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Mitochondrial permeability transition pore

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https://www.readbyqxmd.com/read/28542130/activation-of-transient-receptor-potential-vanilloid-4-involves-in-hypoxia-reoxygenation-injury-in-cardiomyocytes
#1
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
https://www.readbyqxmd.com/read/28536949/exercise-and-doxorubicin-treatment-modulate-cardiac-mitochondrial-quality-control-signaling
#2
I Marques-Aleixo, E Santos-Alves, J R Torrella, P J Oliveira, J Magalhães, A Ascensão
The cross-tolerance effect of exercise against heart mitochondrial-mediated quality control, remodeling and death-related mechanisms associated with sub-chronic Doxorubicin (DOX) treatment is yet unknown. We therefore analyzed the effects of two distinct chronic exercise models (endurance treadmill training-TM and voluntary free wheel activity-FW) performed during the course of the sub-chronic DOX treatment on mitochondrial susceptibility to permeability transition pore (mPTP), apoptotic and autophagic signaling and mitochondrial dynamics...
May 23, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28527718/rotenone-decreases-ischemia-induced-injury-by-inhibiting-mitochondrial-permeability-transition-in-mature-brains
#3
Evelina Rekuviene, Laima Ivanoviene, Vilmante Borutaite, Ramune Morkuniene
The mitochondrial permeability transition pore (mPTP) is thought to be implicated in brain ischemia-induced cell death. Here we sought to determine whether complex I (CI) of the mitochondrial electron transfer system may be involved in regulation of mPTP opening during ischemia and whether a specific inhibitor of this complex - rotenone can protect against ischemia-induced cell death in an experimental model of total ischemia in adult rat brains. Anesthetized Wistar rats were administered a single injection of rotenone (0...
May 17, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28524096/itraq-mitoproteome-analysis-reveals-mechanisms-of-programmed-cell-death-in-arabidopsis-thaliana-induced-by-ochratoxin-a
#4
Yan Wang, Xiaoli Peng, Zhuojun Yang, Weiwei Zhao, Wentao Xu, Junran Hao, Weihong Wu, Xiao Li Shen, Yunbo Luo, Kunlun Huang
Ochratoxin A (OTA) is one of the most common and dangerous mycotoxins in the world. Previous work indicated that OTA could elicit spontaneous HR-like lesions formation Arabidopsis thaliana, reactive oxygen species (ROS) play an important role in OTA toxicity, and their major endogenous source is mitochondria. However, there has been no evidence as to whether OTA induces directly PCD in plants until now. In this study, the presence of OTA in Arabidopsisthaliana leaves triggered accelerated respiration, increased production of mitochondrial ROS, the opening of ROS-dependent mitochondrial permeability transition pores and a decrease in mitochondrial membrane potential as well as the release of cytochrome c into the cytosol...
May 18, 2017: Toxins
https://www.readbyqxmd.com/read/28522037/calcium-and-regulation-of-the-mitochondrial-permeability-transition
#5
REVIEW
Valentina Giorgio, Lishu Guo, Claudio Bassot, Valeria Petronilli, Paolo Bernardi
Recent years have seen renewed interest in the permeability transition pore, a high conductance channel responsible for permeabilization of the inner mitochondrial membrane, a process that leads to depolarization and Ca(2+) release. Transient openings may be involved in physiological Ca(2+) homeostasis while long-lasting openings may trigger and/or execute cell death. In this review we specifically focus (i) on the hypothesis that the PTP forms from the F-ATP synthase and (ii) on the mechanisms through which Ca(2+) can reversibly switch this energy-conserving nanomachine into an energy-dissipating device...
May 10, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28515085/regulation-of-atp-production-dependences-on-calcium-concentration-and-respiratory-state
#6
Brian D Fink, Fan Bai, Liping Yu, William I Sivitz
Nanomolar free calcium enhances oxidative phosphorylation. However, the effects over a broad concentration range, at different respiratory states, or on specific energy substrates are less clear. We examined the action of varying [Ca(2+)] over respiratory states ranging 4 to 3 on skeletal muscle mitochondrial respiration, potential, ATP production, and H2O2 production using ADP recycling to clamp external [ADP]. 450 nM calcium enhanced respiration in mitochondria energized by the complex I substrates, glutamate/malate (but not succinate) at [ADP] of 4-256 µM, but more substantially at intermediate respiratory states and not all at state 4...
May 17, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/28508150/exogenous-bdnf-increases-mitochondrial-pcreb-and-alleviates-neuronal-metabolic-defects-following-mechanical-injury-in-a-mptp-dependent-way
#7
Zhen Xu, Xiao-Ai Lv, Qun Dai, Man Lu, Zhang Jin
Metabolic defects are common pathological phenomena following traumatic brain injury (TBI) which contribute to poor prognosis. Brain-derived neurotrophic factor (BDNF) is an important regulator of neuronal survival, development, function, and plasticity. This study was designed to investigate the potential effects of BDNF on TBI-induced metabolic defects and their underlying molecular mechanisms. BDNF was added into cultured neurons to a concentration of 25, 50, and 100 ng/ml, respectively, right after mechanical injury and metabolite levels were analyzed 4 h post injury...
May 15, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28507163/ca-2-binding-to-f-atp-synthase-%C3%AE-subunit-triggers-the-mitochondrial-permeability-transition
#8
Valentina Giorgio, Victoria Burchell, Marco Schiavone, Claudio Bassot, Giovanni Minervini, Valeria Petronilli, Francesco Argenton, Michael Forte, Silvio Tosatto, Giovanna Lippe, Paolo Bernardi
F-ATP synthases convert the electrochemical energy of the H(+) gradient into the chemical energy of ATP with remarkable efficiency. Mitochondrial F-ATP synthases can also undergo a Ca(2+)-dependent transformation to form channels with properties matching those of the permeability transition pore (PTP), a key player in cell death. The Ca(2+) binding site and the mechanism(s) through which Ca(2+) can transform the energy-conserving enzyme into a dissipative structure promoting cell death remain unknown. Through in vitro, in vivo and in silico studies we (i) pinpoint the "Ca(2+)-trigger site" of the PTP to the catalytic site of the F-ATP synthase β subunit and (ii) define a conformational change that propagates from the catalytic site through OSCP and the lateral stalk to the inner membrane...
May 15, 2017: EMBO Reports
https://www.readbyqxmd.com/read/28501872/a-mechanism-study-underlying-the-protective-effects-of-cyclosporine-a-on-lung-ischemia-reperfusion-injury
#9
Jian''an Li, Zhongya Yan, Qianjin Fang
AIM: This study is aimed at validating the hypothesis that administration of cyclosporine-A (CsA) would be protective in lung ischemia-reperfusion (I/R) injury and in exploring the underlying mechanism. METHODS: Rabbits were divided into 4 groups: the control, sham operation, I/R, and I/R with CsA treatment. Flow cytometry was used to measure the mitochondrial membrane potential. Laser scanning confocal microscope was used to analyze mitochondrion permeability transition pore (MPTP)...
May 10, 2017: Pharmacology
https://www.readbyqxmd.com/read/28492973/fast-therapeutic-hypothermia-prevents-post-cardiac-arrest-syndrome-through-cyclophilin-d-mediated-mitochondrial-permeability-transition-inhibition
#10
Vincent Jahandiez, Martin Cour, Thomas Bochaton, Maryline Abrial, Joseph Loufouat, Abdallah Gharib, Annie Varennes, Michel Ovize, Laurent Argaud
The opening of the mitochondrial permeability transition pore (PTP), which is regulated by the matrix protein cyclophilin D (CypD), plays a key role in the pathophysiology of post-cardiac arrest (CA) syndrome. We hypothesized that therapeutic hypothermia could prevent post-CA syndrome through a CypD-mediated PTP inhibition in both heart and brain. In addition, we investigated whether specific pharmacological PTP inhibition would confer additive protection to cooling. Adult male New Zealand White rabbits underwent 15 min of CA followed by 120 min of reperfusion...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28471109/ethaselen-a-novel-organoselenium-anticancer-agent-targeting-thioredoxin-reductase-1-reverses-cisplatin-resistance-in-drug-resistant-k562-cells-by-inducing-apoptosis
#11
Suo-Fu Ye, Yong Yang, Lin Wu, Wei-Wei Ma, Hui-Hui Zeng
It has been reported that Ethaselen shows inhibitory effects on thioredoxin reductase (TrxR) activity and human tumor cell growth. In order to find an efficient way to reverse cisplatin resistance, we investigated the reversal effects of Ethaselen on cisplatin resistance in K562/cisplatin (CDDP) cells that were established by pulse-inducing human erythrocyte leukemic cell line K562, which are fivefold more resistant to cisplatin compared to K562 cells. The morphology and growth showed that the adhesion of K562/CDDP further decreased while the cell volume increased...
May 2017: Journal of Zhejiang University. Science. B
https://www.readbyqxmd.com/read/28457864/development-or-disease-duality-of-the-mitochondrial-permeability-transition-pore
#12
REVIEW
María José Pérez, Rodrigo A Quintanilla
Mitochondria is not only a dynamic organelle that produces ATP, but is also an important contributor to cell functions in both development and cell death processes. These paradoxical functions of mitochondria are partially regulated by the mitochondrial permeability transition pore (mPTP), a high-conductance channel that can induce loss of mitochondrial membrane potential, impairment of cellular calcium homeostasis, oxidative stress, and a decrease in ATP production upon pathological activation. Interestingly, despite their different etiologies, several neurodegenerative diseases and heart ischemic injuries share mitochondrial dysfunction as a common element...
April 28, 2017: Developmental Biology
https://www.readbyqxmd.com/read/28453529/effect-of-mild-hypothermia-preconditioning-against-low-temperature-4%C3%A2-c-induced-rat-liver-cell-injury-in-vitro
#13
Jiasheng Qin, Yanxing Mai, Yang Li, Zesheng Jiang, Yi Gao
Bioartificial liver holds special position in the field of regenerative medicine, and cold environment at 4℃ is widely used for the short storage of both organ and liver cell for later application. However, the disadvantages of such cold storage could influence cell viability and lead to cell apoptosis in different degrees. In this study, we mainly explore the pre-protective effect of mild hypothermia against low temperature (4℃)-induced rat liver cell injury in vitro. Our results indicated that the precondition with mild hypothermia could increase cell viability, such as cell proliferation, LDH regulation and glycogen synthesis ability of liver cell...
2017: PloS One
https://www.readbyqxmd.com/read/28450114/the-novel-cyclophilin-d-inhibitor-compound-19-protects-retinal-pigment-epithelium-cells-and-retinal-ganglion-cells-from-uv-radiation
#14
Laiqing Xie, Long Cheng, Guoxu Xu, Ji Zhang, Xiaoyan Ji, E Song
Excessive Ultra violet (UV) radiation induces injuries to retinal pigment epithelium (RPE) cells (RPEs) and retinal ganglion cells (RGCs), causing retinal degeneration. Cyclophilin D (Cyp-D)-dependent mitochondrial permeability transition pore (mPTP) opening mediates UV-induced cell death. In this study, we show that a novel Cyp-D inhibitor compound 19 efficiently protected RPEs and RGCs from UV radiation. Compound 19-mediated cytoprotection requires Cyp-D, as it failed to further protect RPEs/RGCs from UV when Cyp-D was silenced by targeted shRNAs...
June 10, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28445457/the-mitochondrial-na-ca-2-exchanger-is-essential-for-ca-2-homeostasis-and-viability
#15
Timothy S Luongo, Jonathan P Lambert, Polina Gross, Mary Nwokedi, Alyssa A Lombardi, Santhanam Shanmughapriya, April C Carpenter, Devin Kolmetzky, Erhe Gao, Jop H van Berlo, Emily J Tsai, Jeffery D Molkentin, Xiongwen Chen, Muniswamy Madesh, Steven R Houser, John W Elrod
Mitochondrial calcium (mCa(2+)) has a central role in both metabolic regulation and cell death signalling, however its role in homeostatic function and disease is controversial. Slc8b1 encodes the mitochondrial Na(+)/Ca(2+) exchanger (NCLX), which is proposed to be the primary mechanism for mCa(2+) extrusion in excitable cells. Here we show that tamoxifen-induced deletion of Slc8b1 in adult mouse hearts causes sudden death, with less than 13% of affected mice surviving after 14 days. Lethality correlated with severe myocardial dysfunction and fulminant heart failure...
May 4, 2017: Nature
https://www.readbyqxmd.com/read/28443506/catestain-a-master-regulator-of-cardiovascular-functions
#16
Sushil K Mahata, Malapaka Kiranmayi, Nitish R Mahapatra
Cardiovascular disease (CVD), the most common cause of death globally, accounts for ~30% of all deaths worldwide. Hypertension is a common contributor to morbidity and mortality from CVD. The plasma concentration of chromogranin A (CgA) is elevated in patients with CVD as well as patients with established human essential hypertension and heart failure (HF). In contrast, the plasma level of the CgA-derived peptide catestatin (CST) is diminished in human essential hypertension. Low conversion of CgA-to-CST has been associated with increased mortality in patients hospitalized with acute HF...
April 24, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28442392/4-chlorodiazepam-is-neuroprotective-against-amyloid-beta-in-organotypic-hippocampal-cultures
#17
B D Arbo, J B Hoppe, K Rodrigues, L M Garcia-Segura, C G Salbego, M F Ribeiro
The translocator protein (TSPO) is an outer mitochondrial membrane protein involved in the transport of cholesterol into the mitochondria, which is the first step for the synthesis of steroid hormones, as well as in the regulation of mitochondrial permeability transition pore opening and apoptosis. Studies have shown that the activation of TSPO may promote neuroprotective actions in experimental models of neurodegeneration and brain injury. In a previous study, our group showed that 4'-chlorodiazepam (4'-CD), a TSPO ligand, was neuroprotective against amyloid-beta (Aβ) in SHSY-5Y neuroblastoma cells...
April 23, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/28441753/coq10-deficiency-may-indicate-mitochondrial-dysfunction-in-cr-vi-toxicity
#18
Xiali Zhong, Xing Yi, Rita de Cássia da Silveira E Sá, Yujing Zhang, Kaihua Liu, Fang Xiao, Caigao Zhong
To investigate the toxic mechanism of hexavalent chromium Cr(VI) and search for an antidote for Cr(VI)-induced cytotoxicity, a study of mitochondrial dysfunction induced by Cr(VI) and cell survival by recovering mitochondrial function was performed. In the present study, we found that the gene expression of electron transfer flavoprotein dehydrogenase (ETFDH) was strongly downregulated by Cr(VI) exposure. The levels of coenzyme 10 (CoQ10) and mitochondrial biogenesis presented by mitochondrial mass and mitochondrial DNA copy number were also significantly reduced after Cr(VI) exposure...
April 24, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28440192/mitochondrial-permeability-transition-pore-as-a-suitable-target-for-neuroprotective-agents-against-alzheimer-disease
#19
Elena F Shevtsova, Daria Vinogradova, Margarita E Neganova, Marco Avila-Rodriguez, G M Ashraf, George E Barreto, Sergey O Bachurin, Gjumrakch Aliev
A considerable amount of data suggests the age-related impairments of mitochondrial functions in the development of sporadic forms of neurodegenerative pathologies. These includes a decrease in the calcium retention capacity of mitochondria, which leads to the disturbance of the functional activity of neurons, and increased sensitivity of mitochondria towards the induction of the permeability transition. This in turn provoke the neuronal death enhancing the development of neurodegenerative processes. Inhibitors of mitochondrial permeability transition, which increases calcium retention capacity of mitochondria, are considered as promising neuroprotective drugs able not only to halt the neurodegenerative cascade, but also to increase the functional activity of neurons...
April 23, 2017: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/28435076/design-synthesis-biological-evaluation-and-molecular-modelling-of-2-2-aryloxyphenyl-1-4-dihydroisoquinolin-3-2h-ones-a-novel-class-of-tspo-ligands-modulating-amyloid-%C3%AE-induced-mptp-opening
#20
Ahmed Elkamhawy, Jung-Eun Park, Ahmed H E Hassan, Ae Nim Pae, Jiyoun Lee, Beoung-Geon Park, Sora Paik, Jimin Do, Jong-Hyun Park, Ki Duk Park, Bongjin Moon, Woo Kyu Park, Heeyeong Cho, Dae Young Jeong, Eun Joo Roh
Translocator protein (TSPO) is involved in modulating mitochondrial permeability transition pore (mPTP) opening/closure leading to either apoptotic cell death via opening of mPTP or cell protection mediated by mPTP blocking and hence intercepting mPTP induced apoptosis. Herein, 2-(2-aryloxyphenyl)-1,4-dihydroisoquinolin-3(2H)-one derivatives have been designed and synthesized as new modulators for amyloid-β-induced mPTP opening. Among all, compound 7c remarkably enhanced mPTP opening while compound 7e showed the highest mPTP blocking activity...
April 21, 2017: European Journal of Pharmaceutical Sciences
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