MTERF2 contributes to MPP+-induced mitochondrial dysfunction and cell damage

Han, Yanyan; Gao, Peiye; Qiu, Shi; Zhang, Linbing; Yang, Ling; Zuo, Jiane; Zhong, Chunjiu; Zhu, Shun; Liu, Wen

doi:10.1016/j.bbrc.2016.01.156

Cited by 8 publications

(6 citation statements)

References 29 publications

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“…ATP adenosine triphosphate, DA dopamine, PD Parkinson’s disease, NDUFS subunits of NADH-ubiquinone oxidoreductase (complex I), ROS reactive oxygen species, NDI-1 yeast NADH dehydrogenase. References: [1] Wirth et al ( 2016 ), [2] Friedrich et al ( 1994 ), [3] Mailloux ( 2015 ), [4] Fernandez-Moreira et al ( 2007 ), [5] Berger et al ( 2008 ), [6] Hoefs et al ( 2008 ), [7] Janssen et al ( 2006 ), [8] Lazarou et al ( 2009 ), [9] Dunning et al ( 2007 ), [10] Ogilvie et al ( 2005 ), [11] Saada et al ( 2008 ), [12] Pagliarini et al ( 2008 ), [13] Koopman et al ( 2007 ), [14] Sheehan et al ( 1997 ), [15] Willems et al ( 2008 ), [16] Ye et al ( 2015 ), [17] Han et al ( 2016 ), [18] Dukes et al ( 2016 ), [19] Wang et al ( 2011 ), [20] Li et al ( 2014 ), [21] Giordano et al ( 2012 ), [22] Piao et al ( 2012 ), [23] Wu et al ( 2009 ), [24] Bi et al ( 2008 ), [25] Nakai et al ( 2003 ), [26] Brownell et al ( 1998 ), [27] Koga et al ( 2006 ), [28] Seo et al ( 1998 ), [29] Sherer et al ( 2003 ), [30] Shults et al ( 2002 ), [31] Moon et al ( 2005 ), [32] Wen et al ( 2011 ), [33] Yang et al ( 2009 ), [34] Matthews et al ( 1999 ), [35] Beal ( 2011 ); [36] Przedborski et al ( 1992 ), [37] Zhang et al ( 2000 ), [38] Filomeni et al ( 2012 ), [39] Wang et al ( 2015 ), [40] Nataraj et al ( 2016 ), [41] Lee et al ( 2011 ), [42] Tseng et al ( 2014 ), [43] Liu et al ( 2015 ), [44] Thomas et al ( 2012 ), [45] Pöltl et al (…”

Section: Key Event Relationships (Kers)mentioning

confidence: 99%

“…Experimental support for a causal relationship between complex I inhibition and mitochondrial dysfunction is largely based on observations made with the complex I inhibitors rotenone and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). A rich experimental basis indicates the direct correlation between complex I inhibition and the emergence of features of mitochondrial dysfunction in cellular and in vivo models exposed to rotenone or MPTP/MPP + (Bi et al 2008 ; Dukes et al 2016 ; Giordano et al 2012 ; Han et al 2016 ; Li et al 2014 ; Nakai et al 2003 ; Piao et al 2012 ; Schildknecht et al 2009 ; Scholz et al 2011 ; Wang et al 2011 ; Wu et al 2009 ; Ye et al 2015 ). Initial studies using proton magnetic resonance spectroscopy ( 1 H-MRS) and positron emission tomography (PET) have illustrated the onset of mitochondrial dysfunction by live measurements in living animals exposed to MPTP (Brownell et al 1998 ; Koga et al 2006 ).…”

Section: Key Event Relationships (Kers)mentioning

confidence: 99%

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An adverse outcome pathway for parkinsonian motor deficits associated with mitochondrial complex I inhibition

et al. 2017

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Epidemiological studies have observed an association between pesticide exposure and the development of Parkinson’s disease, but have not established causality. The concept of an adverse outcome pathway (AOP) has been developed as a framework for the organization of available information linking the modulation of a molecular target [molecular initiating event (MIE)], via a sequence of essential biological key events (KEs), with an adverse outcome (AO). Here, we present an AOP covering the toxicological pathways that link the binding of an inhibitor to mitochondrial complex I (i.e., the MIE) with the onset of parkinsonian motor deficits (i.e., the AO). This AOP was developed according to the Organisation for Economic Co-operation and Development guidelines and uploaded to the AOP database. The KEs linking complex I inhibition to parkinsonian motor deficits are mitochondrial dysfunction, impaired proteostasis, neuroinflammation, and the degeneration of dopaminergic neurons of the substantia nigra. These KEs, by convention, were linearly organized. However, there was also evidence of additional feed-forward connections and shortcuts between the KEs, possibly depending on the intensity of the insult and the model system applied. The present AOP demonstrates mechanistic plausibility for epidemiological observations on a relationship between pesticide exposure and an elevated risk for Parkinson’s disease development.

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Section: Key Event Relationships (Kers)mentioning

confidence: 99%

Section: Key Event Relationships (Kers)mentioning

confidence: 99%

An adverse outcome pathway for parkinsonian motor deficits associated with mitochondrial complex I inhibition

et al. 2017

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“…Impairment in the function and expression of PGC-1α, a key regulator of mitochondrial biogenesis is also responsible for PD [47]. Further, mitochondrial transcription termination factor 2 and 4 (MTERF2 and MTERF4) has been identified in 1-methyl-4-phenylpyridinium (MPP+)-induced PD brain that is responsible for mitochondrial dysfunction [48,49]. Recently, SUMOylation, an epigenetic modification has also been found to be involved in mitochondrial dysfunction associated with PD progression [50].…”

Section: Parkinson's Diseasementioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

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“…The MTERF2 gene belongs to the mitochondrial transcription termination factor ( MTERF ) family, which has been reported to be linked with the regulation of mtDNA replication and transcription [54,55]. In human MTERF2 is highly expressed in tissues that are highly dependent on the mitochondrial energy production and may regulate oxidative phosphorylation by modulating mitochondrial DNA transcription [56,57]. The MTERF family in mammals has four members, named MTERF1 to MTERF4 , in which MTERF1 was explored more widely.…”

Section: Discussionmentioning

confidence: 99%

Marek’s Disease Virus Infection Induced Mitochondria Changes in Chickens

Chu

Ding

Cai

et al. 2019

IJMS

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Mitochondria are crucial cellular organelles in eukaryotes and participate in many cell processes including immune response, growth development, and tumorigenesis. Marek’s disease (MD), caused by an avian alpha-herpesvirus Marek’s disease virus (MDV), is characterized with lymphomas and immunosuppression. In this research, we hypothesize that mitochondria may play roles in response to MDV infection. To test it, mitochondrial DNA (mtDNA) abundance and gene expression in immune organs were examined in two well-defined and highly inbred lines of chickens, the MD-susceptible line 72 and the MD-resistant line 63. We found that mitochondrial DNA contents decreased significantly at the transformation phase in spleen of the MD-susceptible line 72 birds in contrast to the MD-resistant line 63. The mtDNA-genes and the nucleus-genes relevant to mtDNA maintenance and transcription, however, were significantly up-regulated. Interestingly, we found that POLG2 might play a potential role that led to the imbalance of mtDNA copy number and gene expression alteration. MDV infection induced imbalance of mitochondrial contents and gene expression, demonstrating the indispensability of mitochondria in virus-induced cell transformation and subsequent lymphoma formation, such as MD development in chicken. This is the first report on relationship between virus infection and mitochondria in chicken, which provides important insights into the understanding on pathogenesis and tumorigenesis due to viral infection.

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MTERF2 contributes to MPP+-induced mitochondrial dysfunction and cell damage

Cited by 8 publications

References 29 publications

An adverse outcome pathway for parkinsonian motor deficits associated with mitochondrial complex I inhibition

An adverse outcome pathway for parkinsonian motor deficits associated with mitochondrial complex I inhibition

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Marek’s Disease Virus Infection Induced Mitochondria Changes in Chickens

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