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Mitochondrial permeability transition pore

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https://www.readbyqxmd.com/read/28922345/tilianin-post-conditioning-attenuates-myocardial-ischemia-reperfusion-injury-via-mitochondrial-protection-and-inhibition-of-apoptosis
#1
Yangyang Wang, Yong Yuan, Xinchun Wang, Yanfang Wang, Jiang Cheng, Li Tian, Xinhong Guo, Dongmei Qin, Wenjiang Cao
BACKGROUND The aim of this study was to investigate the role of tilianin in modulating mitochondrial functions and mitochondria-mediated apoptosis during cardio-protection. MATERIAL AND METHODS Myocardial ischemia/reperfusion (I/R) injury was induced by 30 minutes coronary occlusion followed by two hours reperfusion in Sprague-Dawley rats. To investigate the cardio-protective effects of tilianin, apoptosis was evaluated by TUNEL. Mitochondrial ultrastructure and function were assessed by transmission electron microscopy, dynamics of mitochondrial permeability transition pore (mPTP) opening and ATP production in the myocardium; Ca2+ content and reactive oxygen species (ROS) were measured to evaluated the level of damage factors in the mitochondria...
September 18, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28921048/antibacterial-and-antitumor-activity-of-bogorol-b-jx-isolated-from-brevibacillus-laterosporus-jx-5
#2
Hongxia Jiang, Chao Ji, Junkang Sui, Rongbo Sa, Xiaohui Wang, Xunli Liu, Tai L Guo
Antimicrobial peptides are promising anti-infective agent candidates because they have a broad antimicrobial spectrum and bioactivity and are unlikely to elicit antibiotic resistance. The bogorols represent a new cationic antibiotic peptide and possess great therapeutic potential because of their bioactivity and precise mode of action. Here, we report that Bogorol B-JX (BBJX), a peptide previously isolated from Brevibacillus laterosporus JX-5 by us, has significant antibacterial and antitumor activities in vitro...
September 18, 2017: World Journal of Microbiology & Biotechnology
https://www.readbyqxmd.com/read/28918598/triacsin-c-reduces-lipid-droplet-formation-and-induces-mitochondrial-biogenesis-in-primary-rat-hepatocytes
#3
Carlos R P Dechandt, Felippe H Zuccolotto-Dos-Reis, Bruno G Teodoro, Anna Maria A P Fernandes, Marcos N Eberlin, Isis C Kettelhut, Carlos Curti, Luciane C Alberici
Intracellular long-chain acyl-CoA synthetases (ACSL) activate fatty acids to produce acyl-CoA, which undergoes β-oxidation and participates in the synthesis of esterified lipids such as triacylglycerol (TAG). Imbalances in these metabolic routes are closely associated with the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Triacsin C is one of the few compounds that inhibit TAG accumulation into lipid droplets (LD) by suppressing ACSL activity. Here we report that treatment of primary rat hepatocytes with triacsin C at concentrations lower than the IC50 (4...
September 16, 2017: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/28913661/discovery-of-non-peptidic-small-molecule-inhibitors-of-cyclophilin-d-as-neuroprotective-agents-in-a%C3%AE-induced-mitochondrial-dysfunction
#4
Insun Park, Ashwini M Londhe, Ji Woong Lim, Beoung-Geon Park, Seo Yun Jung, Jae Yeol Lee, Sang Min Lim, Kyoung Tai No, Jiyoun Lee, Ae Nim Pae
Cyclophilin D (CypD) is a mitochondria-specific cyclophilin that is known to play a pivotal role in the formation of the mitochondrial permeability transition pore (mPTP).The formation and opening of the mPTP disrupt mitochondrial homeostasis, cause mitochondrial dysfunction and eventually lead to cell death. Several recent studies have found that CypD promotes the formation of the mPTP upon binding to β amyloid (Aβ) peptides inside brain mitochondria, suggesting that neuronal CypD has a potential to be a promising therapeutic target for Alzheimer's disease (AD)...
September 14, 2017: Journal of Computer-aided Molecular Design
https://www.readbyqxmd.com/read/28906548/activation-of-g-protein-coupled-estrogen-receptor-1-at-the-onset-of-reperfusion-protects-the-myocardium-against-ischemia-reperfusion-injury-by-reducing-mitochondrial-dysfunction-and-mitophagy
#5
Yansheng Feng, Ngonidzashe B Madungwe, Carolina Victoria da Cruz Junho, Jean C Bopassa
BACKGROUND AND PURPOSE: Recent evidence indicates that Gper1 (G Protein-coupled Estrogen Receptor 1) mediates acute pre-ischemic estrogen-induced protection of the myocardium from ischemia/reperfusion injury via a signaling cascade that includes PKC translocation, ERK1/2 /GSK-3β phosphorylation and the inhibition of the mitochondrial permeability transition pore (mPTP) opening. Here, we investigated the impact and mechanism involved in post-ischemic Gper1 activation in ischemia/reperfusion injury...
September 14, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28899790/alisporivir-rescues-defective-mitochondrial-respiration-in-duchenne-muscular-dystrophy
#6
Marco Schiavone, Alessandra Zulian, Sara Menazza, Valeria Petronilli, Francesco Argenton, Luciano Merlini, Patrizia Sabatelli, Paolo Bernardi
Duchenne muscular dystrophy (DMD) is a severe muscle disease of known etiology without effective, or generally applicable therapy. Mitochondria are affected by the disease in animal models but whether mitochondrial dysfunction is part of the pathogenesis in patients remains unclear. We show that primary cultures obtained from muscle biopsies of DMD patients display a decrease of the respiratory reserve, a consequence of inappropriate opening of the permeability transition pore (PTP). Treatment with the cyclophilin inhibitor alisporivir - a cyclosporin A derivative that desensitizes the PTP but does not inhibit calcineurin - largely restored the maximal respiratory capacity without affecting basal oxygen consumption in cells from patients, thus reinstating a normal respiratory reserve...
September 9, 2017: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/28878624/cell-death-in-the-developing-brain-after-hypoxia-ischemia
#7
REVIEW
Claire Thornton, Bryan Leaw, Carina Mallard, Syam Nair, Masako Jinnai, Henrik Hagberg
Perinatal insults such as hypoxia-ischemia induces secondary brain injury. In order to develop the next generation of neuroprotective therapies, we urgently need to understand the underlying molecular mechanisms leading to cell death. The cell death mechanisms have been shown to be quite different in the developing brain compared to that in the adult. The aim of this review is update on what cell death mechanisms that are operating particularly in the setting of the developing CNS. In response to mild stress stimuli a number of compensatory mechanisms will be activated, most often leading to cell survival...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28874733/mitochondrial-permeability-transition-pore-sensitivity-to-opening-and-mechanistic-dependence-on-substrate-availability
#8
Thomas Briston, Malcolm Roberts, Sian Lewis, Ben Powney, James M Staddon, Gyorgy Szabadkai, Michael R Duchen
Mitochondrial Ca(2+) uptake has a key role in cellular Ca(2+) homeostasis. Excessive matrix Ca(2+) concentrations, especially when coincident with oxidative stress, precipitate opening of an inner mitochondrial membrane, high-conductance channel: the mitochondrial permeability transition pore (mPTP). mPTP opening has been implicated as a final cell death pathway in numerous diseases and therefore understanding conditions dictating mPTP opening is crucial for developing targeted therapies. Here, we have investigated the impact of mitochondrial metabolic state on the probability and consequences of mPTP opening...
September 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28874678/mitochondrial-cyclophilin-d-ablation-is-associated-with-the-activation-of-akt-p70s6k-pathway-in-the-mouse-kidney
#9
Jelena Klawitter, Alexander Pennington, Jost Klawitter, Joshua M Thurman, Uwe Christians
The mitochondrial matrix protein cyclophilin D (CypD) is an essential component of the mitochondrial permeability transition pore (MPTP). Here we characterized the effects of CypD ablation on bioenergetics in the kidney. CypD loss triggers a metabolic shift in Ppif-/- male and female mouse kidneys towards glycolysis and Krebs cycle activity. The shift is accompanied by increased glucose consumption and a transcriptional upregulation of effectors of glucose metabolism in the kidney. These included activation of Akt, AMPK (only in males) and p70S6K kinases...
September 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28866381/cytochrome-c-oxidase-inhibition-by-calcium-at-physiological-ionic-composition-of-the-medium-implications-for-physiological-significance-of-the-effect
#10
Tatiana V Vygodina, Elizaveta Mukhaleva, Natalia V Azarkina, Alexander A Konstantinov
Cytochrome c oxidase (CcO) from mammalian mitochondria binds Ca(2+) and Na(+) in a special cation binding site. Binding of Ca(2+) brings about partial inhibition of the enzyme while Na(+) competes with Ca(2+) for the binding site and protects the enzyme from the inhibition [Vygodina, T., Kirichenko, A. and Konstantinov, A.A. (2013). Direct Regulation of Cytochrome c Oxidase by Calcium Ions. PLoS One 8(9): e74436]. In the original studies, the inhibition was found to depend significantly on the ionic composition of the buffer...
August 31, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28842823/in-vitro-toxicity-of-perfluorooctane-sulfonate-on-rat-liver-hepatocytes-probability-of-distructive-binding-to-cyp-2e1-and-involvement-of-cellular-proteolysis
#11
Mehdi Rajabnia Khansari, Bahareh Sadat Yousefsani, Farzad Kobarfard, Mehrdad Faizi, Jalal Pourahmad
Perfluorooctanesulfonate (PFOS), an anthropogenic fluorosurfactant, is one of the most common global pollutants. PFOS is used in various consumer products to provide soil, oil, and water resistance to materials used in clothing, upholstery, and food packaging. PFOS is persistent, bioaccumulative, and toxic to mammalian species. In this study, the cellular mechanisms involved in PFOS hepatotoxicity were evaluated. For this purpose, we determined oxidative stress markers including cell lysis, ROS generation, lipid peroxidation, glutathione depletion, mitochondrial membrane potential decrease, lysosomal membrane leakiness, and cellular proteolysis...
August 25, 2017: Environmental Science and Pollution Research International
https://www.readbyqxmd.com/read/28840566/photo-induced-oxidative-stress-impairs-mitochondrial-metabolism-in-neurons-and-astrocytes
#12
Elena Berezhnaya, Maria Neginskaya, Anatoly B Uzdensky, Andrey Y Abramov
Photodynamic therapy is selective destruction of cells stained with a photosensitizer upon irradiation with light at a specific wavelength in the presence of oxygen. Cell death upon photodynamic treatment is known to occur mainly due to free radical production and subsequent development of oxidative stress. During photodynamic therapy of brain tumors, healthy cells are also damaged; considering this, it is important to investigate the effect of the treatment on normal neurons and glia. We employed live-cell imaging technique to investigate the cellular mechanism of photodynamic action of radachlorin (200 nM) on neurons and astrocytes in primary rat cell culture...
August 24, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28838811/mitochondrial-calcium-imbalance-in-parkinson-s-disease
#13
REVIEW
Marthe H R Ludtmann, Andrey Y Abramov
Multiple factors are involved in the mechanism(s) of neuronal loss in neurodegenerative disorders whilst mitochondria are thought to play a central role in neurodegeneration of Parkinson's disease. Mitochondria are vital to cellular functions by supplying energy in form of ATP and affect cell physiology via calcium, ROS and signalling proteins. Changes in mitochondrial calcium homeostasis and ROS overproduction can induce cell death by triggering mitochondrial permeability transition pore opening. One of the major triggers for PTP is mitochondrial calcium overload...
August 26, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28827152/neuropathic-pain-attenuates-ischemia-reperfusion-injury-through-%C3%AE-2-adrenergic-pathway
#14
Shigeaki Kawai, Tokuhiro Yamada, Tadashi Matsuura, Tomoharu Funao, Kiyonobu Nishikawa
AIMS: The relationship between neuropathic pain and myocardial infarction (MI) was uncertain because of some medication or underlying diseases. This study investigated the impact of neuropathic pain on ischemia reperfusion injury using isolated rat hearts and cardiomyocytes. MAIN METHODS: Male Sprague-Dawley rats were assigned to the control and allodynia (AL) groups, with the latter subjected to the fifth lumbar spinal-nerve ligation. First, isolated hearts underwent 25-min ischemia and 90-min reperfusion to assess hemodynamic changes and MI area...
October 15, 2017: Life Sciences
https://www.readbyqxmd.com/read/28819942/study-of-the-relationship-between-ages-and-oxidative-stress-damage-to-trophoblast-cell-mitochondria
#15
Lingling Jiang, Jianying Yan, Lixiang Wu
OBJECTIVES: To study the influence of AGEs on placental trophoblast mitochondria oxidative stress, and to explore the possible pathogenesis which may participate in pre-eclampsia. MATERIAL AND METHODS: Human trophoblast cells from early pregnancy were cultured by an enzyme-digestion method. When trophoblast cells reached approximately 70-80% after passages, they were incubated with pre-eclampsia serum for 24 hours. A fluorescent dye assay was applied to measure the mitochondrial membrane potential; ELISA was used to measure the activity of the mitochondrial permeability transition pore...
2017: Ginekologia Polska
https://www.readbyqxmd.com/read/28815521/endoplasmic-reticulum-mitochondria-communication-through-ca-2-signaling-the-importance-of-mitochondria-associated-membranes-mams
#16
Saverio Marchi, Mart Bittremieux, Sonia Missiroli, Claudia Morganti, Simone Patergnani, Luigi Sbano, Alessandro Rimessi, Martijn Kerkhofs, Jan B Parys, Geert Bultynck, Carlotta Giorgi, Paolo Pinton
The execution of proper Ca(2+) signaling requires close apposition between the endoplasmic reticulum (ER) and mitochondria. Hence, Ca(2+) released from the ER is "quasi-synaptically" transferred to mitochondrial matrix, where Ca(2+) stimulates mitochondrial ATP synthesis by activating the tricarboxylic acid (TCA) cycle. However, when the Ca(2+) transfer is excessive and sustained, mitochondrial Ca(2+) overload induces apoptosis by opening the mitochondrial permeability transition pore. A large number of regulatory proteins reside at mitochondria-associated ER membranes (MAMs) to maintain the optimal distance between the organelles and to coordinate the functionality of both ER and mitochondrial Ca(2+) transporters or channels...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28804553/sirt3-attenuates-doxorubicin-induced-cardiac-hypertrophy-and-mitochondrial-dysfunction-via-suppression-of-bnip3
#17
Qiong Du, Bin Zhu, Qing Zhai, Bo Yu
Doxorubicin (Dox) is an anthracycline antibiotic widely used in cancer treatment. Although its antitumor efficacy appears to be dose dependent, its clinical use is greatly restricted by development of cardiotoxicity. Sirtuin-3 (Sirt3) is the major deacetylase within the mitochondrial matrix that plays an important role in regulation of cardiac function. This study was performed to identify the regulatory role of Sirt3 on Dox-induced cardiac hypertrophy and mitochondrial dysfunction in rats in vivo and in vitro...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28804552/in-vivo-opening-of-the-mitochondrial-permeability-transition-pore-in-a-rat-model-of-ventricular-fibrillation-and-closed-chest-resuscitation
#18
Iyad M Ayoub, Jeejabai Radhakrishnan, Raúl J Gazmuri
Opening of the mitochondrial permeability transition pore (mPTP) is considered central to reperfusion injury. Yet, most of our knowledge comes from observations in isolated mitochondria, cells, and organs. We used a rat model of ventricular fibrillation (VF) and closed-chest resuscitation to examine whether the mPTP opens in vivo and whether cyclosporine A (CsA) attenuates the associated myocardial injury. Two series of 26 and 18 rats each underwent 10 minutes of untreated VF before attempting resuscitation...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28802667/different-approaches-to-modeling-analysis-of-mitochondrial-swelling
#19
REVIEW
Sabzali Javadov, Xavier Chapa-Dubocq, Vladimir Makarov
Mitochondria are critical players involved in both cell life and death through multiple pathways. Structural integrity, metabolism and function of mitochondria are regulated by matrix volume due to physiological changes of ion homeostasis in cellular cytoplasm and mitochondria. Ca(2+) and K(+) presumably play a critical role in physiological and pathological swelling of mitochondria when increased uptake (influx)/decreased release (efflux) of these ions enhances osmotic pressure accompanied by high water accumulation in the matrix...
August 10, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28796779/dose-and-timing-of-injections-for-effective-cyclosporine-a-pretreatment-before-renal-ischemia-reperfusion-in-mice
#20
Sandrine Lemoine, Bruno Pillot, Lionel Augeul, Maud Rabeyrin, Annie Varennes, Gabrielle Normand, Delphine Baetz, Michel Ovize, Laurent Juillard
BACKGROUND: There is experimental evidence that lethal ischemia-reperfusion injury (IRI) is largely due to mitochondrial permeability transition pore (mPTP) opening, which can be prevented by cyclosporine A (CsA). The aim of our study is to show that a higher dose of CsA (10 mg/kg) injected just before ischemia or a lower dose of CsA (3 mg/kg) injected further in advance of ischemia (1 h) protects the kidneys and improves mitochondrial function. METHODS: All mice underwent a right unilateral nephrectomy followed by 30 min clamping of the left renal artery...
2017: PloS One
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