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Mitochondrial permeability transition pore

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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
#1
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/28445457/the-mitochondrial-na-ca-2-exchanger-is-essential-for-ca-2-homeostasis-and-viability
#2
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...
April 26, 2017: Nature
https://www.readbyqxmd.com/read/28443506/catestain-a-master-regulator-of-cardiovascular-functions
#3
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
#4
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 22, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/28441753/coq10-deficiency-may-indicate-mitochondrial-dysfunction-in-cr-vi-toxicity
#5
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
#6
Elena F Shevtsova, Daria Vinogradova, Margarita E Neganova, Marco Avila-Rodriguez, 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
#7
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 20, 2017: European Journal of Pharmaceutical Sciences
https://www.readbyqxmd.com/read/28434975/protection-of-pc12%C3%A2-cells-from-cocaine-induced-cell-death-by-inhibiting-mitochondrial-permeability-transition
#8
Frederic Lamarche, Cecile Cottet-Rousselle, Luc Barret, Eric Fontaine
Cocaine abuse induces brain injury and neurodegeneration by a mechanism that has not yet been fully elucidated. Mitochondria play a key role in cell death processes, notably through the opening of the permeability transition pore (PTP). In this work, we examined the involvement of the PTP in cocaine-induced toxicity in PC12 cell lines. We used two different PTP inhibitors -i.e. cyclosporin A (CsA) and metformin-to assess their ability to counteract the cocaine induced effects. We first observed that a 48 h exposure to cocaine strongly sensitized cells to calcium overload, as measured by the calcium retention capacity...
April 20, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28432755/mitochondria-and-ageing-role-in-heart-skeletal-muscle-and-adipose-tissue
#9
REVIEW
Kerstin Boengler, Maik Kosiol, Manuel Mayr, Rainer Schulz, Susanne Rohrbach
Age is the most important risk factor for most diseases. Mitochondria play a central role in bioenergetics and metabolism. In addition, several lines of evidence indicate the impact of mitochondria in lifespan determination and ageing. The best-known hypothesis to explain ageing is the free radical theory, which proposes that cells, organs, and organisms age because they accumulate reactive oxygen species (ROS) damage over time. Mitochondria play a central role as the principle source of intracellular ROS, which are mainly formed at the level of complex I and III of the respiratory chain...
April 21, 2017: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/28428752/desensitizing-mitochondrial-permeability-transition-by-erk-cyclophilin-d-axis-contributes-to-the-neuroprotective-effect-of-gallic-acid-against-cerebral-ischemia-reperfusion-injury
#10
Jing Sun, Da-Dui Ren, Jin-Yi Wan, Chen Chen, Dong Chen, Huan Yang, Chun-Lai Feng, Jing Gao
Ischemic stroke is a devastating disease with complex pathophysiology. Much evidence confirms that opening of the mitochondrial permeability transition pore (MPTP) is related with mitochondrial dysfunction to apoptosis in ischemic stroke, thus elucidating its signaling mechanism and screening novel MPTP inhibitor is therefore of paramount importance. Our earlier studies identified that gallic acid (GA), a naturally occurring plant phenol, endows with effect on inhibition of mitochondrial dysfunction, which has significant neuroprotective effect in cerebral ischemia/reperfusion injury...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28425440/the-valosin-containing-protein-is-a-novel-mediator-of-mitochondrial-respiration-and-cell-survival-in-the-heart-in-vivo
#11
Paulo Lizano, Eman Rashed, Shaunrick Stoll, Ning Zhou, Hairuo Wen, Tristan T Hays, Gangjian Qin, Lai-Hua Xie, Christophe Depre, Hongyu Qiu
The valosin-containing protein (VCP) participates in signaling pathways essential for cell homeostasis in multiple tissues, however, its function in the heart in vivo remains unknown. Here we offer the first description of the expression, function and mechanism of action of VCP in the mammalian heart in vivo in both normal and stress conditions. By using a transgenic (TG) mouse with cardiac-specific overexpression (3.5-fold) of VCP, we demonstrate that VCP is a new and powerful mediator of cardiac protection against cell death in vivo, as evidenced by a 50% reduction of infarct size after ischemia/reperfusion versus wild type...
April 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28424622/pravastatin-chronic-treatment-sensitizes-hypercholesterolemic-mice-muscle-to-mitochondrial-permeability-transition-protection-by-creatine-or-coenzyme-q10
#12
Estela N B Busanello, Ana C Marques, Noelia Lander, Diogo N de Oliveira, Rodrigo R Catharino, Helena C F Oliveira, Anibal E Vercesi
Statins are efficient cholesterol-lowering medicines utilized worldwide. However, 10% of patients suffer from adverse effects specially related to skeletal muscle function. Pro- or anti-oxidant effects of statins have been reported. Here we hypothesized that statins induce muscle mitochondrial oxidative stress leading to mitochondrial permeability transition (MPT) which may explain statin muscle toxicity. Thus, our aims were to investigate the effects of statin chronic treatment on muscle mitochondrial respiration rates, MPT and redox state indicators in the context of hypercholesterolemia...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28420545/gqsar-modeling-and-combinatorial-library-generation-of-4-phenylquinazoline-2-carboxamide-derivatives-as-antiproliferative-agents-in-human-glioblastoma-tumors
#13
Debolina Goswami, Sukriti Goyal, Salma Jamal, Ritu Jain, Divya Wahi, Abhinav Grover
BACKGROUND: TSPO translocator protein, encoded in humans by the Tspo gene plays a crucial role in mitochondria mediated apoptosis and necrotic cell death through its association with Mitochondrial Permeability Transition pore (MPTP). It has been shown that this function can be exploited as a potential treatment for human Glioblastoma Multiforme. In this study, a novel robust fragment based QSAR model has been developed for a series of 4-phenylquinazoline-2-carboxamides experimentally known to be ligands for TSPO, thus triggering apoptotic mechanism cascade...
April 4, 2017: Computational Biology and Chemistry
https://www.readbyqxmd.com/read/28411054/salidroside-protects-rat-liver-against-ischemia-reperfusion-injury-by-regulating-the-gsk-3%C3%AE-nrf2-dependent-antioxidant-response-and-mitochondrial-permeability-transition
#14
Linlin Cai, Yonghua Li, Qingqing Zhang, Haijing Sun, Xiaodi Yan, Tong Hua, Qiufeng Zhu, Haitao Xu, Hailong Fu
Salidroside (Sal) is a natural antioxidant that elicits cardioprotective and neuroprotective effects in vivo and in vitro; however, its impact on hepatic ischemia/reperfusion (I/R) injury remains unclear. The purpose of this study was to investigate the hepatoprotective effects of salidroside against segmental (70%) warm hepatic I/R injury in rats. Animals were randomized into Sham, Sham+salidroside pretreatment (Sal), Sham+Sal+carboxyatractyloside (CATR), Sham+CATR, I/R, I/R+Sal, I/R+Sal+CATR and I/R+CATR groups...
April 12, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28407688/npc-26-kills-human-colorectal-cancer-cells-via-activating-ampk-signaling
#15
Zhen Zhao, Li Feng, Jiqin Wang, Deshan Cheng, Mei Liu, Meirong Ling, Weiping Xu, Keyu Sun
NPC-26 is novel mitochondrion-interfering compound. The current study tested its potential effect against colorectal cancer (CRC) cells. We demonstrated that NPC-26 induced potent anti-proliferative and cytotoxic activities against CRC cell lines (HCT-116, DLD-1 and HT-29). Activation of AMP-activated protein kinase (AMPK) signaling mediated NPC-26-induced CRC cell death. AMPKα1 shRNA knockdown or dominant negative mutation abolished NPC-26-induced AMPK activation and subsequent CRC cell death. NPC-26 disrupted mitochondrial function, causing mitochondrial permeability transition pore (mPTP) opening and reactive oxygen species (ROS) production...
March 14, 2017: Oncotarget
https://www.readbyqxmd.com/read/28398674/melatonin-protects-cardiac-microvasculature-against-ischemia-reperfusion-injury-via-suppression-of-mitochondrial-fission-vdac1-hk2-mptp-mitophagy-axis
#16
Hao Zhou, Ying Zhang, Shunying Hu, Chen Shi, Pingjun Zhu, Qiang Ma, Qinhua Jin, Feng Cao, Feng Tian, Yundai Chen
The cardiac microvascular system, which is primarily composed of monolayer endothelial cells, is the site of blood supply and nutrient exchange to cardiomyocytes. However, microvascular ischemia/reperfusion injury (IRI) following percutaneous coronary intervention is a woefully neglected topic and few strategies are available to reverse such pathologies. Here, we studied the effects of melatonin on microcirculation IRI and elucidated the underlying mechanism. Melatonin markedly reduced infarcted area, improved cardiac function, restored blood flow and lower microcirculation perfusion defects...
April 11, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28395670/absence-of-physiological-ca-2-transients-is-an-initial-trigger-for-mitochondrial-dysfunction-in-skeletal-muscle-following-denervation
#17
Chehade Karam, Jianxun Yi, Yajuan Xiao, Kamal Dhakal, Lin Zhang, Xuejun Li, Carlo Manno, Jiejia Xu, Kaitao Li, Heping Cheng, Jianjie Ma, Jingsong Zhou
BACKGROUND: Motor neurons control muscle contraction by initiating action potentials in muscle. Denervation of muscle from motor neurons leads to muscle atrophy, which is linked to mitochondrial dysfunction. It is known that denervation promotes mitochondrial reactive oxygen species (ROS) production in muscle, whereas the initial cause of mitochondrial ROS production in denervated muscle remains elusive. Since denervation isolates muscle from motor neurons and deprives it from any electric stimulation, no action potentials are initiated, and therefore, no physiological Ca(2+) transients are generated inside denervated muscle fibers...
April 10, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28386342/hydrogen-rich-saline-attenuates-isoflurane-induced-caspase-3-activation-and-cognitive-impairment-via-inhibition-of-isoflurane-induced-oxidative-stress-mitochondrial-dysfunction-and-reduction-in-atp-levels
#18
Cheng Li, Lengchen Hou, Dan Chen, Fuqing Lin, Tao Chang, Mengzhu Li, Lingling Zhang, Xiaoyin Niu, Huiying Wang, Shukun Fu, Junhua Zheng
OBJECTIVES: The inhaled general anesthetic isoflurane has been shown to induce caspase-3 activation in vitro and in vivo. The underlying mechanisms and functional consequences of this activity remain unclear. Isoflurane can induce caspase-3 activation by causing accumulation of reactive oxygen species (ROS), mitochondrial dysfunction, and reduction in adenosine triphosphate (ATP) levels. This study aimed to investigate the protective effect of hydrogen, a novel antioxidant, against isoflurane-induced caspase-3 activation and cognitive impairment...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28381122/argon-exposure-induces-postconditioning-in-myocardial-ischemia-reperfusion
#19
Sandrine Lemoine, Katrien Blanchart, Mathieu Souplis, Adrien Lemaitre, Damien Legallois, Laurent Coulbault, Christophe Simard, Stéphane Allouche, Jacques H Abraini, Jean-Luc Hanouz, René Rouet, Laurent Sallé, Romain Guinamard, Alain Manrique
BACKGROUND AND PURPOSE: Cardioprotection against ischemia-reperfusion (I/R) damages remains a major concern during prehospital management of acute myocardial infarction. Noble gases have shown beneficial effects in preconditioning studies. Because emergency proceedings in the context of myocardial infarction require postconditioning strategies, we evaluated the effects of argon in such protocols on mammalian cardiac tissue. EXPERIMENTAL APPROACHES: In rat, cardiac I/R was induced in vivo by transient coronary artery ligature and cardiac functions were evaluated by magnetic resonance imaging...
January 1, 2017: Journal of Cardiovascular Pharmacology and Therapeutics
https://www.readbyqxmd.com/read/28378042/mitochondrial-permeability-transition-in-cardiac-ischemia-reperfusion-whether-cyclophilin-d-is-a-viable-target-for-cardioprotection
#20
REVIEW
Sabzali Javadov, Sehwan Jang, Rebecca Parodi-Rullán, Zaza Khuchua, Andrey V Kuznetsov
Growing number of studies provide strong evidence that the mitochondrial permeability transition pore (PTP), a non-selective channel in the inner mitochondrial membrane, is involved in the pathogenesis of cardiac ischemia-reperfusion and can be targeted to attenuate reperfusion-induced damage to the myocardium. The molecular identity of the PTP remains unknown and cyclophilin D is the only protein commonly accepted as a major regulator of the PTP opening. Therefore, cyclophilin D is an attractive target for pharmacological or genetic therapies to reduce ischemia-reperfusion injury in various animal models and humans...
April 4, 2017: Cellular and Molecular Life Sciences: CMLS
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