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https://www.readbyqxmd.com/read/28527718/rotenone-decreases-ischemia-induced-injury-by-inhibiting-mitochondrial-permeability-transition-in-mature-brains
#1
Evelina Rekuviene, Laima Ivanoviene, Vilmante Borutaite, Ramune Morkuniene
The mitochondrial permeability transition pore (mPTP) is thought to be implicated in brain ischemia-induced cell death. Here we sought to determine whether complex I (CI) of the mitochondrial electron transfer system may be involved in regulation of mPTP opening during ischemia and whether a specific inhibitor of this complex - rotenone can protect against ischemia-induced cell death in an experimental model of total ischemia in adult rat brains. Anesthetized Wistar rats were administered a single injection of rotenone (0...
May 17, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28511953/small-conductance-ca-2-activated-k-channels-in-the-plasma-membrane-mitochondria-and-the-er-pharmacology-and-implications-in-neuronal-diseases
#2
REVIEW
Birgit Honrath, Inge Krabbendam, Carsten Culmsee, Amalia Dolga
Ca(2+)-activated K(+) (KCa) channels regulate after-hyperpolarization in many types of neurons in the central and peripheral nervous system. Small conductance Ca(2+)-activated K(+) (KCa2/SK) channels, a subfamily of KCa channels, are widely expressed in the central and peripheral nervous system, and in the cardiovascular system. Voltage-independent SK channels are activated by alterations in intracellular Ca(2+) ([Ca(2+)]i) which facilitates the opening of these channels through binding of Ca(2+) to calmodulin that is constitutively bound to the SK2 C-terminus...
May 13, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28509380/amyloid-is-essential-but-insufficient-for-alzheimer-causation-addition-of-subcellular-cofactors-is-required-for-dementia
#3
REVIEW
Jeffrey Fessel
OBJECTIVE: The aim of this study is to examine the hypotheses stating the importance of amyloid or of its oligomers in the pathogenesis of Alzheimer's disease (AD). METHODS: Published studies were examined. RESULTS: The importance of amyloid in the pathogenesis of AD is well established, yet accepting it as the main cause for AD is problematic, because amyloid-centric treatments have provided no clinical benefit and about one-third of cognitively normal, older persons have cerebral amyloid plaques...
May 16, 2017: International Journal of Geriatric Psychiatry
https://www.readbyqxmd.com/read/28508993/14-15-eet-suppresses-neuronal-apoptosis-in-ischemia-reperfusion-through-the-mitochondrial-pathway
#4
Hui-Xia Geng, Rui-Ping Li, Ying-Ge Li, Xiao-Qing Wang, Li Zhang, Jin-Bo Deng, Lai Wang, Jie-Xin Deng
Neuronal apoptosis mediated by the mitochondrial apoptosis pathway is an important pathological process in cerebral ischemia-reperfusion injury. 14,15-EET, an intermediate metabolite of arachidonic acid, can promote cell survival during ischemia/reperfusion. However, whether the mitochondrial apoptotic pathway is involved this survival mechanism is not fully understood. In this study, we observed that infarct size in ischemia-reperfusion injury was reduced in sEH gene knockout mice. In addition, Caspase 3 activation, cytochrome C release and AIF nuclear translocation were also inhibited...
May 16, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28508173/neuroprotective-effects-of-lycium-barbarum-polysaccharide-on-focal-cerebral-ischemic-injury-in-mice
#5
Peng Zhao, Ru Zhou, Xiao-Yun Zhu, Gang Liu, Yu-Ping Zhao, Peng-Sheng Ma, Wei Wu, Yang Niu, Tao Sun, Yu-Xiang Li, Jian-Qiang Yu, Zhong-Ming Qian
Increasing evidence demonstrates inflammation contributes to neuronal death following cerebral ischemia. Lycium barbarum polysaccharide (LBP) has been reported to prevent scopolamine-induced cognitive and memory deficits. We recently indicated that LBP exerts neuroprotective effect against focal cerebral ischemic injury in mice via attenuating the mitochondrial apoptosis pathway. The aim of this study was to investigate the neuroprotective effects of LBP against the behavioral dysfunction induced by focal cerebral ischemia injury in mice...
May 15, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28507314/metabolic-imaging-of-energy-metabolism-in-traumatic-brain-injury-using-hyperpolarized-1-13-c-pyruvate
#6
Stephen J DeVience, Xin Lu, Julie Proctor, Parisa Rangghran, Elias R Melhem, Rao Gullapalli, Gary M Fiskum, Dirk Mayer
Traumatic brain injury (TBI) is known to cause perturbations in the energy metabolism of the brain, but current tests of metabolic activity are only indirect markers of energy use or are highly invasive. Here we show that hyperpolarized (13)C magnetic resonance spectroscopic imaging (MRSI) can be used as a direct, non-invasive method for studying the effects of TBI on energy metabolism. Measurements were performed on rats with moderate TBI induced by controlled cortical impact on one cerebral hemisphere. Following injection of hyperpolarized [1-(13)C]pyruvate, the resulting (13)C-bicarbonate signal was found to be 24 ± 6% lower in the injured hemisphere compared with the non-injured hemisphere, while the hyperpolarized bicarbonate-to-lactate ratio was 33 ± 8% lower in the injured hemisphere...
May 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28492973/fast-therapeutic-hypothermia-prevents-post-cardiac-arrest-syndrome-through-cyclophilin-d-mediated-mitochondrial-permeability-transition-inhibition
#7
Vincent Jahandiez, Martin Cour, Thomas Bochaton, Maryline Abrial, Joseph Loufouat, Abdallah Gharib, Annie Varennes, Michel Ovize, Laurent Argaud
The opening of the mitochondrial permeability transition pore (PTP), which is regulated by the matrix protein cyclophilin D (CypD), plays a key role in the pathophysiology of post-cardiac arrest (CA) syndrome. We hypothesized that therapeutic hypothermia could prevent post-CA syndrome through a CypD-mediated PTP inhibition in both heart and brain. In addition, we investigated whether specific pharmacological PTP inhibition would confer additive protection to cooling. Adult male New Zealand White rabbits underwent 15 min of CA followed by 120 min of reperfusion...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28492551/haploinsufficiency-in-the-mitochondrial-protein-chchd4-reduces-brain-injury-in-a-mouse-model-of-neonatal-hypoxia-ischemia
#8
Yanyan Sun, Tao Li, Cuicui Xie, Yiran Xu, Kai Zhou, Juan Rodriguez, Wei Han, Xiaoyang Wang, Guido Kroemer, Nazanine Modjtahedi, Klas Blomgren, Changlian Zhu
Mitochondria contribute to neonatal hypoxic-ischemic brain injury by releasing potentially toxic proteins into the cytosol. CHCHD4 is a mitochondrial intermembrane space protein that plays a major role in the import of intermembrane proteins and physically interacts with apoptosis-inducing factor (AIF). The purpose of this study was to investigate the impact of CHCHD4 haploinsufficiency on mitochondrial function and brain injury after cerebral hypoxia-ischemia (HI) in neonatal mice. CHCHD4(+/-) and wild-type littermate mouse pups were subjected to unilateral cerebral HI on postnatal day 9...
May 11, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28473298/maintenance-of-neural-activities-in-torpid-rhinolophus-ferrumequinum-bats-revealed-by-2d-gel-based-proteome-analysis
#9
Qiuyuan Yin, Yijian Zhang, Dong Dong, Ming Lei, Shuyi Zhang, Chen-Chung Liao, Yi-Hsuan Pan
Bats are the only mammals capable of self-powered flying. Many bat species hibernate in winter. A reversible control of cerebral activities is critical for bats to accommodate a repeated torpor-arousal cycle during hibernation. Little is known about the molecular mechanisms that regulate neuronal activities in torpid bats. In this study, Rhinolophus ferrumequinum bat brain proteins were fractionated, and their abundance in active and torpid states was compared. Results of 2D gel-based proteomics showed that 38% of identified proteins with a significant change in abundance are involved in synaptic vesicle recycling and cytoskeletal integrity...
May 1, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28453191/naringenin-prevents-ischemic-stroke-damage-via-anti-apoptotic-and-anti-oxidant-effects
#10
Kaihua Wang, Zhenzhen Chen, Jianmin Huang, Longjian Huang, Ning Luo, Xiulin Liang, Mingkun Liang, Wei Xie
Apoptosis and oxidative stress are considered to be the major factors associated with the development and progression of many ischemic cerebrovascular diseases. Naringenin (NAR) is an abundant flavanone in citrus plants and has been found to exhibit anti-oxidant, anti-carcinogenic and anti-apoptotic effects. This study aimed to investigate the anti-apoptotic and anti-oxidant effects of naringenin on ischemic stroke. In vitro, cortical neuron cells isolated from the brains of neonatal Sprague-Dawley rats were randomly divided into control, oxygen and glucose deprivation/reperfusion (OGD/Rep), NAR-L, NAR-M and NAR-H groups...
April 28, 2017: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/28443065/hemoglobin-improved-protection-in-cultured-cerebral-cortical-astroglial-cells-inhibition-of-oxidative-stress-and-caspase-activation
#11
Fatma Amri, Ikram Ghouili, Marie-Christine Tonon, Mohamed Amri, Olfa Masmoudi-Kouki
Oxidative stress plays a major role in triggering astroglial cell death in diverse neuropathological conditions such as ischemia and neurodegenerative diseases. Numerous studies indicate that hemoglobin (Hb) is expressed in both resting and reactive glia cells, but nothing is known regarding a possible role of Hb on astroglial cell survival. Thus, the purpose of the present study was to investigate the potential glioprotective effect of Hb on hydrogen peroxide (H2O2)-induced oxidative stress and apoptosis in cultured rat astrocytes...
2017: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/28440425/mitochondrial-transcription-factor-a-tfam-is-upregulated-in-glioma
#12
Hyunji Lee, Jisoo Park, Quangdon Tran, Dohoon Kim, Youngeun Hong, Hyeonjeong Cho, So Hee Kwon, Derek Brazil, Seon-Hwan Kim, Jongsun Park
Mitochondrial transcription factor A (TFAM), which was initially discovered as a transcription factor for mitochondrial DNA, has known to be critical for the regulation of mitochondrial DNA. However the possible involvement of TFAM in cancer is largely unknown. In this study, we have provided some evidence that TFAM may have a potential role in brain tumor. Western blot analysis with anti‑TFAM antibody indicated that TFAM is overexpressed in glioblastoma cell lines including U87MG and U251MG. Transcriptome profiling of U87MG and U251MG cells by using deep‑sequencing revealed that TFAM transcripts were upregulated in these cells compared to its of cerebral cortex...
June 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28438718/the-effect-of-50-compared-to-100-inspired-oxygen-fraction-on-brain-oxygenation-and-post-cardiac-arrest-mitochondrial-function-in-experimental-cardiac-arrest
#13
Annika Nelskylä, Jouni Nurmi, Milla Jousi, Alexey Schramko, Eero Mervaala, Giuseppe Ristagno, Markus B Skrifvars
BACKGROUND AND AIM: We hypothesised that the use of 50% compared to 100% oxygen maintains cerebral oxygenation and ameliorates the disturbance of cardiac mitochondrial respiration during cardiopulmonary resuscitation (CPR). METHODS: Ventricular fibrillation (VF) was induced electrically in anaesthetised healthy adult pigs and left untreated for seven minutes followed by randomisation to manual ventilation with 50% or 100% oxygen and mechanical chest compressions (LUCAS(®))...
April 22, 2017: Resuscitation
https://www.readbyqxmd.com/read/28436815/moyamoya-in-a-patient-with-fires-a-first-case-report
#14
Taylor Kaufman, Andrew White
Febrile infection-related epilepsy syndrome (FIRES) is a form of epileptic encephalopathy with severe refractory epilepsy that presents in previously healthy, school-aged children after significant febrile illness with concomitant rise in body temperature. Suspected causes include genetic or acquired channelopathies, as well as mitochondrial disturbances. In FIRES, the EEG shows diffuse slowing, generalized, and/or multifocal discharges. Seizures are present and resistant to treatment. Moyamoya angiopathy (MMA) is characterized by progressive stenosis of cerebral arteries and subsequent development of a network of collateral circulation that is prone to rupture...
2017: Neurodiagnostic Journal
https://www.readbyqxmd.com/read/28431972/mitochondrial-energy-metabolism-of-rat-hippocampus-after-treatment-with-the-antidepressants-desipramine-and-fluoxetine
#15
Roberto Federico Villa, Federica Ferrari, Laura Bagini, Antonella Gorini, Nicoletta Brunello, Fabio Tascedda
Alterations in mitochondrial functions have been hypothesized to participate in the pathogenesis of depression, because brain bioenergetic abnormalities have been detected in depressed patients by neuroimaging in vivo studies. However, this hypothesis is not clearly demonstrated in experimental studies: some suggest that antidepressants are inhibitors of mitochondrial metabolism, while others observe the opposite. In this study, the effects of 21-day treatment with desipramine (15 mg/kg) and fluoxetine (10 mg/kg) were examined on the energy metabolism of rat hippocampus, evaluating the catalytic activity of regulatory enzymes of mitochondrial energy-yielding metabolic pathways...
April 18, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28429368/-aralar-agc1-deficiency-a-neurodevelopmental-disorder-with-severe-impairment-of-neuronal-mitochondrial-respiration-does-not-produce-a-primary-increase-in-brain-lactate
#16
Inés Juaristi, María L García-Martin, Tiago B Rodrigues, Jorgina Satrústegui, Irene Llorente-Folch, Beatriz Pardo
ARALAR/AGC1 (aspartate-glutamate mitochondrial carrier 1) is an important component of the NADH malate-aspartate shuttle (MAS). AGC1-deficiency is a rare disease causing global cerebral hypomyelination, developmental arrest, hypotonia, and epilepsy (OMIM ID #612949); the aralar-KO mouse recapitulates the major findings in humans. This study was aimed at understanding the impact of ARALAR-deficiency in brain lactate levels as a biomarker. We report that lactate was equally abundant in wild-type and aralar-KO mouse brain in vivo at PND 17...
April 21, 2017: Journal of Neurochemistry
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
#17
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/28427446/respiratory-chain-complex-iii-deficiency-due-to-mutated-bcs1l-a-novel-phenotype-with-encephalomyopathy-partially-phenocopied-in-a-bcs1l-mutant-mouse-model
#18
Saara Tegelberg, Nikica Tomašić, Jukka Kallijärvi, Janne Purhonen, Eskil Elmér, Eva Lindberg, David Gisselsson Nord, Maria Soller, Nicole Lesko, Anna Wedell, Helene Bruhn, Christoph Freyer, Henrik Stranneheim, Rolf Wibom, Inger Nennesmo, Anna Wredenberg, Erik A Eklund, Vineta Fellman
BACKGROUND: Mitochondrial diseases due to defective respiratory chain complex III (CIII) are relatively uncommon. The assembly of the eleven-subunit CIII is completed by the insertion of the Rieske iron-sulfur protein, a process for which BCS1L protein is indispensable. Mutations in the BCS1L gene constitute the most common diagnosed cause of CIII deficiency, and the phenotypic spectrum arising from mutations in this gene is wide. RESULTS: A case of CIII deficiency was investigated in depth to assess respiratory chain function and assembly, and brain, skeletal muscle and liver histology...
April 20, 2017: Orphanet Journal of Rare Diseases
https://www.readbyqxmd.com/read/28413987/alzheimer-s-disease-like-early-phase-brain-pathogenesis-self-curing-amelioration-of-neurodegeneration-from-pro-inflammatory-wounding-to-anti-inflammatory-healing
#19
Jiang He, Tao Liao, Guo-Xin Zhong, Ji-Da Zhang, Yan-Ping Chen, Qi Wang, Qing-Ping Zeng
The etiological initiators of neuroinflammation remain inclusive, and effective interventions to block neurodegeneration are unavailable. Surprisingly, we found collagen II-combined complete Freund's adjuvant (CC) that usually induces rheumatoid arthritis (RA) also drives Alzheimer's disease (AD)-like neurodegeneration in mice. CC not only upregulates the cerebral pro-inflammatory cytokines including tumor necrosis factor α (TNF-α) and interleukin 8 (IL-8), but also downregulates the cerebral interleukin 10 (IL-10), an anti-inflammatory cytokine, and tyrosine hydroxylase (TH), a rate-limiting enzyme for biosynthesis of the anti-inflammatory neurotransmitter dopamine...
April 17, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28401402/ischemia-reperfusion-induced-translocation-of-pkc%C3%AE-ii-to-mitochondria-as-an-important-mediator-of-a-protective-signaling-mechanism-in-an-ischemia-resistant-region-of-the-hippocampus
#20
Olga Krupska, Anna Sarnowska, Bartlomiej Fedorczyk, Magdalena Gewartowska, Aleksandra Misicka, Barbara Zablocka, Malgorzata Beresewicz
Emerging reports indicate that activated PKC isoforms that translocate to the mitochondria are pro- or anti-apoptotic to mitochondrial function. Here, we concentrate on the role of PKCβ translocated to mitochondria in relation to the fate of neurons following cerebral ischemia. As we have demonstrated previously ischemia/reperfusion injury (I/R) results in translocation of PKCβ from cytoplasm to mitochondria, but only in ischemia-resistant regions of the hippocampus (CA2-4, DG), we hypothesize that this translocation may be a mediator of a protective signaling mechanism in this region...
April 12, 2017: Neurochemical Research
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