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Mitochondrial permeability transition pore

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https://www.readbyqxmd.com/read/28197936/salvianolic-acid-a-protects-neonatal-cardiomyocytes-against-hypoxia-reoxygenation-induced-injury-by-preserving-mitochondrial-function-and-activating-akt-gsk-3%C3%AE-signals
#1
Xue-Li Li, Ji-Ping Fan, Jian-Xun Liu, Li-Na Liang
OBJECTIVE: To investigate the effects of salvianolic acid A (SAA) on cardiomyocyte apoptosis and mitochondrial dysfunction in response to hypoxia/reoxygenation (H/R) injury and to determine whether the Akt signaling pathway might play a role. METHODS: An in vitro model of H/R injury was used to study outcomes on primary cultured neonatal rat cardiomyocytes. The cardiomyocytes were treated with 12.5, 25, 50 μg/mL SAA at the beginning of hypoxia and reoxygenation, respectively...
February 15, 2017: Chinese Journal of Integrative Medicine
https://www.readbyqxmd.com/read/28197079/sirt3-in-neural-stem-cells-attenuates-microglia-activation-induced-oxidative-stress-injury-through-mitochondrial-pathway
#2
De-Qi Jiang, Yan Wang, Ming-Xing Li, Yan-Jiao Ma, Yong Wang
Sirtuin 3 (SIRT3), a mitochondrial protein, is involved in energy metabolism, cell apoptosis and mitochondrial function. However, the role of SIRT3 in neural stem cells (NSCs) remains unknown. In previous studies, we found that microglia activation-induced cytotoxicity negatively regulated survival of NSCs, along with mitochondrial dysfunction. The aim of this study was to investigate the potential neuroprotective effects of SIRT3 on the microglia activation-induced oxidative stress injury in NSCs and its possible mechanisms...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28194639/ultrafine-particulate-matter-increases-cardiac-ischemia-reperfusion-injury-via-mitochondrial-permeability-transition-pore
#3
Nathan A Holland, Chad R Fraiser, Ruben C Sloan, Robert B Devlin, David A Brown, Christopher J Wingard
Ultrafine particulate matter (UFP) has been associated with increased cardiovascular morbidity and mortality. However, the mechanisms that drive PM-associated cardiovascular disease and dysfunction remain unclear. We examined the impact of oropharyngeal aspiration of 100 μg UFP from the Chapel Hill, NC, air shed in Sprague-Dawley rats on cardiac function, arrhythmogenesis, and cardiac ischemia/reperfusion (I/R) injury using a Langendorff working heart model. We found that exposure to UFP was capable of significantly exacerbating cardiac I/R injury without changing overall cardiac function or major changes in arrhythmogenesis...
February 13, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28191472/suppression-of-excessive-histone-deacetylases-activity-in-diabetic-hearts-attenuates-myocardial-ischemia-reperfusion-injury-via-mitochondria-apoptosis-pathway
#4
Yang Wu, Yan Leng, Qingtao Meng, Rui Xue, Bo Zhao, Liying Zhan, Zhongyuan Xia
Background. Histone deacetylases (HDACs) play a pivotal role in signaling modification and gene transcriptional regulation that are essential for cardiovascular pathophysiology. Diabetic hearts with higher HDACs activity were more vulnerable to myocardial ischemia/reperfusion (MI/R) injury compared with nondiabetic hearts. We are curious about whether suppression of excessive HDACs activity in diabetic heart protects against MI/R injury. Methods. Diabetic rats were subjected to 45 min of ischemia, followed by 3 h of reperfusion...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28186490/atomistic-simulations-indicate-the-c-subunit-ring-of-the-f1fo-atp-synthase-is-not-the-mitochondrial-permeability-transition-pore
#5
Wenchang Zhou, Fabrizio Marinelli, Corrine Nief, José D Faraldo-Gómez
Pathological metabolic conditions such as ischemia induce the rupture of the mitochondrial envelope and the release of pro-apoptotic proteins, leading to cell death. At the onset of this process, the inner mitochondrial membrane becomes depolarized and permeable to osmolytes, due to the opening of a non-selective protein channel of unknown molecular identity. A recent study purports that this channel, referred to as Mitochondrial Permeability Transition Pore (MPTP), is the lumen of the c-subunit ring of the ATP synthase, upon dissociation from the catalytic domain...
February 10, 2017: ELife
https://www.readbyqxmd.com/read/28181692/irisin-plays-a-pivotal-role-to-protect-the-heart-against-ischemia-and-reperfusion-injury
#6
Hao Wang, Yu Tina Zhao, Shouyan Zhang, Patrycja M Dubielecka, Jianfeng Du, Naohiro Yano, Y Eugene Chin, Shougang Zhuang, Gangjian Qin, Ting C Zhao
Irisin, a newly identified hormone, is critical to modulating body metabolism, thermogenesis and reducing oxidative stresses. However, whether irisin protects the heart against myocardial ischemia and reperfusion (I/R) injury remains unknown. In this study, we determine the effect of irisin on myocardial I/R injury in the Langendorff perfused heart and cultured myocytes. Adult C57/BL6 mice were treated with irisin (100mg/kg) or vehicle for 30 minutes to elicit preconditioning. The isolated hearts were subjected to 30 min ischemia followed by 30 min reperfusion...
February 9, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28179991/a-homolog-of-cyclophilin-d-is-expressed-in-trypanosoma-cruzi-and-is-involved-in-the-oxidative-stress-damage-response
#7
Patricia L Bustos, Bibiana J Volta, Alina E Perrone, Natalia Milduberger, Jacqueline Bua
Mitochondria have an important role in energy production, homeostasis and cell death. The opening of the mitochondrial permeability transition pore (mPTP) is considered one of the key events in apoptosis and necrosis, modulated by cyclophilin D (CyPD), a crucial component of this protein complex. In Trypanosoma cruzi, the protozoan parasite that causes Chagas disease, we have previously described that mitochondrial permeability transition occurs after oxidative stress induction in a cyclosporin A-dependent manner, a well-known cyclophilin inhibitor...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28167533/glyceraldehyde-3-phosphate-dehydrogenase-gapdh-aggregation-causes-mitochondrial-dysfunction-during-oxidative-stress-induced-cell-death
#8
Hidemitsu Nakajima, Masanori Itakura, Takeya Kubo, Akihiro Kaneshige, Naoki Harada, Takeshi Izawa, Yasu-Taka Azuma, Mitsuru Kuwamura, Ryouichi Yamaji, Tadayoshi Takeuchi
Glycolytic glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a multifunctional protein that also mediates cell death under oxidative stress. We previously reported that the active-site cysteine (Cys-152) of GAPDH plays an essential role in oxidative stress-induced aggregation of GAPDH associated with cell death, and a C152A-GAPDH mutant rescues nitric oxide (NO)-induced cell death by interfering with aggregation of wild type (WT)-GAPDH. However, the detailed mechanism underlying GAPDH-aggregate-induced cell death remains elusive...
February 6, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28167264/surface-modified-particles-loaded-with-camkii-inhibitor-protect-cardiac-cells-against-mitochondrial-injury
#9
Amaraporn Wongrakpanich, Angie S Morris, Sean M Geary, Mei-Ling A Joiner, Aliasger K Salem
An excess of calcium (Ca(2+)) influx into mitochondria during mitochondrial re-energization is one of the causes of myocardial cell death during ischemic/reperfusion injury. This overload of Ca(2+) triggers the mitochondrial permeability transition pore (mPTP) opening which leads to programmed cell death. During the ischemic/reperfusion stage, the activated Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) enzyme is responsible for Ca(2+) influx. To reduce CaMKII-related cell death, sub-micron particles composed of poly(lactic-co-glycolic acid) (PLGA), loaded with a CaMKII inhibitor peptide were fabricated...
February 3, 2017: International Journal of Pharmaceutics
https://www.readbyqxmd.com/read/28160133/cardioprotective-kinase-signaling-to-subsarcolemmal-and-interfibrillar-mitochondria-is-mediated-by-caveolar-structures
#10
Wylly Ramsés García-Niño, Francisco Correa, Julia Isabel Rodríguez-Barrena, Juan Carlos León-Contreras, Mabel Buelna-Chontal, Elizabeth Soria-Castro, Rogelio Hernández-Pando, José Pedraza-Chaverri, Cecilia Zazueta
The demonstration that caveolin-3 overexpression reduces myocardial ischemia/reperfusion injury and our own finding that multiprotein signaling complexes increase in mitochondria in association with caveolin-3 levels, led us to investigate the contribution of caveolae-driven extracellular signal-regulated kinases 1/2 (ERK1/2) on maintaining the function of cardiac mitochondrial subpopulations from reperfused hearts subjected to postconditioning (PostC). Rat hearts were isolated and subjected to ischemia/reperfusion and to PostC...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28152427/discovery-of-1-3-benzyloxy-pyridin-2-yl-3-2-piperazin-1-yl-ethyl-urea-a-new-modulator-for-amyloid-beta-induced-mitochondrial-dysfunction
#11
Ahmed Elkamhawy, Jung-Eun Park, Ahmed H E Hassan, Hyunhwa Ra, Ae Nim Pae, Jiyoun Lee, Beoung-Geon Park, Bongjin Moon, Hyun-Mee Park, Eun Joo Roh
Herein, we report a new series of aliphatic substituted pyridyl-urea small molecules synthesized as potential modulators for amyloid beta (Aβ) induced mitochondrial dysfunction. Their blocking activities against Aβ-induced mitochondrial permeability transition pore (mPTP) opening were evaluated by JC-1 assay which measures the change of mitochondrial membrane potential (ΔΨm). The inhibitory activity of sixteen compounds against Aβ-induced mPTP opening was superior or almost similar to that of the standard Cyclosporin A (CsA)...
December 29, 2016: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28141910/the-mechanism-of-valproic-acid-induced-fanconi-syndrome-involves-mitochondrial-dysfunction-and-oxidative-stress-in-rat-kidney
#12
Reza Heidari, Faezeh Jafari, Forouzan Khodaei, Babak Shirazi Yeganeh, Hossein Niknahad
AIM: Drug-induced kidney proximal tubular injury and renal failure (Fanconi syndrome; FS) is a clinical complication. Valproic acid (VPA) is among the FS-inducing drugs. The current investigation was designed to evaluate the role of mitochondrial dysfunction and oxidative stress in VPA-induced renal injury. METHODS: Animals received VPA (250 and 500 mg/kg, i.p., 15 consecutive days). Serum biomarkers of kidney injury and markers of oxidative stress were assessed...
January 31, 2017: Nephrology
https://www.readbyqxmd.com/read/28141792/preventing-permeability-transition-pore-opening-increases-mitochondrial-maturation-myocyte-differentiation-and-cardiac-function-in-the-neonatal-mouse-heart
#13
Jayson V Lingan, Ryan E Alanzalon, George A Porter
BACKGROUND: In embryonic myocytes, closure of the mitochondrial permeability transition pore (PTP) drives mitochondrial maturation and cardiac myocyte differentiation. Since neonatal cardiac myocytes remain relatively immature, we hypothesized that inducing PTP closure at this age, by inhibiting the PTP regulator, cyclophilin D (CyPD), genetically or with Cyclosporin A (CsA) and NIM811, would increase cardiac function by increasing mitochondrial maturation and myocyte differentiation...
January 31, 2017: Pediatric Research
https://www.readbyqxmd.com/read/28135002/ischemia-reperfusion
#14
Theodore Kalogeris, Christopher P Baines, Maike Krenz, Ronald J Korthuis
Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload)...
December 6, 2016: Comprehensive Physiology
https://www.readbyqxmd.com/read/28132831/transient-opening-of-the-mitochondrial-permeability%C3%A2-transition-pore-induces-microdomain-calcium-transients-in-astrocyte-processes
#15
Amit Agarwal, Pei-Hsun Wu, Ethan G Hughes, Masahiro Fukaya, Max A Tischfield, Abraham J Langseth, Denis Wirtz, Dwight E Bergles
Astrocytes extend highly branched processes that form functionally isolated microdomains, facilitating local homeostasis by redistributing ions, removing neurotransmitters, and releasing factors to influence blood flow and neuronal activity. Microdomains exhibit spontaneous increases in calcium (Ca(2+)), but the mechanisms and functional significance of this localized signaling are unknown. By developing conditional, membrane-anchored GCaMP3 mice, we found that microdomain activity that occurs in the absence of inositol triphosphate (IP3)-dependent release from endoplasmic reticulum arises through Ca(2+) efflux from mitochondria during brief openings of the mitochondrial permeability transition pore...
February 8, 2017: Neuron
https://www.readbyqxmd.com/read/28120038/compensatory-role-of-the-nbcn1-sodium-bicarbonate-cotransporter-on-ca-2-induced-mitochondrial-swelling-in-hypertrophic-hearts
#16
Lorena A Vargas, Fernanda Carrizo Velasquez, Bernardo V Alvarez
NBC Na(+)/HCO3(-) cotransporter (NBCn1) and NHE1 Na(+)/H(+) exchanger have been associated with cardiac disorders and recently located in coronary endothelial cells (CEC) and cardiomyocytes mitochondria, respectively. Mitochondrial NHE1 blockade delays permeability transition pore (MPTP) opening and reduces superoxide levels, two critical events exacerbated in cells of diseased hearts. Conversely, activation of NBCn1 prevented apoptosis in CEC subjected to ischemic stress. We characterized the role of the NHE1 and NBCn1 transporters in heart mitochondria from hypertrophic (SHR) and control (Wistar) rats...
March 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28119815/synthesis-of-hydroxycinnamic-acid-derivatives-as-mitochondria-targeted-antioxidants-and-cytotoxic-agents
#17
Jiyu Li, Dian He, Baitao Wang, Ling Zhang, Kun Li, Qinjian Xie, Lifang Zheng
In order to develop agents with superior chemopreventive and chemotherapeutic properties against hepatocellular carcinomas, mitochondria-targeted hydroxycinnamic acids (MitoHCAs) were synthesized by conjugation with a triphenylphosphonium cation. These synthetic compounds were evaluated for their antioxidant activities in hepatic mitochondria, including against OH(∙-) and ROO(∙-) induced lipid peroxidation. H2O2 production was decreased significantly by increasing glutathione peroxidase and catalase activities...
January 2017: Acta Pharmaceutica Sinica. B
https://www.readbyqxmd.com/read/28118671/mechanistic-approach-for-toxic-effects-of-bupropion-in-primary-rat-hepatocytes
#18
Elham Ahmadian, Hossein Babaei, Alireza Mohajjel Nayebi, Aziz Eftekhari, Mohammad Ali Eghbal
Bupropion is a widely prescribed antidepressant/smoke cessation drug. However, hepatotoxicity is one of its side effects reported in some recipients. The mechanisms by which bupropion induces hepatotoxicity is not clear yet. This experiment was intended to assess the cytotoxic mechanisms of bupropion toward primary rat hepatocytes. Additionally, the effect of α-tocopherol succinate (ALPHA-TOS) and N-acetyl cysteine (NAC) and mitochondrial permeability transition (MPT) pore sealing agent cyclosporine A (Cs A) on this toxicity was investigated...
January 24, 2017: Drug Research
https://www.readbyqxmd.com/read/28110593/new-insight-into-mitochondrial-changes-in-vascular-endothelial-cells-irradiated-by-gamma-ray
#19
Shunying Hu, Yajing Gao, Hao Zhou, Fanxuan Kong, Fengjun Xiao, Pingkun Zhou, Yundai Chen
PURPOSE: To investigate alterations of mitochondria in irradiated endothelial cells so that to further elucidate the mechanism underlying radiation-induced heart disease. MATERIALS AND METHODS: Experiments were performed using human umbilical vein endothelial cells (HUVECs). HUVECs were irradiated with single gamma ray dose of 0Gy, 5Gy, 10Gy, 20Gy, respectively. Apoptosis was assessed by flow cytometry at 24h, 48h, 72h post-irradiation, respectively. The intracellular reactive oxygen species (ROS) was measured with 2',7'-dichlorofluorescein-diacetate (DCFH-DA) at 24h post- irradiation...
January 23, 2017: International Journal of Radiation Biology
https://www.readbyqxmd.com/read/28109286/acetaminophen-attenuates-lipopolysaccharide-induced-cognitive-impairment-through-antioxidant-activity
#20
Wei-Xing Zhao, Jun-Han Zhang, Jiang-Bei Cao, Wei Wang, Dong-Xin Wang, Xiao-Ying Zhang, Jun Yu, Yong-Yi Zhang, You-Zhi Zhang, Wei-Dong Mi
BACKGROUND: Considerable evidence has shown that neuroinflammation and oxidative stress play an important role in the pathophysiology of postoperative cognitive dysfunction (POCD) and other progressive neurodegenerative disorders. Increasing evidence suggests that acetaminophen (APAP) has unappreciated antioxidant and anti-inflammatory properties. However, the impact of APAP on the cognitive sequelae of inflammatory and oxidative stress is unknown. The objective of this study is to explore whether APAP could have neuroprotective effects on lipopolysaccharide (LPS)-induced cognitive impairment in mice...
January 21, 2017: Journal of Neuroinflammation
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