MTERF4 regulates the mitochondrial dysfunction induced by MPP+ in SH-SY5Y cells

Ye, Xiaofei; Han, Yanyan; Zhang, Linbing; Liu, Wen; Zuo, Jiane

doi:10.1016/j.bbrc.2015.06.119

Cited by 14 publications

(12 citation statements)

References 22 publications

(30 reference statements)

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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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“…MTERF4 contributes to the regulation of mitochondrial translation by targeting NOP2/sun RNA methyltransferase family member 4 (NSUN4) to large mitochondrial ribosome, and MTERF4-knockout also leads to mouse embryo death (16). A previous study also provided a novel insight into the association between MTERF4 and MPP + -induced mitochondrial damage (17). In addition, MTERF4 has been hypothesized to be one of the triggering genes for Parkinson's disease, which is induced by an environmental toxin (17).…”

Section: Introductionmentioning

confidence: 95%

Prognostic roles of mitochondrial transcription termination factors in non‑small cell lung cancer

Sun

Yang

et al. 2019

Oncol Lett

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Mitochondrial transcription termination factors (MTERFs) regulate mitochondrial gene transcription and metabolism in numerous types of cells. Previous studies have indicated that MTERFs serve pivotal roles in the pathogenesis of various cancer types. However, the expression and prognostic roles of MTERFs in patients with non-small cell lung cancer (NSCLC) remain elusive. The present study investigated the gene alteration frequency and expression level using Gene Expression Omnibus datasets and reverse transcription-quantitative polymerase chain reaction, and evaluated the prognostic roles of MTERFs in patients with NSCLC using the Kaplan-Meier plotter database. In human lung cancer tissues, it was observed that the mRNA levels of MTERF1, 2, 3 and 4 were positively associated with the copy number of these genes. The mRNA expression levels of MTERF1 and 3 were significantly increased in NSCLC tissues compared with adjacent non-tumor tissues; however, the mRNA expression of MTERF2 was significantly decreased in NSCLC tissues. High mRNA expression levels of MTERF1, 2, 3 and 4 were strongly associated with an improved overall survival rate (OS) in patients with lung adenocarcinoma. Additionally, high mRNA expression levels of MTERF1, 2, 3 and 4 were also strongly associated with an improved OS of patients with NSCLC in the earlier stages of disease (stage I) or patients with negative surgical margins. These results indicate the critical prognostic values of MTERF expression levels in NSCLC. The findings of the present study may be beneficial for understanding the molecular biology mechanism of NSCLC and for generating effective therapeutic approaches for patients with NSCLC.

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MTERF4 regulates the mitochondrial dysfunction induced by MPP+ in SH-SY5Y cells

Cited by 14 publications

References 22 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

Prognostic roles of mitochondrial transcription termination factors in non‑small cell lung cancer

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