Read by QxMD icon Read

Mitochondrial permeability transition pore

Zuolei Chen, Donat R Spahn, Xuewei Zhang, Yingzhi Liu, Haichen Chu, Zhongkai Liu
BACKGROUND/AIMS: The purpose of this study was to investigate the implications of protein kinase C-epsilon (PKCε), Extracellular Signal-regulated Kinase 1/2 (ERK1/2) and mitochondrial permeability transition pore (mPTP) in myocardial protection induced by morphine postconditioning (MpostC). METHODS: The isolated rat hearts were randomly assigned into one of eight groups. Hearts in time control (TC) group were constantly perfused for 105min. Hearts in ischemia-reperfusion (I/R) group were subjected to 45 min of ischemia followed by 1 h of reperfusion...
October 24, 2016: Cellular Physiology and Biochemistry
Zhi-Yong Xu, Ming-Xue Zheng, Yan Zhang, Xiao-Zhen Cui, Sha-Sha Yang, Rui-Li Liu, Shan Li, Rou Xi, Xin Gong, Rui Bai
The purpose of the present study was to investigate the dynamic changes in the main regulatory genes of the mitochondrial permeability transition pore in E. tenella host cells. Primary chick embryo cecum epithelial cell culture techniques, spectrophotometer technology, Hoechst-Annexin V-PI apoptosis staining and ELISA were used to detect the apoptosis rate and dynamic changes of Bcl-2, Bcl-xl, Bax, Bak, Bid, Bad, HK-II, and ATP content in E. tenella host cells at 4, 24, 48, 72, 96, and 120 h. The rates of early apoptosis, late apoptosis, and necrosis of group T0 were significantly lower (P < 0...
October 17, 2016: Experimental Parasitology
Wenwen Wang, Yanqin Yang, Zhewen Xiong, Jiamin Kong, Xinlu Fu, Feihai Shen, Zhiying Huang
Triptolide (TP), a diterpene triepoxide, is a major active component of Tripterygium wilfordii extracts, which are prepared as tablets and has been used clinically for the treatment of inflammation and autoimmune disorders. However, TP's therapeutic potential is limited by severe adverse effects. In a previous study, we reported that TP induced mitochondria dependent apoptosis in cardiomyocytes. Glycogen synthase kinase-3β (GSK-3β) is a multifunctional serine/threonine kinase that plays important roles in the necrosis and apoptosis of cardiomyocytes...
October 14, 2016: Toxicology and Applied Pharmacology
Carola Stockburger, Davide Miano, Thea Pallas, Kristina Friedland, Walter E Müller
The mitochondrial cascade hypothesis of dementia assumes mitochondrial dysfunction leading to reduced energy supply, impaired neuroplasticity, and finally cell death as one major pathomechanism underlying the continuum from brain aging over mild cognitive impairment to initial and advanced late onset Alzheimer's disease. Accordingly, improving mitochondrial function has become an important strategy to treat the early stages of this continuum. The metabolic enhancer piracetam has been proposed as possible prototype for those compounds by increasing impaired mitochondrial function and related aspects like mechanisms of neuroplasticity...
2016: Neural Plasticity
Shangcheng Xu, Pei Wang, Huiliang Zhang, Guohua Gong, Nicolas Gutierrez Cortes, Weizhong Zhu, Yisang Yoon, Rong Tian, Wang Wang
Mitochondrial permeability transition pore (mPTP) is involved in cardiac dysfunction during chronic β-adrenergic receptor (β-AR) stimulation. The mechanism by which chronic β-AR stimulation leads to mPTP openings is elusive. Here, we show that chronic administration of isoproterenol (ISO) persistently increases the frequency of mPTP openings followed by mitochondrial damage and cardiac dysfunction. Mechanistically, this effect is mediated by phosphorylation of mitochondrial fission protein, dynamin-related protein 1 (Drp1), by Ca(2+)/calmodulin-dependent kinase II (CaMKII) at a serine 616 (S616) site...
October 14, 2016: Nature Communications
Zhou Ou, Teng Jiang, Qing Gao, You-Yong Tian, Jun-Shan Zhou, Liang Wu, Jian-Quan Shi, Ying-Dong Zhang
INTRODUCTION: We recently demonstrated that angiotensin II (Ang II) was involved in the etiology of Parkinson's disease (PD) via induction of apoptosis of dopaminergic neurons, but the mechanisms are not completely elucidated. Here, we asked whether mitochondrial-dependent mechanisms contributed to the Ang II-induced dopaminergic neuronal apoptosis. MATERIALS AND METHODS: CATH.a cells were incubated with Ang II in combination with mitochondrial permeability transition pore (mPTP) inhibitors or angiotensin receptor antagonists, and apoptosis rate, caspase-3 activity, cytochrome c levels, and mPTP opening were assessed...
October 2016: Journal of the Renin-angiotensin-aldosterone System: JRAAS
Fang Ye, Xiaoyi Li, Fen Li, Jianxin Li, Wei Chang, Jing Yuan, Jun Chen
Mitochondria play a key role in the process of lead (Pb)-induced impairment in nervous system. To further clarify the underlying mechanism of Pb neurotoxicity, this study was designed to investigate the role of mitochondrial permeability transition (MPT) and cyclophilin D (CyPD), a component of MPT pore (MPTP), in Pb-induced mitochondrial apoptosis in nerve cells. In SH-SY5Y and PC12 cells, Cyclosporin A (CSA), a special inhibitor of CyPD, could alleviate cell death, lactate dehydrogenase (LDH) leakage and adenosine 5 triphosphate (ATP) decrease caused by PbAc...
October 7, 2016: Neurotoxicology
Sophie Le Page, Marjorie Niro, Jérémy Fauconnier, Laura Cellier, Sophie Tamareille, Abdallah Gharib, Arnaud Chevrollier, Laurent Loufrani, Céline Grenier, Rima Kamel, Emmanuelle Sarzi, Alain Lacampagne, Michel Ovize, Daniel Henrion, Pascal Reynier, Guy Lenaers, Delphine Mirebeau-Prunier, Fabrice Prunier
BACKGROUND: Recent data suggests the involvement of mitochondrial dynamics in cardiac ischemia/reperfusion (I/R) injuries. Whilst excessive mitochondrial fission has been described as detrimental, the role of fusion proteins in this context remains uncertain. OBJECTIVES: To investigate whether Opa1 (protein involved in mitochondrial inner-membrane fusion) deficiency affects I/R injuries. METHODS AND RESULTS: We examined mice exhibiting Opa1delTTAG mutations (Opa1+/-), showing 70% Opa1 protein expression in the myocardium as compared to their wild-type (WT) littermates...
2016: PloS One
Yunqing Chen, Junjun Zheng, Shuyun Chen, Min Zhu, Daojun Hong
AIMS: To investigate the underlying mechanisms of how the defects of desmin cause mitochondrial abnormalities in desminopathy. MATERIAL AND METHODS: Primary myoblasts were isolated from muscle biopsy of a desminopathy patient with mitochondrial abnormalities. Two-dimensional gel electrophoresis analyses of mitochondrial proteins were performed in mitochondria isolated from myoblasts. Immunostaining, immunoblot, and mitochondrial function tests were carried out to confirm the proteomic results...
October 10, 2016: Clinical Neuropathology
Xiang-Bin Song, Gang Liu, Zhen-Yong Wang, Lin Wang
Puerarin (PU) is a potent free radical scavenger with a protective effect in nephrotoxin-mediated oxidative damage. Here, we show a novel molecular mechanism by which PU exerts its anti-apoptotic effects in cadmium (Cd)-exposed primary rat proximal tubular (rPT) cells. Morphological assessment and flow cytometric analysis revealed that PU significantly decreased Cd-induced apoptotic cell death of rPT cells. Administration of PU protected cells against Cd-induced depletion of mitochondrial membrane potential (ΔΨm) and lipid peroxidation...
October 4, 2016: Chemico-biological Interactions
Alessandra Zulian, Marco Schiavone, Valentina Giorgio, Paolo Bernardi
The hypothesis that mitochondrial dysfunction can be a general mechanism for cell death in muscle diseases is 40 years old. The key elements of the proposed pathogenetic sequence (cytosolic Ca(2+) overload followed by excess mitochondrial Ca(2+) uptake, functional and then structural damage of mitochondria, energy shortage, worsened elevation of cytosolic Ca(2+) levels, hypercontracture of muscle fibers, cell necrosis) have been confirmed in amazing detail by subsequent work in a variety of models. The explicit implication of the hypothesis was that it "may provide the basis for a more rational treatment for some conditions even before their primary causes are known" (Wrogemann and Pena, 1976, Lancet, 1, 672-674)...
September 30, 2016: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
Jin Yu, Yiliyaer Maimaitili, Peng Xie, Jianjiang Wu, Jiang Wang, Yining Yang, Haiping Ma, Hong Zheng
AIM: Hyperglycaemia-induced cell injury is a primary cause of cardiovascular complications in diabetic patients. In vivo studies demonstrated that sevoflurane postconditioning (SpostC) was cardioprotective against ischaemia/reperfusion injury, which was blocked by hyperglycaemia. This study investigated whether high glucose concentration abrogated SpostC cardioprotection in vitro by advancing mitochondrial fission and whether mitochondrial division inhibitor-1 (Mdivi-1) restored SpostC cardioprotection in cultured primary neonatal rat cardiomyocytes (NCMs)...
September 29, 2016: Acta Physiologica
Piet Kramer, Alexander T Jung, Andrea Hamann, Heinz D Osiewacz
The mitochondrial permeability transition pore plays a key role in programmed cell death and the induction of autophagy. Opening of the pore is regulated by the mitochondrial peptidyl prolyl-cis, trans-isomerase cyclophilin D (CYPD). Previously it was shown in the aging model organism Podospora anserina that PaCYPD abundance increases during aging and that PaCypD overexpressors are characterized by accelerated aging. Here, we describe a role of PaCYPD in the regulation of autophagy. We found that the accelerated aging phenotype observed in a strain overexpressing PaCypD is not metacaspase-dependent but is accompanied by an increase of general autophagy and mitophagy, the selective autophagic degradation of mitochondria...
2016: Frontiers in Genetics
Ngonidzashe B Madungwe, Netanel F Zilberstein, Yansheng Feng, Jean C Bopassa
Reactive oxygen species (ROS) generation has been implicated in many pathologies including ischemia/reperfusion (I/R) injury. This led to multiple studies on antioxidant therapies to treat cardiovascular diseases but paradoxically, results have so far been mixed as ROS production can be beneficial as a signaling mechanism and in cardiac protection via preconditioning interventions. We investigated whether the differential impact of increased ROS in injury as well as in protection could be explained by their site of production on the mitochondrial electron transport chain...
2016: American Journal of Cardiovascular Disease
Farinoosh Fakharnia, Fariba Khodagholi, Leila Dargahi, Abolhassan Ahmadiani
The mitochondrial permeability transition pore (mPTP) is a complex channel of the inner membrane, the opening of which leads to mitochondrial swelling and dissipation of mitochondrial membrane potential (MMP). Here, we aimed to evaluate the role of the cyclophilin D (CypD) as a prominent mediator of mPTP, on necroptosis and autophagy as well as apoptosis, beyond the global cerebral ischemia-reperfusion (I/R) injury. We showed that while cerebral I/R injury is accompanied by loss of MMP, mitochondrial swelling and programmed cell death, pretreatment with cyclosporine-A (CsA) as a potent inhibitor of CypD, led to partial but significant reduction in necroptosis markers, RIP1 and RIP3 as well as activity of glutamate-ammonia ligase (GLUL) and glutamate dehydrogenase 1 (GLUD1), downstream enzymes of RIP3...
September 23, 2016: Journal of Molecular Neuroscience: MN
R J Aitken, L Muscio, S Whiting, H S Connaughton, B A Fraser, B Nixon, N D Smith, G N De Iuliis
The need to protect human spermatozoa from oxidative stress during assisted reproductive technology, has prompted a detailed analysis of the impacts of phenolic compounds on the functional integrity of these cells. Investigation of 16 individual compounds revealed a surprising variety of negative effects including: (i) a loss of mitochondrial membrane potential (Δψm) via mechanisms that were not related to opening of the permeability transition pore but associated with a reduction in thiol expression, (ii) a decline in intracellular reduced glutathione, (iii) the stimulation of pro-oxidant activity including the induction of ROS generation from mitochondrial and non-mitochondrial sources, (iv) stimulation of lipid peroxidation, (v) the generation of oxidative DNA damage, and (vi) impaired sperm motility...
September 19, 2016: Biochemical Pharmacology
Yang-Yang Dong, Yi-Huang Zhuang, Wen-Jie Cai, Yan Liu, Wen-Bing Zou
The development of novel anti-pancreatic cancer agents is extremely important. Here, we investigated the anti-pancreatic cancer activity by NPC-26, a novel mitochondrion interfering compound. We showed that NPC-26 was anti-proliferative and cytotoxic to human pancreatic cancer cells, possibly via inducing caspase-9-dependent cell apoptosis. Pharmacological inhibition or shRNA-mediated silence of caspase-9 attenuated NPC-26-induced pancreatic cancer cell death and apoptosis. Further, NPC-26 treatment led to mitochondrial permeability transition pore (mPTP) opening in the cancer cells, which was evidenced by mitochondrial depolarization, ANT-1(adenine nucleotide translocator-1)-Cyp-D (cyclophilin-D) association and oxidative phosphorylation disturbance...
September 22, 2016: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Tim König, Simon E Tröder, Kavya Bakka, Anne Korwitz, Ricarda Richter-Dennerlein, Philipp A Lampe, Maria Patron, Mareike Mühlmeister, Sergio Guerrero-Castillo, Ulrich Brandt, Thorsten Decker, Ines Lauria, Angela Paggio, Rosario Rizzuto, Elena I Rugarli, Diego De Stefani, Thomas Langer
Mutations in subunits of mitochondrial m-AAA proteases in the inner membrane cause neurodegeneration in spinocerebellar ataxia (SCA28) and hereditary spastic paraplegia (HSP7). m-AAA proteases preserve mitochondrial proteostasis, mitochondrial morphology, and efficient OXPHOS activity, but the cause for neuronal loss in disease is unknown. We have determined the neuronal interactome of m-AAA proteases in mice and identified a complex with C2ORF47 (termed MAIP1), which counteracts cell death by regulating the assembly of the mitochondrial Ca(2+) uniporter MCU...
October 6, 2016: Molecular Cell
Rodrigo A Quintanilla, Cheril Tapia, María José Pérez
Huntington disease (HD) is a devastating neurological disorder that affects the striatum and cortex of patients. HD patients develop progressive motor dysfunction and psychiatric disturbances with gradual dementia. HD is caused by a pathological expansion of CAG repeats in the huntingtin gene that codifies for a protein called huntingtin (Htt), which principal function is not completely understood. Accumulative evidence shows that this pathological expansion modifies Htt function affecting different neuronal targets, including mitochondrial function which is an important factor that contributes to HD...
September 13, 2016: Biochemical and Biophysical Research Communications
Armen V Gyulkhandanyan, David J Allen, Sergiy Mykhaylov, Elena Lyubimov, Heyu Ni, John Freedman, Valery Leytin
Availability of universal marker for the diagnosis of platelet apoptosis is an important but currently unresolved goal of platelet physiology investigations. Mitochondrial inner transmembrane potential (ΔΨm) depolarization is frequently used as a marker of apoptosis in nucleated cells and anucleate platelets. Since ΔΨm depolarization in platelets is also frequently associated with concurrent induction of other apoptotic responses, it may appear that ΔΨm depolarization is a good universal marker of platelet apoptosis...
September 16, 2016: Clinical and Applied Thrombosis/hemostasis
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"