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Condition: Mitochondrial Disease

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Total 454 results found since Jan 2013.

Exendin-4 attenuates endoplasmic reticulum stress through a SIRT1-dependent mechanism.
In conclusion, increased SIRT1 by exendin-4 attenuates PA-induced ER stress and mitochondrial dysfunction in hepatocytes. PMID: 24446069 [PubMed - as supplied by publisher]
Source: Cell Stress and Chaperones - January 21, 2014 Category: Cytology Authors: Lee J, Hong SW, Park SE, Rhee EJ, Park CY, Oh KW, Park SW, Lee WY Tags: Cell Stress Chaperones Source Type: research

Mortalin Inhibition and Mitochondrial Dysfunction Cell Biology
Mitochondrial dynamics greatly influence the biogenesis and morphology of mitochondria. Mitochondria are particularly important in neurons, which have a high demand for energy. Therefore, mitochondrial dysfunction is strongly associated with neurodegenerative diseases. Until now various post-translational modifications for mitochondrial dynamic proteins and several regulatory proteins have explained complex mitochondrial dynamics. However, the precise mechanism that coordinates these complex processes remains unclear. To further understand the regulatory machinery of mitochondrial dynamics, we screened a mitochondrial siRN...
Source: Journal of Biological Chemistry - January 24, 2014 Category: Chemistry Authors: Park, S. J., Shin, J. H., Jeong, J. I., Song, J. H., Jo, Y. K., Kim, E. S., Lee, E. H., Hwang, J. J., Lee, E. K., Chung, S. J., Koh, J.-Y., Jo, D.-G., Cho, D.-H. Tags: Neurobiology Source Type: research

A Role for Myosin II in Mammalian Mitochondrial Fission.
Abstract Mitochondria are dynamic organelles, undergoing both fission and fusion regularly in interphase cells. Mitochondrial fission is thought to be part of a quality-control mechanism whereby damaged mitochondrial components are segregated from healthy components in an individual mitochondrion, followed by mitochondrial fission and degradation of the damaged daughter mitochondrion [1]. Fission also plays a role in apoptosis [2]. Defects in mitochondrial dynamics can lead to neurodegenerative diseases such as Alzheimer's disease [3]. Mitochondrial fission requires the dynamin GTPase Drp1, which assembles in a ri...
Source: Current Biology - January 28, 2014 Category: Biology Authors: Korobova F, Gauvin TJ, Higgs HN Tags: Curr Biol Source Type: research

Evidence for association of mitochondrial metabolism alteration with lipid accumulation in aging rats.
Abstract Adipogenesis and lipid accumulation during aging have a great impact on the aging process and the pathogenesis of chronic, age-related diseases. However, little is known about the age-related molecular changes in lipid accumulation and the mechanisms underlying them. Here, using 5-month- and 25-month-old rats (young and old, respectively), we found that epididymal fat is the only tissue to accumulate during aging. By testing tissues rich with mitochondria in old and young animals, we found that the old animals had elevated levels of triglycerides in their muscle, heart and liver tissues but not in their k...
Source: Experimental Gerontology - February 8, 2014 Category: Geriatrics Authors: Zhao L, Zou X, Feng Z, Luo C, Liu J, Li H, Chang L, Wang H, Li Y, Long J, Gao F, Liu J Tags: Exp Gerontol Source Type: research

Role of hOgg1 and Aco-2 in Oxidant-induced mtDNA Damage Molecular Bases of Disease
Mitochondria-targeted human 8-oxoguanine DNA glycosylase (mt-hOgg1) and aconitase-2 (Aco-2) each reduce oxidant-induced alveolar epithelial cell (AEC) apoptosis, but it is unclear whether protection occurs by preventing AEC mitochondrial DNA (mtDNA) damage. Using quantitative PCR-based measurements of mitochondrial and nuclear DNA damage, mtDNA damage was preferentially noted in AEC after exposure to oxidative stress (e.g. amosite asbestos (5–25 μg/cm2) or H2O2 (100–250 μm)) for 24 h. Overexpression of wild-type mt-hOgg1 or mt-long α/β 317–323 hOgg1 mutant incapable of DNA repair (mt-hOgg1-Mut) each blocked A549 ...
Source: Journal of Biological Chemistry - February 27, 2014 Category: Chemistry Authors: Kim, S.-J., Cheresh, P., Williams, D., Cheng, Y., Ridge, K., Schumacker, P. T., Weitzman, S., Bohr, V. A., Kamp, D. W. Tags: Cell Biology Source Type: research

δ-Opioid receptor activation reduces ɑ-synuclein overexpression and oligomer formation induced by MPP(+) and/or hypoxia.
Abstract Hypoxic/ischemic brain injury is a potential cause of Parkinson's disease (PD) with ɑ-synuclein playing a critical role in the pathophysiology. Since δ-Opioid receptor (DOR) is neuroprotective against hypoxic/ischemic insults, we sought to determine if DOR regulates ɑ-synuclein under hypoxia and/or MPP(+) stress. We found that in HEK293 cells 1) MPP(+) in normoxia enhanced ɑ-synuclein expression and the formation of ɑ-synuclein oligomers thereby causing cytotoxic injury; 2) hypoxia at 1% O2 for 48hrs or at 0.5% O2 for 24hrs also induced ɑ-synuclein overexpression and its oligomer formation with cell...
Source: Experimental Neurology - March 5, 2014 Category: Neurology Authors: Chen T, Li J, Chao D, Sandhu HK, Liao X, Zhao J, Wen G, Xia Y Tags: Exp Neurol Source Type: research

Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance.
CONCLUSIONS: A mutual enhancement between DRP1 and ROS could promote mitochondrial dysfunction and inhibition of insulin signal transduction. However, other mechanisms, including lipid metabolite-induced mitochondrial dysfunction, may be involved in palmitate-induced insulin resistance. PMID: 24631294 [PubMed - as supplied by publisher]
Source: Experimental Cell Research - March 11, 2014 Category: Cytology Authors: Watanabe T, Saotome M, Nobuhara M, Sakamoto A, Urushida T, Katoh H, Satoh H, Funaki M, Hayashi H Tags: Exp Cell Res Source Type: research

Amelioration of Ischemic Mitochondrial Injury and Bax-Dependent Outer Membrane Permeabilization by Mdivi-1.
CONCLUSIONS: Down-regulation or inhibition of Drp1 may reduce cerebral ischemic damage through maintaining normal mitochondrial morphology and function, and decreasing Bax insertion and oligomerization in mitochondria. PMID: 24712408 [PubMed - as supplied by publisher]
Source: CNS Neuroscience and Therapeutics - April 8, 2014 Category: Neuroscience Authors: Zhao YX, Cui M, Chen SF, Dong Q, Liu XY Tags: CNS Neurosci Ther Source Type: research

Metabolic profiling reveals that pnpla3 induces widespread effects on metabolism beyond triacylglycerol remodeling in huh-7 hepatoma cells.
METABOLIC PROFILING REVEALS THAT PNPLA3 INDUCES WIDESPREAD EFFECTS ON METABOLISM BEYOND TRIACYLGLYCEROL REMODELING IN HUH-7 HEPATOMA CELLS. Am J Physiol Gastrointest Liver Physiol. 2014 Apr 24; Authors: Min HK, Sookoian SC, Pirola CJ, Cheng J, Mirshahi F, Sanyal AJ Abstract PNPLA3 was recently associated with the susceptibility to nonalcoholic fatty liver disease, a common cause of chronic liver disease characterized by abnormal triglyceride accumulation. While it is established that PNPLA3 has both triacylglycerol lipase and acylglycerol O-acyltransferase activities, is still unknown whether the gene...
Source: American Journal of Physiology. Gastrointestinal and Liver Physiology - April 24, 2014 Category: Physiology Authors: Min HK, Sookoian SC, Pirola CJ, Cheng J, Mirshahi F, Sanyal AJ Tags: Am J Physiol Gastrointest Liver Physiol Source Type: research

Nucleic acid-based tissue biomarkers of urologic malignancies.
This article provides an overview of nucleic acid-based biomarkers in tissues for the management of urologic malignancies, i.e. tumors of the prostate, testis, kidney, penis, urinary bladder, renal pelvis, ureter and other urinary organs. Special emphasis is put on genomic, transcriptomic and epigenomic biomarkers (SNPs, mutations [genomic and mitochondrial], microsatellite instabilities, viral and bacterial DNA, DNA methylation and hydroxymethylation, mRNA expression, and non-coding RNAs [lncRNA, miRNA, siRNA, piRNA, snRNA, snoRNA]). Due to the multitude of published biomarker candidates, special focus is given to the gen...
Source: Clinical Prostate Cancer - May 30, 2014 Category: Cancer & Oncology Authors: Dietrich D, Meller S, Uhl B, Ralla B, Stephan C, Jung K, Ellinger J, Kristiansen G Tags: Crit Rev Clin Lab Sci Source Type: research

Effect of Tacrine-3-caffeic Acid, A Novel Multifunctional Anti-Alzheimer's Dimer, Against Oxidative-Stress-Induced Cell Death in HT22 Hippocampal Neurons: Involvement of Nrf2/HO-1 Pathway.
CONCLUSIONS: Taken together, these results clearly demonstrate that T3CA protects neurons against OS-induced cell death partially through Nrf2/ARE/HO-1 signaling pathway, which further supports that T3CA might be a promising novel therapeutic agent for OS-associated diseases. PMID: 24922524 [PubMed - as supplied by publisher]
Source: CNS Neuroscience and Therapeutics - June 12, 2014 Category: Neuroscience Authors: Chao XJ, Chen ZW, Liu AM, He XX, Wang SG, Wang YT, Liu PQ, Ramassamy C, Mak SH, Cui W, Kong AN, Yu ZL, Han YF, Pi RB Tags: CNS Neurosci Ther Source Type: research

Metabolic profiling reveals that PNPLA3 induces widespread effects on metabolism beyond triacylglycerol remodeling in Huh-7 hepatoma cells
PNPLA3 was recently associated with the susceptibility to nonalcoholic fatty liver disease, a common cause of chronic liver disease characterized by abnormal triglyceride accumulation. Although it is established that PNPLA3 has both triacylglycerol lipase and acylglycerol O-acyltransferase activities, is still unknown whether the gene has any additional role in the modulation of the human liver metabolome. To uncover the functional role of PNPLA3 on liver metabolism, we performed high-throughput metabolic profiling of PNPLA3 siRNA-silencing and overexpression of wild-type and mutant Ile148Met variants (isoleucine/methionin...
Source: AJP: Gastrointestinal and Liver Physiology - July 1, 2014 Category: Gastroenterology Authors: Min, H.-K., Sookoian, S., Pirola, C. J., Cheng, J., Mirshahi, F., Sanyal, A. J. Tags: LIVER AND BILIARY TRACT Source Type: research

Involvement of activation of the Nrf2/ARE pathway in protection against 6-OHDA-induced SH-SY5Y cell death by α-iso-cubebenol.
This study was carried out in an attempt to clarify the neuroprotective effect of α-iso-cubebenol on toxin-insulted dopaminergic neuronal death using 6-hydroxy-dopamine (6-OHDA)-induced dopaminergic SH-SY5Y cells. α-iso-cubebenol significantly attenuated the loss of mitochondrial function (MTT assay) and membrane integrity (lactate dehydrogenase assay) associated with 6-OHDA-induced neurotoxicity. Pretreatment of the cells with α-iso-cubebenol diminished the intracellular accumulation of reactive oxygen species (ROS) and calcium in response to 6-OHDA. Moreover, α-iso-cubebenol protected against 6-OHDA-induced neurotoxi...
Source: Neurotoxicology - July 2, 2014 Category: Neurology Authors: Park SY, Kim DY, Kang JK, Park G, Choi YW Tags: Neurotoxicology Source Type: research

LOX-1, mtDNA damage, and NLRP3 inflammasome activation in macrophages: implications in atherogenesis
Conclusions This study based on THP-1 macrophages and primary macrophages indicates that LOX-1-mediated autophagy and mtDNA damage play an essential role in NLRP3 inflammasome activation in inflammatory disease states.
Source: Cardiovascular Research - August 26, 2014 Category: Cardiology Authors: Ding, Z., Liu, S., Wang, X., Dai, Y., Khaidakov, M., Deng, X., Fan, Y., Xiang, D., Mehta, J. L. Tags: Vascular biology Source Type: research

p53 Is Required for Mitochondrial Fragmentation Cell Biology
Mitochondria are highly dynamic organelles, and mitochondrial fission is a crucial step of apoptosis. Although Oma1 is believed to be responsible for long form Opa1 (L-Opa1) processing during mitochondrial fragmentation, whether and how Oma1 is involved in L-Opa1 processing and participates in the regulation of chemoresistance is unknown. Chemosensitive and chemoresistant ovarian (OVCA) and cervical (CECA) cancer cells were treated with cisplatin (CDDP). Mitochondrial dynamics and protein contents were assessed by immunofluorescence and Western blot, respectively. The requirements of Oma1 and p53 for CDDP-induced L-Opa1 pr...
Source: Journal of Biological Chemistry - September 25, 2014 Category: Chemistry Authors: Kong, B., Wang, Q., Fung, E., Xue, K., Tsang, B. K. Tags: Molecular Bases of Disease Source Type: research