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Mitochondrial permeability transition pore

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https://www.readbyqxmd.com/read/29781984/mitochondrial-ca2-retention-capacity-assay-and-ca2-triggered-mitochondrial-swelling-assay
#1
Wei Li, Chen Zhang, Xiulian Sun
The production of ATP by oxidative phosphorylation is the primary function of mitochondria. Mitochondria in higher eukaryotes also participate in cytosolic Ca2+ buffering, and the ATP production in mitochondrial can be mediated by intramitochondrial free Ca2+ concentration. Ca2+ retention capacity can be regarded as the capability of mitochondria to retain calcium in the mitochondrial matrix. Accumulated intracellular Ca2+ leads to the permeability of the inner mitochondrial membrane, termed the opening of mitochondrial permeability transition pore (mPTP), which leads to the leakage of molecules with a molecular weight less than 1...
May 1, 2018: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/29770487/inhibitory-effect-of-melatonin-on-necroptosis-via-repressing-the-ripk3-pgam5-cypd-mptp-pathway-attenuates-cardiac-microvascular-ischemia-reperfusion-injury
#2
Hao Zhou, Dandan Li, Pingjun Zhu, Qiang Ma, Toan Sam, Jin Wang, Shunying Hu, Yundai Chen, Yingmei Zhang
The molecular features of necroptosis in cardiac ischemia reperfusion (IR) injury have been extensively explored. However, there have been no studies investigating the physiological regulatory mechanisms of melatonin acting on necroptosis in cardiac IR injury. This study was designed to determine the role of necroptosis in microvascular IR injury, and investigate the contribution of melatonin in repressing necroptosis and preventing IR-mediated endothelial system collapse. Our results demonstrated that Ripk3 was primarily activated by IR injury and consequently aggravated endothelial necroptosis, microvessel barrier dysfunction, capillary hyperpermeability, the inflammation response, microcirculatory vasospasms and microvascular perfusion defects...
May 16, 2018: Journal of Pineal Research
https://www.readbyqxmd.com/read/29766336/ischaemic-preconditioning-protects-cardiomyocytes-from-anthracycline-induced-toxicity-via-the-pi3k-pathway
#3
Angshuman Maulik, Sean M Davidson, Izabela Piotrowska, Malcolm Walker, Derek M Yellon
PURPOSE: Anthracyclines cause chronic irreversible cardiac failure, but the mechanism remains poorly understood. Emerging data indicate that cardiac damage begins early, suggesting protective modalities delivered in the acute stage may confer prolonged benefit. Ischaemic preconditioning (IPC) activates the pro-survival reperfusion injury salvage kinase (RISK) pathway which involves PI3-kinase and MAPK/ERK1/2. METHODS: We investigated whether simulated IPC (sIPC), in the form of a sublethal exposure to a hypoxic buffer simulating ischaemic conditions followed by reoxygenation, protects primary adult rat cardiomyocytes against anthracycline-induced injury...
May 15, 2018: Cardiovascular Drugs and Therapy
https://www.readbyqxmd.com/read/29765507/ex-vivo-cardiotoxicity-of-antineoplastic-casiopeinas-is-mediated-through-energetic-dysfunction-and-triggered-mitochondrial-dependent-apoptosis
#4
Christian Silva-Platas, César A Villegas, Yuriana Oropeza-Almazán, Mariana Carrancá, Alejandro Torres-Quintanilla, Omar Lozano, Javier Valero-Elizondo, Elena C Castillo, Judith Bernal-Ramírez, Evaristo Fernández-Sada, Luis F Vega, Niria Treviño-Saldaña, Héctor Chapoy-Villanueva, Lena Ruiz-Azuara, Carmen Hernández-Brenes, Leticia Elizondo-Montemayor, Carlos E Guerrero-Beltrán, Karla Carvajal, María E Bravo-Gómez, Gerardo García-Rivas
Casiopeinas are a group of copper-based antineoplastic molecules designed as a less toxic and more therapeutic alternative to cisplatin or Doxorubicin; however, there is scarce evidence about their toxic effects on the whole heart and cardiomyocytes. Given this, rat hearts were perfused with Casiopeinas or Doxorubicin and the effects on mechanical performance, energetics, and mitochondrial function were measured. As well, the effects of Casiopeinas-triggered cell death were explored in isolated cardiomyocytes...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29765325/mequindox-induced-kidney-toxicity-is-associated-with-oxidative-stress-and-apoptosis-in-the-mouse
#5
Qianying Liu, Zhixin Lei, Jingchao Guo, Aimei Liu, Qirong Lu, Zainab Fatima, Haseeb Khaliq, Muhammad A B Shabbir, Muhammad Kashif Maan, Qinghua Wu, Menghong Dai, Xu Wang, Yuanhu Pan, Zonghui Yuan
Mequindox (MEQ), belonging to quinoxaline-di- N -oxides (QdNOs), is a synthetic antimicrobial agent widely used in China. Previous studies found that the kidney was one of the main toxic target organs of the QdNOs. However, the mechanisms underlying the kidney toxicity caused by QdNOs in vivo still remains unclear. The present study aimed to explore the molecular mechanism of kidney toxicity in mice after chronic exposure to MEQ. MEQ led to the oxidative stress, apoptosis, and mitochondrial damage in the kidney of mice...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29763919/inhalation-of-hydrogen-of-different-concentrations-ameliorates-spinal-cord-injury-in-mice-by-protecting-spinal-cord-neurons-from-apoptosis-oxidative-injury-and-mitochondrial-structure-damages
#6
Xiao Chen, Jin Cui, Xiao Zhai, Jun Zhang, Zhengrong Gu, Xin Zhi, Weizong Weng, Panpan Pan, Liehu Cao, Fang Ji, Zhiwei Wang, Jiacan Su
BACKGROUND/AIMS: Hydrogen selectively neutralizes reactive oxygen species (ROS) and ameliorates various ROS-induced injuries. Spinal cord injury (SCI) is a serious injury to the central nervous system, and secondary SCI is closely related to excessive ROS generation. We hypothesized that hydrogen inhalation ameliorates SCI, and the mechanism of action may be related to the protective effects of hydrogen against oxidative stress, apoptosis, and mitochondrial damage. METHODS: Mechanically injured spinal cord neurons were incubated with different concentrations of hydrogen in vitro...
May 10, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29763901/5-aminolevulinic-acid-mediated-sonodynamic-therapy-alleviates-atherosclerosis-via-enhancing-efferocytosis-and-facilitating-a-shift-in-the-th1-th2-balance-toward-th2-polarization
#7
Yang Yang, Yuanyuan Liu, Xi Chen, Jie Gong, Zhen Huang, Wei Wang, Yuanqi Shi, Yu Wang, Jianting Yao, Zhaoqian Shen, Zhen Tian, Hong Jin, Ye Tian
BACKGROUND/AIMS: We and other groups have demonstrated that 5-aminolevulinic acid (ALA)-mediated sonodynamic therapy (ALA-SDT) induces macrophage and foam cell apoptosis and stabilizes atherosclerosis (AS) plaques in animal models. Lymphocytes also play vital roles in the development of AS. The primary purpose of the present study was to investigate the effects of ALA-SDT on T helper (Th) cell fate and function, Th subset differentiation, and atherosclerotic lesion stability. METHODS: We utilized ALA-SDT on Western diet-fed apoE-/-mice in vivo and human Jurkat cells in vitro...
May 9, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29749475/mir-125a-induces-apoptosis-metabolism-disorder-and-migrationimpairment-in-pancreatic-cancer-cells-by-targeting-mfn2-related-mitochondrial-fission
#8
Lichao Pan, Lin Zhou, Weijia Yin, Jia Bai, Rong Liu
Mitochondrial fission is important for the development and progression of pancreatic cancer (PC). However, little is known regarding its role in pancreatic cancer apoptosis, metabolism and migration. In the current study, the mechanism by which mitochondrial fission modifies the biological characteristics of PC was explored. MicroRNA‑125a (miR‑125a) had the ability to inhibit mitochondrial fission and contributed to cellular survival. Suppressed mitochondrial fission led to a reduction in mitochondrial debris, preserved the mitochondrial membrane potential, inhibited mitochondrial permeability transition pore opening, ablated cytochrome c leakage into the cytoplasm and reduced the pro‑apoptotic protein contents, finally blocking mitochondria related apoptosis pathways...
April 26, 2018: International Journal of Oncology
https://www.readbyqxmd.com/read/29746847/csa-attenuates-compression-induced-nucleus-pulposus-mesenchymal-stem-cells-apoptosis-via-alleviating-mitochondrial-dysfunction-and-oxidative-stress
#9
Zhiliang Li, Songfeng Chen, Kaige Ma, Xiao Lv, Hui Lin, Binwu Hu, Ruijun He, Zengwu Shao
AIMS: This study aims to investigate the protective effects and potential mechanisms of cyclosporine A (CsA), which efficiently inhibits mitochondrial permeability transition pore (MPTP) opening, on compression-induced apoptosis of human nucleus pulposus mesenchymal stem cells (NP-MSCs). MATERIALS AND METHODS: Human NP-MSCs were subjected to various periods of 1.0 MPa compression. Cell viability was evaluated using cell counting kit-8 (CCK-8) assay. The cellular ultrastructure and ATP level were analyzed via transmission electron microscopy (TEM) and ATP detection kit respectively...
May 7, 2018: Life Sciences
https://www.readbyqxmd.com/read/29717349/the-release-of-cytochrome-c-and-the-regulation-of-the-programmed-cell-death-progress-in-the-endosperm-of-winter-wheat-triticum-aestivum-l-under-waterlogging
#10
Yuan-Hong Qi, Fang-Fang Mao, Zhu-Qing Zhou, Dong-Cheng Liu, Min-Yu, Xiang-Yi Deng, Ji-Wei Li, Fang-Zhu Mei
It has been shown in mammalian systems that the mitochondria can play a key role in the regulation of apoptosis by releasing intermembrane proteins (such as cytochrome c) into the cytosol. Cytochrome c released from the mitochondria to the cytoplasm activates proteolytic enzyme cascades, leading to specific nuclear DNA degradation and cell death. This pathway is considered to be one of the important regulatory mechanisms of apoptosis. Previous studies have shown that endosperm cell development in wheat undergoes specialized programmed cell death (PCD) and that waterlogging stress accelerates the PCD process; however, little is known regarding the associated molecular mechanism...
May 2, 2018: Protoplasma
https://www.readbyqxmd.com/read/29705943/critical-contribution-of-ripk1-mediated-mitochondrial-dysfunction-and-oxidative-stress-to-compression-induced-rat-nucleus-pulposus-cells-necroptosis-and-apoptosis
#11
Songfeng Chen, Xiao Lv, Binwu Hu, Lei Zhao, Shuai Li, Zhiliang Li, Xiangcheng Qing, Hongjian Liu, Jianzhong Xu, Zengwu Shao
The aim of this study was to investigate whether RIPK1 mediated mitochondrial dysfunction and oxidative stress contributed to compression-induced nucleus pulposus (NP) cells necroptosis and apoptosis, together with the interplay relationship between necroptosis and apoptosis in vitro. Rat NP cells underwent various periods of 1.0 MPa compression. To determine whether compression affected mitochondrial function, we evaluated the mitochondrial membrane potential, mitochondrial permeability transition pore (mPTP), mitochondrial ultrastructure and ATP content...
April 28, 2018: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/29694881/miro-1-determines-mitochondrial-shape-transition-upon-gpcr-activation-and-ca-2-stress
#12
Neeharika Nemani, Edmund Carvalho, Dhanendra Tomar, Zhiwei Dong, Andrea Ketschek, Sarah L Breves, Fabián Jaña, Alison M Worth, Julie Heffler, Palaniappan Palaniappan, Aparna Tripathi, Ramasamy Subbiah, Massimo F Riitano, Ajay Seelam, Thomas Manfred, Kie Itoh, Shuxia Meng, Hiromi Sesaki, William J Craigen, Sudarsan Rajan, Santhanam Shanmughapriya, Jeffrey Caplan, Benjamin L Prosser, Donald L Gill, Peter B Stathopulos, Gianluca Gallo, David C Chan, Prashant Mishra, Muniswamy Madesh
Mitochondria shape cytosolic calcium ([Ca2+ ]c ) transients and utilize the mitochondrial Ca2+ ([Ca2+ ]m ) in exchange for bioenergetics output. Conversely, dysregulated [Ca2+ ]c causes [Ca2+ ]m overload and induces permeability transition pore and cell death. Ablation of MCU-mediated Ca2+ uptake exhibited elevated [Ca2+ ]c and failed to prevent stress-induced cell death. The mechanisms for these effects remain elusive. Here, we report that mitochondria undergo a cytosolic Ca2+ -induced shape change that is distinct from mitochondrial fission and swelling...
April 24, 2018: Cell Reports
https://www.readbyqxmd.com/read/29692032/-effects-of-p-hydroxybenzoic-acid-and-phloroglucinol-on-mitochondria-function-and-root-growth-in-cotton-gossypium-hirsutum-l-seedling-roots
#13
Guo Wei Zhang, Chang Qin Yang, Rui Xian Liu, Wan Chao Ni
With early-maturing cotton cultivar CCRI-50 widely grown in China as experimental material, water culture experiment was conducted to study the effects of p-hydroxybenzoic acid and phloroglucinol with different concentrations (0.8, 4.0, and 20.0 mmol·L-1 ) on generation rate of reactive oxygen, changes of antioxidant enzyme activities and mitochondria function of cotton roots. Results showed that p-hydroxybenzoic acid and phloroglucinol treatments inhibited the cotton root growth, reduced SOD, POD, CAT and H+ -ATPase activities in root mitochondria, increased the generation rate of O2- · and H2 O2 content...
January 2018: Ying Yong Sheng Tai Xue Bao, the Journal of Applied Ecology
https://www.readbyqxmd.com/read/29682760/protective-role-of-parkin-in-skeletal-muscle-contractile-and-mitochondrial-function
#14
Gilles Gouspillou, Richard Godin, Jérome Piquereau, Martin Picard, Mahroo Mofarrahi, Jasmin Mathew, Fennigje M Purves-Smith, Nicolas Sgarioto, Russell T Hepple, Yan Burelle, Sabah Na Hussain
KEY POINTS SUMMARY: Parkin, an E3 ubiquitin ligase encoded by the Park2 gene, has been implicated in the regulation of mitophagy, a quality control process whereby defective mitochondria are degraded. The exact physiological significance of Parkin in regulating mitochondrial function and contractility in skeletal muscle remains largely unexplored. Using Park2-/- mice, we show that Parkin ablation causes a decrease in muscle specific force, a severe decrease in mitochondrial respiration, mitochondrial uncoupling and an increased susceptibility to opening of the permeability transition pore...
April 22, 2018: Journal of Physiology
https://www.readbyqxmd.com/read/29682614/oxidant-stress-and-lipid-peroxidation-in-acetaminophen-hepatotoxicity
#15
Hartmut Jaeschke, Anup Ramachandran
Acetaminophen (APAP) overdose is the most frequent cause of liver injury and acute liver failure in many western countries. The mechanism of APAP-induced hepatocyte necrosis has been investigated extensively. The formation of a reactive metabolite and its binding to cellular proteins was initially thought to be responsible for cell death. A competing hypothesis was introduced that questioned the relevance of protein binding and instead suggested that P450-derived oxidant stress and lipid peroxidation causes APAP-induced liver injury...
May 2018: Reactive Oxygen Species (Apex, N.C.)
https://www.readbyqxmd.com/read/29679372/paraneoplastic-cerebellar-degeneration-yo-antibody-alters-mitochondrial-calcium-buffering-capacity
#16
Debabrata Panja, Christian A Vedeler, Manja Schubert
AIM: Neurodegeneration is associated with dysfunction of calcium buffering capacity and thereby sustained cellular and mitochondrial calcium overload. Paraneoplastic cerebellar degeneration (PCD), characterized by progressive Purkinje neuron degeneration following paraneoplastic Yo antibody internalisation and binding to cerebellar degeneration-related protein CDR2 and CDR2L, has been linked to intracellular calcium homeostasis imbalance due to calbindin D28k malfunction. Therefore, we hypothesized that Yo antibody internalisation affects not only calbindin calcium binding capacity but also calcium-sensitive mitochondrial-associated signalling, causing mitochondrial calcium overload and thereby Purkinje neuron death...
April 21, 2018: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/29679227/cypd-mptp-axis-regulates-mitochondrial-functions-contributing-to-osteogenic-dysfunction-of-mc3t3-e1-cells-in-inflammation
#17
Xueqi Gan, Ling Zhang, Beilei Liu, Zhuoli Zhu, Yuting He, Junsheng Chen, Junfei Zhu, Haiyang Yu
Bone is a dynamic organ, the bone-forming osteoblasts and bone-resorbing osteoclasts form the physiological basis of bone remodeling process. During pathological process of numerous inflammatory diseases, these two aspects are uncoupled and the balance is usually tipped in favor of bone destruction. Evidence suggests that the inflammatory destruction of bone is mainly attributed to oxidative stress and is closely related to mitochondrial dysfunction. The mechanisms underlying osteogenic dysfunction in inflammation still need further investigation...
April 20, 2018: Journal of Physiology and Biochemistry
https://www.readbyqxmd.com/read/29671396/composite-mathematical-modeling-of-calcium-signaling-behind-neuronal-cell-death-in-alzheimer-s-disease
#18
Bobby Ranjan, Ket Hing Chong, Jie Zheng
BACKGROUND: Alzheimer's disease (AD) is a progressive neurological disorder, recognized as the most common cause of dementia affecting people aged 65 and above. AD is characterized by an increase in amyloid metabolism, and by the misfolding and deposition of β-amyloid oligomers in and around neurons in the brain. These processes remodel the calcium signaling mechanism in neurons, leading to cell death via apoptosis. Despite accumulating knowledge about the biological processes underlying AD, mathematical models to date are restricted to depicting only a small portion of the pathology...
April 11, 2018: BMC Systems Biology
https://www.readbyqxmd.com/read/29671257/glycogen-synthase-kinase-3%C3%AE-opens-mitochondrial-permeability-transition-pore-through-mitochondrial-hexokinase-ii-dissociation
#19
Takamitsu Tanaka, Masao Saotome, Hideki Katoh, Terumori Satoh, Prottoy Hasan, Hayato Ohtani, Hiroshi Satoh, Hideharu Hayashi, Yuichiro Maekawa
Accumulating evidence has revealed pivotal roles of glycogen synthase kinase-3β (GSK3β) inactivation on cardiac protection. Because the precise mechanisms of cardiac protection against ischemia/reperfusion (I/R) injury by GSK3β-inactivation remain elusive, we investigated the relationship between GSK3β-mediated mitochondrial hexokinase II (mitoHK-II; a downstream target of GSK3β) dissociation and mitochondrial permeability transition pore (mPTP) opening. In Langendorff-perfused hearts, GSK3β inactivation by SB216763 improved the left ventricular-developed pressure and retained mitoHK-II binding after I/R...
April 18, 2018: Journal of Physiological Sciences: JPS
https://www.readbyqxmd.com/read/29671020/luteolin-alleviates-cardiac-ischemia-reperfusion-injury-in-the-hypercholesterolemic-rat-via-activating-akt-nrf2-signaling
#20
Jin-Ting Yang, Jue Wang, Xin-Ru Zhou, Chi Xiao, Yang-Yun Lou, Li-Hui Tang, Feng-Jiang Zhang, Ling-Bo Qian
Myocardial ischemia/reperfusion (I/R) injury in hypercholesterolemia is associated with oxidative stress, while luteolin is known to reduce oxidative stress by activating Akt/nuclear factor erythroid-2-related factor 2 (Nrf2) signaling and alleviate cardiac I/R injury. Here, we investigated whether luteolin pretreatment diminishes myocardial I/R injury in hypercholesterolemic rats by activating Akt/Nrf2 signaling. Hypercholesterolemic rats were produced by 2% cholesterol diet for 8 weeks. Luteolin (100 mg/kg/day, i...
April 18, 2018: Naunyn-Schmiedeberg's Archives of Pharmacology
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