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Mitochondrial permeability transition pore

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https://www.readbyqxmd.com/read/28096195/the-multifunctional-mitochondrial-epac1-controls-myocardial-cell-death
#1
Loubina Fazal, Marion Laudette, Sílvia Paula-Gomes, Sandrine Pons, Caroline Conte, Florence Tortosa, Pierre Sicard, Yannis Sainte-Marie, Malik Bisserier, Olivier Lairez, Alexandre Lucas, Jérôme Roy, Bijan Ghaleh, Jeremy Fauconnier, Jeanne Mialet-Perez, Frank Lezoualc'h
RATIONALE: Although the second messenger cyclic AMP (cAMP) is physiologically beneficial in the heart, it largely contributes to cardiac disease progression when dysregulated. Current evidence suggests that cAMP is produced within mitochondria. However, mitochondrial cAMP signaling and its involvement in cardiac pathophysiology are far from being understood. OBJECTIVE: To investigate the role of mitochondrial exchange protein directly activated by cAMP 1 (MitEpac1) in ischemia/reperfusion (I/R) injury...
January 17, 2017: Circulation Research
https://www.readbyqxmd.com/read/28089921/penehyclidine-hydrochloride-prevents-anoxia-reoxygenation-injury-and-induces-h9c2-cardiomyocyte-apoptosis-via-a-mitochondrial-pathway
#2
Zhaoqi Wang, Duomao Lin, Liang Zhang, Wenjun Liu, Hongbao Tan, Jun Ma
Penehyclidine hydrochloride (PHC) is an anticholinergic drug that has been widely used in the clinic for years, evaluating for anesthetic premedication, anti-muscarinic, or improving microcirculation. However, very little is known about its protective effects against anoxia/reoxygenation (A/R) injury in myocardiocytes. The aim of our study was to investigate the protective effects of PHC pretreatment on A/R injury, as well as the underlying mechanisms involved. To investigate apoptosis, we used the cell viability assay, Annexin-V/PI assay, and lactate dehydrogenase (LDH) and creatine kinase (CK) activity measurements...
January 12, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28078995/sphingolipids-in-genetic-and-acquired-forms-of-chronic-kidney-diseases
#3
Norishi Ueda
Sphingolipids (SLs) regulate apoptosis, proliferation, and stress response. SLs, including ceramide, glycosphingolipids (glucosylceramide, lactosylceramide, and gangliosides) and sphingosine-1-phosphate (S1P), play a role in the pathogenesis and progression of genetic (lysosomal storage disease, congenital nephrotic syndrome and polycystic kidney disease) and non-genetic forms of chronic kidney diseases (CKDs). SLs metabolism defects promote complications (cardiovascular events, etc.) via oxidant stress in CKDs...
January 12, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28070860/energetic-oxidative-and-ionic-exchange-in-rat-brain-and-liver-mitochondria-at-experimental-audiogenic-epilepsy-krushinsky-molodkina-model
#4
Natalya I Venediktova, Olga S Gorbacheva, Natalia V Belosludtseva, Irina B Fedotova, Natalia M Surina, Inga I Poletaeva, Oleg V Kolomytkin, Galina D Mironova
The role of brain and liver mitochondria at epileptic seizure was studied on Krushinsky-Molodkina (KM) rats which respond to sound with an intensive epileptic seizure (audiogenic epilepsy). We didn't find significant changes in respiration rats of brain and liver mitochondria of KM and control rats; however the efficiency of АТР synthesis in the KM rat mitochondria was 10% lower. In rats with audiogenic epilepsy the concentration of oxidative stress marker malondialdehyde in mitochondria of the brain (but not liver) was 2-fold higher than that in the control rats...
January 9, 2017: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/28065984/the-possible-role-of-nonbilayer-structures-in-regulating-atp-synthase-activity-in-mitochondrial-membranes
#5
S E Gasanov, A A Kim, R K Dagda
The effects of temperature and of the membrane-active protein CTII on the formation of nonbilayer structures in mitochondrial membranes were studied by (31)P-NMR. Increasing the temperature of isolated mitochondrial fractions correlated with an increase in ATP synthase activity and the formation of nonbilayer packed phospholipids with immobilized molecular mobility. Computer modeling was employed for analyzing the interaction of mitochondrial membrane phospholipids with the molecular surface of CTII, which behaves like a dicyclohexylcarbodiimide-binding protein (DCCD-BP) of the F0 group in a lipid phase...
July 2016: Biophysics
https://www.readbyqxmd.com/read/28065786/cisplatin-induced-necroptosis-in-tnf%C3%AE-dependent-and-independent-pathways
#6
Yanfang Xu, Hua-Bin Ma, Yu-Lu Fang, Zhi-Rong Zhang, Jing Shao, Mao Hong, Chao-Jun Huang, Jing Liu, Rui-Qing Chen
Cisplatin is a chemotherapeutic drug for treatment of many solid tumors. It has been shown to induce apoptosis and/or necrosis in different types of cancer cells. However, the underlying mechanisms remain elusive. In this study, we provide evidences that cisplatin induces necroptosis in receptor-interacting protein 3 (RIP3)-expressing cell lines, but not in cell lines lacking RIP3 protein expression. Deficiency of core components of necroptotic pathway, RIP1, RIP3, or mixed lineage kinase domain-like protein (MLKL) blocked cisplatin-induced cell death in L929 cells...
January 6, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28064403/knockdown-of-clusterin-alters-mitochondrial-dynamics-facilitates-necrosis-in-camptothecin-induced-cancer-stem-cells
#7
Parthasarathy Arumugam, Annie Samson, Jieun Ki, Joon Myong Song
The existence of a well-established drug resistance mechanism in cancer stem cells (CSC) complicates the cancer treatment. Clusterin (CLU) plays a key role in maintaining the integrity of endoplasmic reticulum (ER) during drug-induced stress. Hence, silencing the CLU could significantly reduce the inherent drug resistance mechanism of CSC. The combination of drug-induced cytotoxicity, as well as the suppression of drug resistance in CSC, could circumvent the recurrence capability of the tumor. In the present study, camptothecin (CPT)-induced apoptosis and necrosis in CSC with and without siCLU treatment were simultaneously measured using Qdot-based total internal reflection fluorescence microscope (TIRF)...
January 7, 2017: Cell Biology and Toxicology
https://www.readbyqxmd.com/read/28060833/wnt-signaling-prevents-the-a%C3%AE-oligomer-induced-mitochondrial-permeability-transition-pore-opening-preserving-mitochondrial-structure-in-hippocampal-neurons
#8
Macarena S Arrázola, Eva Ramos-Fernández, Pedro Cisternas, Daniela Ordenes, Nibaldo C Inestrosa
Alzheimer's disease (AD) is a neurodegenerative disorder mainly known for synaptic impairment and neuronal cell loss, affecting memory processes. Beside these damages, mitochondria have been implicated in the pathogenesis of AD through the induction of the mitochondrial permeability transition pore (mPTP). The mPTP is a non-selective pore that is formed under apoptotic conditions, disturbing mitochondrial structure and thus, neuronal viability. In AD, Aβ oligomers (Aβos) favor the opening of the pore, activating mitochondria-dependent neuronal cell death cascades...
2017: PloS One
https://www.readbyqxmd.com/read/28034298/effective-agents-targeting-the-mitochondria-and-apoptosis-to-protect-the-heart
#9
Eltyeb Abdelwahid, Aurimas Stulpinas, Audrone Kalvelyte
A wide variety of agents have been traditionally used in cardiovascular medicine worldwide and their precise mechanisms of action have been demonstrated to be largely related to the cardiomyocyte mitochondria and apoptosis. Abnormalities in the structure and function of the mitochondria and mutations in mitochondrial DNA can decrease energy production, alter the redox system, impair calcium homeostasis, and induce the mitochondrial permeability transition pore (MPTP), causing cell death. All of these data provide evidence of mitochondrial signaling pathways as targets to downregulate cardiac cell apoptosis and thus to prevent and treat cardiovascular diseases...
December 29, 2016: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28033580/extracellular-cl-free-induced-cardioprotection-against-hypoxia-reoxygenation-is-associated-with-attenuation-of-mitochondrial-permeability-transition-pore
#10
Xian-Gui Zhang, Le Zhao, Yi Zhang, Yuan-Yuan Li, Huan Wang, Guang-Ling Duan, Lin Xiao, Xiao-Ran Li, He-Ping Chen
The isotonic substitution of extracellular chloride by gluconate (extracellular Cl(-)-free) has been demonstrated to elicit cardioprotection by attenuating ischaemia/reperfusion-induced elevation of intracellular chloride ion concentration ([Cl(-)]i). However, the downstream mechanism underlying the cardioprotective effect of extracellular Cl(-)-free is not fully established. Here, it was investigated whether extracellular Cl(-)-free attenuates mitochondrial dysfunction after hypoxia/reoxygenation (H/R) and whether mitochondrial permeability transition pore (mPTP) plays a key role in the extracellular Cl(-)-free cardioprotection...
December 26, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28017206/sevoflurane-pre-conditioning-increases-phosphorylation-of-erk1-2-and-ho-1-expression-via-inhibition-of-mptp-in-primary-rat-cortical-neurons-exposed-to-ogd-r
#11
Li-Min Zhang, Dong-Xue Zhang, Xiao-Chun Zhao, Wen-Bo Sun, Xiao-Jing Jiang
BACKGROUND: As an indispensable clinical inhalation anesthetic, sevoflurane is widely used for peri-operative sedation. The neuroprotective effect of sevoflurane pre-conditioning against cerebral ischemia/reperfusion has been gradually realized, but the underlying mechanism during the early reperfusion period has not been established. METHOD: Primary cultured cortical neurons were treated with 2% sevoflurane pre-conditioning for 30min, exposed to oxygen-glucose deprivation for 90min, and followed by 60min of reperfusion (OGD/R)...
January 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28011391/pathophysiology-of-status-epilepticus
#12
REVIEW
Matthew C Walker
Status epilepticus (SE) is the maximal expression of epilepsy with a high morbidity and mortality. It occurs due to the failure of mechanisms that terminate seizures. Both human and animal data indicate that the longer a seizure lasts, the less likely it is to stop. Recent evidence suggests that there is a critical transition from an ictal to a post-ictal state, associated with a transition from a spatio-temporally desynchronized state to a highly synchronized state, respectively. As SE continues, it becomes progressively resistant to drugs, in particular benzodiazepines due partly to NMDA receptor-dependent internalization of GABA(A) receptors...
December 20, 2016: Neuroscience Letters
https://www.readbyqxmd.com/read/28005946/the-mitochondrial-permeability-transition-pore-regulator-cyclophilin-d-exhibits-tissue-specific-control-of-metabolic-homeostasis
#13
Rhianna C Laker, Evan P Taddeo, Yasir N Akhtar, Mei Zhang, Kyle L Hoehn, Zhen Yan
The mitochondrial permeability transition pore (mPTP) is a key regulator of mitochondrial function that has been implicated in the pathogenesis of metabolic disease. Cyclophilin D (CypD) is a critical regulator that directly binds to mPTP constituents to facilitate the pore opening. We previously found that global CypD knockout mice (KO) are protected from diet-induced glucose intolerance; however, the tissue-specific function of CypD and mPTP, particularly in the control of glucose homeostasis, has not been ascertained...
2016: PloS One
https://www.readbyqxmd.com/read/28000313/a-review-of-the-protective-role-of-melatonin-during-phosphine-induced-cardiotoxicity-focus-on-mitochondrial-dysfunction-oxidative-stress-and-apoptosis
#14
REVIEW
Mohammad Hossein Asghari, Mohammad Abdollahi, Marcos Roberto de Oliveira, Seyed Mohammad Nabavi
OBJECTIVES: Acute poisoning with aluminium phosphide (AlP) is a major cause of mortality in developing countries. AlP mortality is due to cardiac dysfunction leading to cardiomyocyte death. The main mechanism is an inhibition of cytochrome c oxidase in the cardiomyocyte mitochondria, resulting in a decreased ATP production and oxidative stress. Unfortunately, the administration of exogenous drugs does not meet the desired requirements of an effective therapy. Melatonin is an amphiphilic molecule and can easily pass through all cellular compartments with the highest concentration recorded in mitochondria...
December 20, 2016: Journal of Pharmacy and Pharmacology
https://www.readbyqxmd.com/read/27999288/melatonin-a-mitochondrial-targeting-molecule-involving-mitochondrial-protection-and-dynamics
#15
REVIEW
Dun-Xian Tan, Lucien C Manchester, Lilan Qin, Russel J Reiter
Melatonin has been speculated to be mainly synthesized by mitochondria. This speculation is supported by the recent discovery that aralkylamine N-acetyltransferase/serotonin N-acetyltransferase (AANAT/SNAT) is localized in mitochondria of oocytes and the isolated mitochondria generate melatonin. We have also speculated that melatonin is a mitochondria-targeted antioxidant. It accumulates in mitochondria with high concentration against a concentration gradient. This is probably achieved by an active transportation via mitochondrial melatonin transporter(s)...
December 16, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27995363/unacylated-ghrelin-analog-prevents-myocardial-reperfusion-injury-independently-of-permeability-transition-pore
#16
Rania Harisseh, Bruno Pillot, Abdallah Gharib, Lionel Augeul, Noelle Gallo-Bona, René Ferrera, Joseph Loufouat, Thomas Delale, Soraya Allas, Thierry Abribat, Claire Crola Da Silva, Michel Ovize
Reperfusion injury is responsible for an important part of myocardial infarct establishment due notably to triggering cardiomyocytes death at the first minutes of reperfusion. AZP-531 is an optimized analog of unacylated ghrelin currently in clinical development in several metabolic diseases. We investigated a potential cardioprotective effect of AZP-531 in ischemia/reperfusion (IR) and the molecular underlying mechanism(s) involved in this protection. In vivo postconditioning with AZP-531 in C57BL6 mouse IR model decreased infarct size...
January 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/27993675/the-cyclophilin-d-drp1-axis-regulates-mitochondrial-fission-contributing-to-oxidative-stress-induced-mitochondrial-dysfunctions-in-sh-sy5y-cells
#17
Anqi Xiao, Xueqi Gan, Ruiqi Chen, Yanming Ren, Haiyang Yu, Chao You
Oxidative stress plays a central role in the pathogenesis of various neurodegenerative diseases. Increasing evidences have demonstrated that structural abnormalities in mitochondria are involved in oxidative stress related nerve cell damage. And Drp1 plays a critical role in mitochondrial dynamic imbalance insulted by oxidative stress-derived mitochondria. However, the status of mitochondrial fusion and fission pathway and its relationship with mitochondrial properties such as mitochondrial membrane permeability transition pore (mPTP) have not been fully elucidated...
December 18, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27991671/the-mitochondrial-calcium-uniporter-in-the-heart-energetics-and-beyond
#18
Jennifer Q Kwong
Ca(2+) and mitochondria are inextricably linked to cardiac function and dysfunction. Ca(2+) is central cardiac excitation-contraction coupling and stimulates mitochondrial energy production to fuel contraction. Under pathological conditions of dysregulated Ca(2+) cycling, mitochondrial Ca(2+) overload activates cellular death pathways. Thus, in the cardiomyocyte, the mitochondrial Ca(2+) microdomain is where contraction, energy and death collide. A key component of mitochondrial Ca(2+) signalling is the mitochondrial Ca(2+) uniporter (MCU) complex (uniplex), an inner membrane Ca(2+) transporter and major pathway of mitochondrial Ca(2+) entry...
December 19, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27983605/effect-of-the-crac-peptide-vlnyyvw-on-mptp-opening-in-rat-brain-and-liver-mitochondria
#19
Tamara Azarashvili, Olga Krestinina, Yulia Baburina, Irina Odinokova, Vladimir Akatov, Igor Beletsky, John Lemasters, Vassilios Papadopoulos
The translocator protein (TSPO; 18 kDa) is a high-affinity cholesterol-binding protein located in the outer membrane of mitochondria. A domain in the C-terminus of TSPO was characterized as the cholesterol recognition/interaction amino acid consensus (CRAC). The ability of the CRAC domain to bind to cholesterol led us to hypothesize that this peptide may participate in the regulation of mitochondrial membrane permeability. Herein, we report the effect of the synthetic CRAC peptide, VLNYYVW, on mitochondrial permeability transition pore (mPTP) opening...
December 13, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27982058/shengmai-formula-suppressed-over-activated-ras-mapk-pathway-in-c-elegans-by-opening-mitochondrial-permeability-transition-pore-via-regulating-cyclophilin-d
#20
Yan Liu, Dejuan Zhi, Menghui Li, Dongling Liu, Xin Wang, Zhengrong Wu, Zhanxin Zhang, Dongqing Fei, Yang Li, Hongmei Zhu, Qingjian Xie, Hui Yang, Hongyu Li
Since about 30% of all human cancers contain mutationally activated Ras, down regulating the over-activation of Ras/MAPK pathway represents a viable approach for treating cancers. Over-activation of Ras/MAPK pathway is accompanied by accumulation of reactive oxygen species (ROS). One approach for developing anti-cancer drugs is to target ROS production and their accumulation. To test this idea, we have employed C. elegans of let-60 (gf) mutant, which contain over-activated let-60 (the homolog of mammalian ras) and exhibit tumor-like symptom of multivulva phenotype, to determine whether anti-oxidants can affect their tumor-like phenotype...
December 16, 2016: Scientific Reports
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