 2018: Basic Research in Cardiology
Lei Hou, Junjie Guo, Feng Xu, Xinyu Weng, Wenhui Yue, Junbo Ge
Asymmetric dimethylarginine (ADMA) is a risk factor for heart diseases. Dimethylarginine dimethylaminohydrolase (DDAH) enzymes are key proteins for ADMA degradation. Endothelial DDAH1 is a vital regulator of angiogenesis. DDAH1 is also expressed in cardiomyocytes. However, the role of DDAH1 in cardiomyocytes needs further clarification. Herein, we used an inducible cardiac-specific DDAH1 knockdown mouse (cardiac DDAH1-/- ) to investigate the role of cardiomyocyte DDAH1 in left-ventricular (LV) remodeling after acute myocardial infarction (AMI)...
June 11, 2018: Basic Research in Cardiology
Felix Wiedmann, Jan S Schulte, Bruna Gomes, Maria-Patapia Zafeiriou, Antonius Ratte, Franziska Rathjens, Edda Fehrmann, Beatrix Scholz, Niels Voigt, Frank Ulrich Müller, Dierk Thomas, Hugo A Katus, Constanze Schmidt
Understanding molecular mechanisms involved in atrial tissue remodeling and arrhythmogenesis in atrial fibrillation (AF) is essential for developing specific therapeutic approaches. Two-pore-domain potassium (K2P ) channels modulate cellular excitability, and TASK-1 (K2P 3.1) currents were recently shown to alter atrial action potential duration in AF and heart failure (HF). Finding animal models of AF that closely resemble pathophysiological alterations in human is a challenging task. This study aimed to analyze murine cardiac expression patterns of K2P channels and to assess modulation of K2P channel expression in murine models of AF and HF...
June 7, 2018: Basic Research in Cardiology
Alan J Mouton, Kristine Y DeLeon-Pennell, Osvaldo J Rivera Gonzalez, Elizabeth R Flynn, Tom C Freeman, Jeffrey J Saucerman, Michael R Garrett, Yonggang Ma, Romain Harmancey, Merry L Lindsey
In response to myocardial infarction (MI), cardiac macrophages regulate inflammation and scar formation. We hypothesized that macrophages undergo polarization state changes over the MI time course and assessed macrophage polarization transcriptomic signatures over the first week of MI. C57BL/6 J male mice (3-6 months old) were subjected to permanent coronary artery ligation to induce MI, and macrophages were isolated from the infarct region at days 1, 3, and 7 post-MI. Day 0, no MI resident cardiac macrophages served as the negative MI control...
June 4, 2018: Basic Research in Cardiology
Marina V Basalay, Sean M Davidson, Andrey V Gourine, Derek M Yellon
Remote ischaemic conditioning (RIC) is a promising method of cardioprotection, with numerous clinical studies having demonstrated its ability to reduce myocardial infarct size and improve prognosis. On the other hand, there are several clinical trials, in particular those conducted in the setting of elective cardiac surgery, that have failed to show any benefit of RIC. These contradictory data indicate that there is insufficient understanding of the mechanisms underlying RIC. RIC is now known to signal indiscriminately, protecting not only the heart, but also other organs...
June 1, 2018: Basic Research in Cardiology
Min Park, Peter Sandner, Thomas Krieg
The nitric oxide (NO)-protein kinase G (PKG) pathway has been known for some time to be an important target for cardioprotection against ischaemia/reperfusion injury and heart failure. While many approaches for reducing infarct size in patients have failed in the past, the advent of novel drugs that modulate cGMP and its downstream targets shows very promising results in recent preclinical and clinical studies. Here, we review main aspects of the NO-PKG pathway in light of recent drug development and summarise potential cardioprotective strategies in which cGMP is the main player...
May 15, 2018: Basic Research in Cardiology
Watthana Nuntaphum, Wanpitak Pongkan, Suwakon Wongjaikam, Savitree Thummasorn, Pongpan Tanajak, Juthamas Khamseekaew, Kannaporn Intachai, Siriporn C Chattipakorn, Nipon Chattipakorn, Krekwit Shinlapawittayatorn
Vagus nerve stimulation (VNS) has been shown to exert cardioprotection against myocardial ischemia/reperfusion (I/R) injury. However, whether the cardioprotection of VNS is mainly due to direct activation through its ipsilateral efferent fibers (motor) rather than indirect effects mediated by the afferent fibers (sensory) have not been clearly understood. We hypothesized that VNS exerts cardioprotection predominantly through its efferent vagal fibers. Thirty swine (30-35 kg) were randomized into five groups: I/R no VNS (I/R), and left mid-cervical VNS with both vagal trunks intact (LC-VNS), with left vagus nerve transection (LtVNX), with right vagus nerve transection (RtVNX) and with atropine pretreatment (Atropine), respectively...
May 9, 2018: Basic Research in Cardiology
Hao Zhou, Jin Wang, Pingjun Zhu, Hong Zhu, Sam Toan, Shunying Hu, Jun Ren, Yundai Chen
Mitochondrial fission and mitophagy are considered key processes involved in the pathogenesis of cardiac microvascular ischemia reperfusion (IR) injury although the upstream regulatory mechanism for fission and mitophagy still remains unclear. Herein, we reported that NR4A1 was significantly upregulated following cardiac microvascular IR injury, and its level was positively correlated with microvascular collapse, endothelial cellular apoptosis and mitochondrial damage. However, NR4A1-knockout mice exhibited resistance against the acute microvascular injury and mitochondrial dysfunction compared with the wild-type mice...
May 9, 2018: Basic Research in Cardiology
Lorena A Vargas, Fernanda Carrizo Velasquez, Bernardo V Alvarez
The authors have retracted this article [1] because of modifications in the control lanes of Figs. 2a and 8a of the COX1 blot obtained for 18-week-old rats (rotation, horizontal flipping and re-use of the control lanes for the 35-week-old rats blot). In light of the concerns raised, the conclusions drawn in this article cannot be relied upon.
April 18, 2018: Basic Research in Cardiology
Derek M Yellon, Zhenhe He, Rayomand Khambata, Amrita Ahluwalia, Sean M Davidson
There remains a significant un-met need to reduce the extent of myocardial injury caused by ischaemia and reperfusion injury in patients experiencing an ST-elevation MI. Although nitric oxide is central to many cardioprotective strategies currently undergoing investigation, cardioprotection from the delivery of nitrates/nitrites has been inconsistently observed. The route of administration appears to be a critical variable. The glyceryl trinitrate (GTN) patch is commonly used as a simple and practical means of delivering nitric oxide to patients with ischaemic heart disease, but whether acute cardioprotection can be achieved by application of a GTN patch has not been investigated before...
April 17, 2018: Basic Research in Cardiology
Zhen-Guo Ma, Jia Dai, Yu-Pei Yuan, Zhou-Yan Bian, Si-Chi Xu, Ya-Ge Jin, Xin Zhang, Qi-Zhu Tang
Previous studies have suggested the involvement of CD4 + T lymphocytes in cardiac remodelling. T-bet can direct Th1 lineage commitment. This study aimed to investigate the functional significance of T-bet in cardiac remodelling induced by pressure overload using T-bet global knockout rats. Increased T-bet levels were observed in rodent and human hypertrophied hearts. T-bet deficiency resulted in a less severe hypertrophic phenotype in rats. CD4 + T-lymphocyte reconstitution in T-bet-/- rats resulted in aggravated cardiac remodelling...
March 21, 2018: Basic Research in Cardiology
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