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Mitochondrial permeability transition pore

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https://www.readbyqxmd.com/read/28630136/atp-synthase-complex-and-the-mitochondrial-permeability-transition-pore-poles-of-attraction
#1
Christos Chinopoulos
No abstract text is available yet for this article.
June 19, 2017: EMBO Reports
https://www.readbyqxmd.com/read/28630004/co-releasing-molecules-2-attenuates-ox-ldl-induced-injury-in-huvecs-by-ameliorating-mitochondrial-function-and-inhibiting-wnt-%C3%AE-catenin-pathway
#2
Hai-Jian Sun, Dong-Yan Xu, Yi-Xin Sun, Tong Xue, Chen-Xing Zhang, Zhi-Xuan Zhang, Wei Lin, Ke-Xue Li
Oxidized low-density lipoprotein (ox-LDL) is well known to disrupt normal functionality of endothelium, which plays a prominent role in endothelial dysfunction in many cardiovascular diseases. CO-releasing molecule 2 (CORM-2) is a promising candidate for treatment of cardiovascular diseases. However, it has not been defined whether CORM-2 might improve endothelial injury induced by ox-LDL. The present study was undertaken to determine the regulatory role of CORM-2 in cell injury of ox-LDL-treated human umbilical vein endothelial cells (HUVECs)...
June 16, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28625317/sphingosine-1-phosphate-postconditioning-protects-against-myocardial-ischemia-reperfusion-injury-in-rats-via-mitochondrial-signaling-and-akt-gsk3%C3%AE-phosphorylation
#3
Rui Fang, Lu-Lu Zhang, Li-Zhi Zhang, Wenchang Li, Mengmeng Li, Ke Wen
BACKGROUND AND AIMS: Although preconditioning of sphingosine 1-phosphate (S1P) has been shown to protect myocytes from hypoxia reoxgenation injury in vitro, the role of S1P postconditioning on myocardial ischemia reperfusion injury (MIRI) in vivo and its related mechanism are unknown. The aim of this study was to investigate the protective role of sphingosine 1-phosphate (S1P) postconditioning in MIRI via its effects on mitochondrial signaling and Akt/Gsk3β phosphorylation. METHODS: Rats were subjected to MIRI, consisting of 30 min of ischemia followed by 120 min of reperfusion, with S1P administered at the beginning of the reperfusion...
February 2017: Archives of Medical Research
https://www.readbyqxmd.com/read/28624490/bioenergetics-dysfunction-mitochondrial-permeability-transition-pore-opening-and-lipid-peroxidation-induced-by-hydrogen-sulfide-as-relevant-pathomechanisms-underlying-the-neurological-dysfunction-characteristic-of-ethylmalonic-encephalopathy
#4
Gabriela Miranda Fernandez Cardoso, Julia Tauana Pletsch, Belisa Parmeggiani, Mateus Grings, Nícolas Manzke Glanzel, Larissa Daniele Bobermin, Alexandre Umpierrez Amaral, Moacir Wajner, Guilhian Leipnitz
Hydrogen sulfide (sulfide) accumulates at high levels in the brains of patients with ethylmalonic encephalopathy (EE). In the present study, we evaluated whether sulfide could disturb energy and redox homeostasis, and induce mitochondrial permeability transition (mPT) pore opening in rat brain aiming to better clarify the neuropathophysiology of EE. Sulfide decreased the activities of citrate synthase and aconitase in rat cerebral cortex mitochondria, and of creatine kinase (CK) in rat cerebral cortex, striatum and hippocampus supernatants...
June 14, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28608233/alleviation-by-gabab-receptors-of-neurotoxicity-mediated-by-mitochondrial-permeability-transition-pore-in-cultured-murine-cortical-neurons-exposed-to-n-methyl-d-aspartate
#5
Toshihiko Kinjo, Yoshino Ashida, Hiroshi Higashi, Satoshi Sugimura, Miho Washida, Hiroki Niihara, Kiyokazu Ogita, Yukio Yoneda, Nobuyuki Kuramoto
Mitochondrial permeability transition pore (PTP) is supposed to at least in part participate in molecular mechanisms underlying the neurotoxicity seen after overactivation of N-methyl-D-aspartate (NMDA) receptor (NMDAR) in neurons. In this study, we have evaluated whether activation of GABAB receptor (GABABR), which is linked to membrane G protein-coupled inwardly-rectifying K(+) ion channels (GIRKs), leads to protection of the NMDA-induced neurotoxicity in a manner relevant to mitochondrial membrane depolarization in cultured embryonic mouse cortical neurons...
June 12, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28600454/the-slo-w-path-to-identifying-the-mitochondrial-channels-responsible-for-ischemic-protection
#6
REVIEW
Charles Owen Smith, Keith Nehrke, Paul S Brookes
Mitochondria play an important role in tissue ischemia and reperfusion (IR) injury, with energetic failure and the opening of the mitochondrial permeability transition pore being the major causes of IR-induced cell death. Thus, mitochondria are an appropriate focus for strategies to protect against IR injury. Two widely studied paradigms of IR protection, particularly in the field of cardiac IR, are ischemic preconditioning (IPC) and volatile anesthetic preconditioning (APC). While the molecular mechanisms recruited by these protective paradigms are not fully elucidated, a commonality is the involvement of mitochondrial K(+) channel opening...
June 9, 2017: Biochemical Journal
https://www.readbyqxmd.com/read/28598232/exercise-reestablishes-autophagic-flux-and-mitochondrial-quality-control-in-heart-failure
#7
Juliane C Campos, Bruno B Queliconi, Luiz H M Bozi, Luiz R G Bechara, Paulo M M Dourado, Allen M Andres, Paulo R Jannig, Kátia M S Gomes, Vanessa O Zambelli, Cibele Rocha-Resende, Silvia Guatimosim, Patricia C Brum, Daria Mochly-Rosen, Roberta A Gottlieb, Alicia J Kowaltowski, Julio C B Ferreira
We previously reported that facilitating the clearance of damaged mitochondria through macroautophagy/autophagy protects against acute myocardial infarction. Here we characterized the impact of exercise, a safe strategy against cardiovascular disease, on cardiac autophagy and its contribution to mitochondrial quality control, bioenergetics and oxidative damage in a post-myocardial infarction-induced heart failure animal model. We found that failing hearts displayed reduced autophagic flux depicted by accumulation of autophagy-related markers and loss of responsiveness to chloroquine treatment at 4 and 12 weeks after myocardial infarction...
June 9, 2017: Autophagy
https://www.readbyqxmd.com/read/28591721/ginkgolide-k-attenuates-neuronal-injury-after-ischemic-stroke-by-inhibiting-mitochondrial-fission-and-gsk-3%C3%AE-dependent-increases-in-mitochondrial-membrane-permeability
#8
Xu Zhou, Hui-Ying Wang, Bin Wu, Cai-Yi Cheng, Wei Xiao, Zhen-Zhong Wang, Yu-Yu Yang, Ping Li, Hua Yang
Ginkgolide K (GK) belongs to the ginkgolide family of natural compounds found in Ginkgo biloba leaves, which have been used for centuries to treat cerebrovascular and cardiovascular diseases. We evaluated the protective effects of GK against neuronal apoptosis by assessing its ability to sustain mitochondrial integrity and function. Co-immunoprecipitation showed that Drp1 binding to GSK-3β was increased after an oxygen-glucose deprivation/reperfusion (OGD/R) insult in cultured neuroblastoma cells. This induced Drp1 and GSK-3β translocation to mitochondria and mitochondrial dysfunction, which was attenuated by GK...
May 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28578275/mitochondria-meditated-pathways-of-organ-failure-upon-inflammation
#9
REVIEW
Andrey V Kozlov, Jack R Lancaster, Andras T Meszaros, Adelheid Weidinger
Liver failure induced by systemic inflammatory response (SIRS) is often associated with mitochondrial dysfunction but the mechanism linking SIRS and mitochondria-mediated liver failure is still a matter of discussion. Current hypotheses suggest that causative events could be a drop in ATP synthesis, opening of mitochondrial permeability transition pore, specific changes in mitochondrial morphology, impaired Ca(2+) uptake, generation of mitochondrial reactive oxygen species (mtROS), turnover of mitochondria and imbalance in electron supply to the respiratory chain...
May 25, 2017: Redox Biology
https://www.readbyqxmd.com/read/28575497/loss-of-hepatic-lrpprc-alters-mitochondrial-bioenergetics-regulation-of-permeability-transition-and-trans-membrane-ros-diffusion
#10
Alexanne Cuillerier, Shamisa Honarmand, Virgilio J J Cadete, Matthieu Ruiz, Anik Forest, Sonia Deschênes, Claudine Beauchamp, Guy Charron, John D Rioux, Christine Des Rosiers, Eric A Shoubridge, Yan Burelle
BACKGROUND AND AIMS: The French-Canadian variant of Leigh Syndrome (LSFC) is an autosomal recessive oxidative phosphorylation (OXPHOS) disorder caused by a mutation in LRPPRC, coding for a protein involved in the stability of mitochondrially-encoded mRNAs. Low levels of LRPPRC are present in all patient tissues, but result in a disproportionately severe OXPHOS defect in the brain and liver, leading to unpredictable subacute metabolic crises. METHODS: To investigate the impact of the OXPHOS defect in the liver, we analyzed the mitochondrial phenotype in mice harboring an hepatocyte-specific inactivation of Lrpprc...
May 31, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28572055/estrogen-regulates-spatially-distinct-cardiac-mitochondrial-subpopulations
#11
Rogério Faustino Ribeiro Junior, Paula Lopes Rodrigues, Elis Aguiar Morra, Karoline Sousa Ronconi, Patrícia Ribeiro Do Val Lima, Marcella Leite Porto, Maylla Ronacher Simões, Dalton Valentim Vassallo, Suely Gomes Figueiredo, Ivanita Stefanon
Increased susceptibility to permeability transition pore (mPTP) is a significant concern to decreased cardiac performance in postmenopausal females. The goal of this study was to assess the effects of estrogen deficiency on the two spatially distinct mitochondrial subpopulations from left ventricle: subsarcolemmal mitochondria (SSM) and intermyofibrillar mitochondria (IFM) based on: morphology, membrane potential, oxidative phosphorylation, mPTP and reactive oxygen species production. Female rats (8weeks old) that underwent bilateral ovariectomy were randomly assigned to receive daily treatment with placebo (OVX), estrogen replacement (OVX+E2) and Sham for 60days...
May 29, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28566520/mitochondrial-permeability-transition-involves-dissociation-of-f1fo-atp-synthase-dimers-and-c-ring-conformation
#12
Massimo Bonora, Claudia Morganti, Giampaolo Morciano, Gaia Pedriali, Magdalena Lebiedzinska-Arciszewska, Giorgio Aquila, Carlotta Giorgi, Paola Rizzo, Gianluca Campo, Roberto Ferrari, Guido Kroemer, Mariusz R Wieckowski, Lorenzo Galluzzi, Paolo Pinton
The impact of the mitochondrial permeability transition (MPT) on cellular physiology is well characterized. In contrast, the composition and mode of action of the permeability transition pore complex (PTPC), the supramolecular entity that initiates MPT, remain to be elucidated. Specifically, the precise contribution of the mitochondrial F1FO ATP synthase (or subunits thereof) to MPT is a matter of debate. We demonstrate that F1FO ATP synthase dimers dissociate as the PTPC opens upon MPT induction. Stabilizing F1FO ATP synthase dimers by genetic approaches inhibits PTPC opening and MPT Specific mutations in the F1FO ATP synthase c subunit that alter C-ring conformation sensitize cells to MPT induction, which can be reverted by stabilizing F1FO ATP synthase dimers...
May 31, 2017: EMBO Reports
https://www.readbyqxmd.com/read/28560396/mitochondrial-ca2-removal-amplifies-trail-cytotoxicity-toward-apoptosis-resistant-tumor-cells-via-promotion-of-multiple-cell-death-modalities
#13
Natsuhiko Takata, Yohei Ohshima, Miki Suzuki-Karasaki, Yukihiro Yoshida, Yasuaki Tokuhashi, Yoshihiro Suzuki-Karasaki
Ca2+ has emerged as a new target for cancer treatment since tumor-specific traits in Ca2+ dynamics contributes to tumorigenesis, malignant phenotypes, drug resistance, and survival in different tumor types. However, Ca2+ has a dual (pro-death and pro-survival) function in tumor cells depending on the experimental conditions. Therefore, it is necessary to minimize the onset of the pro-survival Ca2+ signals caused by the therapy. For this purpose, a better understanding of pro-survival Ca2+ pathways in cancer cells is critical...
May 25, 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/28560002/prostaglandin-e1-protects-coronary-microvascular-function-via-the-glycogen-synthase-kinase-3%C3%AE-mitochondrial-permeability-transition-pore-pathway-in-rat-hearts-subjected-to-sodium-laurate-induced-coronary-microembolization
#14
Houyong Zhu, Yu Ding, Xiaoqun Xu, Meiya Li, Yangliang Fang, Beibei Gao, Hengyi Mao, Guoxin Tong, Liang Zhou, Jinyu Huang
Prostaglandin E1 (PGE1) is used as a pretreatment for ischemia reperfusion injury in many biological systems. However, its value as a pretreatment for coronary microembolization (CME) is unknown. The goal of this study was to determine whether PGE1 would protect against CME. In a CME rat model, we observed microthrombi and early myocardial ischemia, with endothelium appearing exfoliated and mitochondria having irregular morphology and decreased internal complexity. The level of fibrinogen-like protein 2 prothrombinase was increased and superoxide dismutase and catalase levels were decreased...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28559847/high-sensitivity-of-sirt3-deficient-hearts-to-ischemia-reperfusion-is-associated-with-mitochondrial-abnormalities
#15
Rebecca M Parodi-Rullán, Xavier Chapa-Dubocq, Pedro J Rullán, Sehwan Jang, Sabzali Javadov
Aim: Sirtuins are NAD(+)-dependent deacetylases that regulate cell metabolism through protein acetylation/deacetylation, and SIRT3 is the major deacetylase among mitochondrial isoforms. Here, we elucidated the possible role of acetylation of cyclophilin D, a key regulator of the mitochondrial permeability transition pore (mPTP), in mitochondria-mediated cardiac dysfunction induced by ischemia-reperfusion (IR) in wild type (WT) and SIRT3 knockout (SIRT3(-/-)) mice. Materials and Methods: Isolated and Langendorff-mode perfused hearts of WT and SIRT3(-/-) mice were subjected to 25-min global ischemia followed by 60-min of reperfusion in the presence or absence of the mPTP inhibitor, sanglifehrin A (SfA)...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28551789/mitochondria-and-cardiac-hypertrophy
#16
Heberty di Tarso Fernandes Facundo, Robert Eli Brainard, Francisco Rodrigo de Lemos Caldas, Aline Maria Brito Lucas
Cardiac tissue responds to long-term hemodynamic load through initiation of a hypertrophic remodeling program. Importantly, if not counteracted this response will eventually lead to organ failure. Cardiac hypertrophic adaptations are complex, and involve multiple cellular events and the mechanisms underlying the development of cardiac hypertrophy are not well understood. Mitochondrial dysfunction has been indicated as a potential and important player in the development of cardiac hypertrophy. Additionally, substantial evidence shows that a significant portion of mitochondrial processes, necessary for normal cardiomyocyte physiology, are impacted by these hypertrophic changes...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28551787/mechanistic-role-of-mptp-in-ischemia-reperfusion-injury
#17
Giampaolo Morciano, Massimo Bonora, Gianluca Campo, Giorgio Aquila, Paola Rizzo, Carlotta Giorgi, Mariusz R Wieckowski, Paolo Pinton
Acute myocardial infarction (MI) is a major cause of death and disability worldwide. The treatment of choice for reducing ischemic injury and limiting infarct size (IS) in patients with ST-segment elevation MI (STEMI) is timely and effective myocardial reperfusion via primary percutaneous coronary intervention (PCI). However, myocardial reperfusion itself may induce further cardiomyocyte death, a phenomenon known as reperfusion injury (RI). The opening of a large pore in the mitochondrial membrane, namely, the mitochondrial permeability transition pore (mPTP), is widely recognized as the final step of RI and is responsible for mitochondrial and cardiomyocyte death...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28551785/mitochondria-in-ischemic-heart-disease
#18
L Maximilian Buja
A core feature of ischemic heart disease is injury to cardiomyocytes (CMC). Ischemic CMC manifest the molecular mechanisms to undergo the major forms of cell injury and death, namely, oncotic necrosis, necroptosis, apoptosis and unregulated autophagy. Important modulators of ischemic injury are reperfusion and conditioning. Mitochondria have a major role in mediating the injury to CMC through membrane protein complexes referred to as death channels. Apoptosis is mediated by activation of a channel regulated by the Bcl-2 protein family leading to mitochondrial outer membrane permeabilization (MOMP)...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28551242/effect-of-mitochondrial-apoptotic-activation-through-the-mitochondrial-membrane-permeability-transition-pore-on-yak-meat-tenderness-during-postmortem-aging
#19
Lin-Lin Wang, Ling Han, Xiu-Li Ma, Qun-Li Yu, Suo-Nan Zhao
The effect of membrane permeability transition pore dependent mitochondrial apoptotic activation on yak meat tenderness was investigated. Results indicate that MPTP opening increased significantly and the mitochondrial membrane potential decreased markedly in the early aging process (P<0.05). Cytochrome c was released from the mitochondria to the cytoplasm via the MPTP in the early period. Meanwhile, the activation of procaspase-9 occurred earlier than that of procaspase-3. Cyclosporin A suppressed the MPTP opening, depolarization of the mitochondrial membrane potential, activities of caspase-9 and caspase-3, apoptosis rate, myofibril fragmentation index, reactive oxygen species generation, and Ca(2+) levels...
November 1, 2017: Food Chemistry
https://www.readbyqxmd.com/read/28542130/activation-of-transient-receptor-potential-vanilloid-4-involves-in-hypoxia-reoxygenation-injury-in-cardiomyocytes
#20
Qiong-Feng Wu, Cheng Qian, Ning Zhao, Qian Dong, Jing Li, Bin-Bin Wang, Lei Chen, Lixiu Yu, Bing Han, Yi-Mei Du, Yu-Hua Liao
Transient receptor potential vanilloid 4 (TRPV4) is highly expressed in heart and vessels and can be activated during myocardial ischemia/reperfusion (I/R). Recently, we found that treatment with a selective TRPV4 antagonist HC-067047 significantly reduced infarct size, decreased troponin T levels and improved cardiac function in murine model myocardial I/R. This study was undertaken to investigate the mechanism underlying TRPV4-mediated myocardial I/R injury. To mimic myocardial I/R injury, we established a hypoxia/reoxygenation (H/R) model in H9C2 cells and neonatal rat ventricle myocytes (NRVMs) in vitro...
May 25, 2017: Cell Death & Disease
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