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heart and ischemia and mitochondria

Nidhi Kuksal, Danielle Gardiner, Dake Qi, Ryan J Mailloux
Recent work has found that complex I is the sole source of reactive oxygen species (ROS) during myocardial ischemia-reperfusion (IR) injury. However, it has also been reported that heart mitochondria can also generate ROS from other sources in the respiratory chain and Krebs cycle. This study examined the impact of partial complex I deficiency due to selective loss of the Ndufs4 gene on IR injury to heart tissue. Mice heterozygous for NDUFS4 (NDUFS4+/-) did not display any significant changes in overall body or organ weight when compared to wild-type (WT) littermates...
March 1, 2018: Biochemical and Biophysical Research Communications
Amanda Bundgaard, Andrew M James, William Joyce, Michael P Murphy, Angela Fago
Freshwater turtles ( Trachemys scripta ) are among the very few vertebrates capable of tolerating severe hypoxia and reoxygenation without suffering from damage to the heart. As myocardial ischemia and reperfusion causes a burst of mitochondrial reactive oxygen species (ROS) in mammals, the question arises as to whether, and if so how, this ROS burst is prevented in the turtle heart. We find here that heart mitochondria isolated from turtles acclimated to anoxia produce less ROS than mitochondria from normoxic turtles when consuming succinate...
March 1, 2018: Journal of Experimental Biology
Xiaoou Sun, Yingying Yang, Yanxiang Xie, Xingjuan Shi, Lijie Huang, Wen Tan
It has been reported that isosteviol, a widely known sweeteners, can protect against myocardial ischemia-reperfusion (IR) injury in isolated guinea pig heart. Here, we aim to confirm the cardioprotective effect of its sodium salt, isosteviol sodium (STVNa), against IR injury and its potential molecular mechanism in H9c2 cardiomyocytes. STVNa significantly improved cell viability, restored mitochondrial membrane potential, decreased cellular reactive oxygen species generation, and inhibited cell apoptosis. Furthermore, STVNa treatment changed the morphology of mitochondria from fragmented, discontinuous forms to normal elongated, tubular forms...
January 5, 2018: Oncotarget
Erfei Song, Sofhia V Ramos, Xiaojing Huang, Ying Liu, Amy Botta, Hye Kyoung Sung, Patrick C Turnbull, Michael B Wheeler, Thorsten Berger, Derek J Wilson, Christopher G R Perry, Tak W Mak, Gary Sweeney
Lipocalin-2 (Lcn2), a critical component of the innate immune response which binds siderophores and limits bacterial iron acquisition, can elicit spillover adverse proinflammatory effects. Here we show that holo-Lcn2 (Lcn2-siderophore-iron, 1:3:1) increases mitochondrial reactive oxygen species (ROS) generation and attenuates mitochondrial oxidative phosphorylation in adult rat primary cardiomyocytes in a manner blocked by N-acetyl-cysteine or the mitochondria-specific antioxidant SkQ1. We further demonstrate using siderophores 2,3-DHBA (2,3-dihydroxybenzoic acid) and 2,5-DHBA that increased ROS and reduction in oxidative phosphorylation are direct effects of the siderophore component of holo-Lcn2 and not due to apo-Lcn2 alone...
January 29, 2018: Proceedings of the National Academy of Sciences of the United States of America
Sriram Ravindran, Kausthubh Ramachandran, Gino A Kurian
Sodium thiosulfate (STS) has shown promising effects in amelioration of myocardial ischemia-reperfusion injury (IR) in a rat model and is clinically useful in the treatment of chronic kidney disease (CKD) associated calciphylaxis. As the prevalence of cardiac complications is higher in CKD, we tested the effectiveness of STS in a rat model of adenine-induced vascular calcification and subjected the heart to IR. We observed an increased infarct size (29%) by TTC staining, lactate dehydrogenase (54%) and creatine kinase (32%) release in the coronary perfusate and altered hemodynamics compared to a normal rat treated with STS and subjected to IR...
January 20, 2018: Biochimie
Valentina M Parra, Francisco Altamirano, Carolina P Hernández-Fuentes, Dan Tong, Viktoriia Kyrychenko, David Rotter, Zully R Pedrozo, Joseph A Hill, Veronica Eisner, Sergio Lavandero, Jay W Schneider, Beverly A Rothermel
Rationale: The Regulator of Calcineurin 1 (RCAN1) inhibits calcineurin (CN), a Ca2+-activated protein phosphatase important in cardiac remodeling. In humans, RCAN1 is located on chromosome 21 in proximity to the "Down syndrome critical region." The hearts and brains of Rcan1 KO mice are more susceptible to damage from ischemia/reperfusion (I/R), however, the underlying cause is not known. Objective: Mitochondria are key mediators of I/R damage. The goal of these studies was to determine the impact of RCAN1 on mitochondrial dynamics and function...
January 23, 2018: Circulation Research
Qun Chen, Masood S Younus, Jeremy Thompson, Ying Hu, John M Hollander, Edward J Lesnefsky
BACKGROUND: Cardiac ischemia-reperfusion (IR) damages the electron transport chain (ETC) causing mitochondrial and cardiomyocyte injury. Reversible blockade of the ETC at complex I during ischemia protects the ETC and decreases cardiac injury. In the present study, we used an unbiased proteomic approach to analyze the extent of ETC-driven mitochondrial injury during IR. METHODS: Isolated-perfused mouse (C57BL/6) hearts underwent 25 min global ischemia (37{degree sign}C) and 30 min reperfusion...
December 29, 2017: American Journal of Physiology. Heart and Circulatory Physiology
Sri Rahavi Boovarahan, Gino A Kurian
Air pollution has become an environmental burden with regard to non-communicable diseases, particularly heart disease. It has been reported that air pollution can accelerate the development of heart failure and atrial fibrillation. Air pollutants encompass various particulate matters (PMs), which change the blood composition and heart rate and eventually leads to cardiac failure by triggering atherosclerotic plaque ruptures or by developing irreversible ischemia. A series of major epidemiological and observational studies have established the noxious effect of air pollutants on cardiovascular diseases (CVD), but the underlying molecular mechanisms of its susceptibility and the pathological disease events remain largely elusive and are predicted to be initiated in the cell organelle...
January 18, 2018: Reviews on Environmental Health
Terumori Satoh, Masao Saotome, Hideki Katoh, Daishi Nonaka, Prottoy Hasan, Hideharu Hayashi, Yuichiro Maekawa
Although beneficial effects of non-secreting intracellular renin (ns-renin) against ischemia have been reported, the precise mechanism remains unclear. In this study, we investigated the roles of ns-renin and mitochondrial extracellular signal-related kinase (ERK) 1/2 on mitochondrial permeability transition pore (mPTP) opening during ischemia in diabetes mellitus (DM) hearts. When isolated hearts from Wistar rats (non-DM hearts) and Goto-Kakizaki rats (DM hearts) were subjected to ischemia for 70 min by left anterior descending coronary artery ligation, DM hearts exhibited higher left ventricular (LV) developed pressure and lower LV end-diastolic pressure than non-DM hearts, suggesting ischemic resistance...
December 25, 2017: International Journal of Molecular Sciences
Douglas B Cowan, Rouan Yao, Jerusha K Thedsanamoorthy, David Zurakowski, Pedro J Del Nido, James D McCully
Tissue ischemia adversely affects the function of mitochondria, which results in impairment of oxidative phosphorylation and compromised recovery of the affected organ. The impact of ischemia on mitochondrial function has been extensively studied in the heart because of the morbidity and mortality associated with injury to this organ. As conventional methods to preserve cardiac cell viability and contractile function following ischemia are limited in their efficacy, we developed a unique approach to protect the heart by transplanting respiration-competent mitochondria to the injured region...
December 12, 2017: Scientific Reports
Michael Coronado, Giovanni Fajardo, Kim Nguyen, Mingming Zhao, Kristina B Kooiker, Gwanghyun Jung, Dong-Qing Hu, Sushma Reddy, Erik Sandoval, Aleksandr Stotland, Roberta A Gottlieb, Daniel Bernstein
Rationale: Mitochondria play a dual role in the heart, responsible for meeting energetic demands and regulating cell death. Paradigms have held that mitochondrial fission and fragmentation are the result of pathologic stresses such as ischemia, are an indicator of poor mitochondrial health, and lead to mitophagy and cell death. However, recent studies demonstrate that inhibiting fission also results in decreased mitochondrial function and cardiac impairment, suggesting that fission is important for maintaining cardiac and mitochondrial bioenergetic homeostasis...
December 12, 2017: Circulation Research
Daniel J Herr, Mauhamad Baarine, Sverre E Aune, Xiaoyang Li, Lauren E Ball, John J Lemasters, Craig C Beeson, James C Chou, Donald R Menick
RATIONALE: Recent evidence indicates that histone deacetylase enzymes (HDACs) contribute to ischemia reperfusion (I/R) injury, and pan-HDAC inhibitors have been shown to be cardioprotective when administered either before an ischemic insult or during reperfusion. We have shown previously that selective inhibition of class I HDACs provides superior cardioprotection when compared to pan-HDAC inhibition in a pretreatment model, but selective class I HDAC inhibition has not been tested during reperfusion, and specific targets of class I HDACs in I/R injury have not been identified...
January 2018: Journal of Molecular and Cellular Cardiology
Juan-Xia Zhu, Ling-Heng Kong, Chao-Feng Zhang, Na Sun, Jin-Rui Chang, Yan Xu
OBJECTIVE: To investigate the role of capsaicin (CAP) in myocardial ischemia reperfusion injury and its underlying mechanisms. METHODS: Twentyfour adult male SD rats were randomized into 4 groups,namely the control group,ischemia reperfusion group,ischemia reperfusion with CAP group,and ischemia reperfusion with CAPZ and CAP group. Isolated rat hearts underwent Langendorff perfusion. Left ventricular enddiastolic pressure (LVEDP) andleft ventricular developed pressure (LVDP) was calculated to evaluate myocardial performance at 30 min of reperfusion...
September 2017: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
Hongbao Tan, Li Chen, Jun Ma
Ischemic heart disease is a major cause of mortality and disability worldwide. Timely reperfusion is currently the most effective method of treating ischemic heart disease; however, abrupt reperfusion may cause ischemia/reperfusion (I/R) injury. Apoptosis serves an important role in the progression of myocardial I/R injury and it has been demonstrated that the mitochondria are the center of regulation for apoptosis. Penehyclidine hydrochloride (PHC) is used during surgery and has recently been identified as a new type of anticholinergic drug...
November 2017: Experimental and Therapeutic Medicine
Jessica M Bradley, Zhen Li, Chelsea L Organ, David J Polhemus, Hiroyuki Otsuka, Shashi Bhushan, Olena M Gorodnya, Mykhaylo Ruchko, Mark N Gillespie, Glenn L Wilson, David J Lefer
BACKGROUND: Oxidative stress results in mitochondrial DNA (mtDNA) damage and contributes to myocardial cell death. mtDNA repair enzymes are crucial for mtDNA repair and cell survival. We investigated a novel, mitochondrial-targeted fusion protein (Exscien1-III) containing endonuclease III in myocardial ischemia/reperfusion (MI/Rep) injury and transverse aortic constriction (TAC) induced heart failure. METHODS AND RESULTS: Male C57/BL6J mice (10-12 wks) were subjected to 45 min...
November 3, 2017: American Journal of Physiology. Heart and Circulatory Physiology
Sanhitha Nandi, Sriram Ravindran, Gino A Kurian
Cardio-protective effect of hydrogen sulfide (H2S) against myocardial ischemia reperfusion injury (I/R) via preservation of mitochondria is well documented. But the distinct role of exogenous and endogenous H2S in cardio-protection and its dependency on functional cardiac mitochondria is not understood. The present study was designed to investigate the role of exogenous H2S preconditioning on cardiac mitochondrial subpopulation namely interfibrillar (IFM) and subsarcolemmal (SSM), in attenuating I/R injury in an isolated rat heart model in the absence of endogenous H2S production...
October 26, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Run-Qing Xue, Man Xu, Xiao-Jiang Yu, Long-Zhu Liu, Wei-Jin Zang
Ischemic heart disease (IHD) is the life-threatening cardiovascular disease. Mitochondria have emerged as key participants and regulators of cellular energy demands and signal transduction. Mitochondrial quality is controlled by a number of coordinated mechanisms including mitochondrial fission, fusion and mitophagy, which plays an important role in maintaining healthy mitochondria and cardiac function. Recently, dysfunction of each process in mitochondrial quality control has been observed in the ischemic hearts...
October 25, 2017: Sheng Li Xue Bao: [Acta Physiologica Sinica]
Ayeshah A Rosdah, Simon T Bond, Priyadharshini Sivakumaran, Ashfaqul Hoque, Jonathan S Oakhill, Brian G Drew, Lea M D Delbridge, Shiang Y Lim
Cardiac stem cell (CSC) therapy is a promising approach to treat ischemic heart disease. However, the poor survival of transplanted stem cells in the ischemic myocardium has been a major impediment in achieving an effective cell-based therapy against myocardial infarction. Inhibiting mitochondrial fission has been shown to promote survival of several cell types. However, the role of mitochondrial morphology in survival of human CSC remains unknown. In this study, we investigated whether mitochondrial division inhibitor-1 (Mdivi-1), an inhibitor of mitochondrial fission protein dynamin-related protein-1 (Drp1), can improve survival of a novel population of human W8B2+ CSCs in hydrogen peroxide (H2 O2 )-induced oxidative stress and simulated ischemia-reperfusion injury models...
December 15, 2017: Stem Cells and Development
Kerstin Boengler, Péter Bencsik, János Palóczi, Krisztina Kiss, Márton Pipicz, Judit Pipis, Péter Ferdinandy, Klaus-Dieter Schlüter, Rainer Schulz
Whereas high amounts of reactive oxygen species (ROS) contribute to cardiac damage following ischemia and reperfusion (IR), low amounts function as trigger molecules in the cardioprotection by ischemic preconditioning (IPC). The mitochondrial translocation and contribution of the hydrogen peroxide-generating protein p66shc in the cardioprotection by IPC is unclear yet. In the present study, we investigated the mitochondrial translocation of p66shc, addressed the impact of p66shc on ROS formation after IR, and characterized the role of p66shc in IR injury per se and in the cardioprotection by IPC...
2017: Frontiers in Physiology
Qun Chen, Jeremy Thompson, Ying Hu, Anindita Das, Edward J Lesnefsky
Endoplasmic reticulum (ER) stress, a disturbance of the ER function, contributes to cardiac injury. ER and mitochondria are closely connected organelles within cells. ER stress contributes to mitochondrial dysfunction, which is a key factor to increase cardiac injury. Metformin, a traditional anti-diabetic drug, decreases cardiac injury during ischemia-reperfusion. Metformin also inhibits ER stress in cultured cells. We hypothesized that metformin can attenuate the ER stress-induced mitochondrial dysfunction and subsequent cardiac injury...
December 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
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