Assignment of the Human Mitochondrial NAD+-Specific Isocitrate Dehydrogenase α Subunit (IDH3A) Gene to 15q25.1 → q25.2 byin SituHybridization

Huh, Tae‐Lin; Kim, Yong-Ou; Oh, Il-Ung; Song, Byoung Joon; Inazawa, Johji

doi:10.1006/geno.1996.0120

Cited by 19 publications

(10 citation statements)

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“…This process is considered to be one of the key enzymes in the tricarboxylic acid (TCA) cycle. In mammals, there are three types of isoenzymes represented by cytosolic NADP-specific IDH (IDH1), mitochondrial NADP-specific IDH (IDH2), and mitochondrial NAD-specific IDH (IDH3) [67]. IDH3 is composed of three distinct types of subunits in the ratio 2alpha:1beta:1gamma [68].…”

Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of Mesenchymal Stem Cells from Normal and Deep Carious Dental Pulp

Cui

Gao

et al. 2014

PLoS ONE

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Dental pulp stem cells (DPSCs), precursor cells of odontoblasts, are ideal seed cells for tooth tissue engineering and regeneration. Our previous study has demonstrated that stem cells exist in dental pulp with deep caries and are called carious dental pulp stem cells (CDPSCs). The results indicated that CDPSCs had a higher proliferative and stronger osteogenic differentiation potential than DPSCs. However, the molecular mechanisms responsible for the biological differences between DPSCs and CDPSCs are poorly understood. The aim of this study was to define the molecular features of DPSCs and CDPSCs by comparing the proteomic profiles using two-dimensional fluorescence difference gel electrophoresis (2-D DIGE) in combination with matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS). Our results revealed that there were 18 protein spots differentially expressed between DPSCs and CDPSCs in a narrow pH range of 4 to 7. These differently expressed proteins are mostly involved in the regulation of cell proliferation, differentiation, cell cytoskeleton and motility. In addition, our results suggested that CDPSCs had a higher expression of antioxidative proteins that might protect CDPSCs from oxidative stress. This study explores some potential proteins responsible for the biological differences between DPSCs and CDPSCs and expands our understanding on the molecular mechanisms of mineralization of DPSCs in the formation of the dentin-pulp complex.

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Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of Mesenchymal Stem Cells from Normal and Deep Carious Dental Pulp

Cui

Gao

et al. 2014

PLoS ONE

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“…Idh3a promotes ATP production by catalyzing the oxidative decarboxylation of isocitrate to 2-oxoglutarate. Cpt1b generates ATP from lipids via beta-oxidation of fatty acids (62–64). Expression of ATP5C1 is enhanced.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Gene Expression Profiles and Metabolic Pathways in the Amygdala Associated with Exaggerated Fear in an Animal Model of PTSD

Smerin

et al. 2014

Front. Neurol.

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The metabolic mechanisms underlying the development of exaggerated fear in post-traumatic stress disorder (PTSD) are not well defined. In the present study, alteration in the expression of genes associated with mitochondrial function in the amygdala of an animal model of PTSD was determined. Amygdala tissue samples were excised from 10 non-stressed control rats and 10 stressed rats, 14 days post-stress treatment. Total RNA was isolated, cDNA was synthesized, and gene expression levels were determined using a cDNA microarray. During the development of the exaggerated fear associated with PTSD, 48 genes were found to be significantly upregulated and 37 were significantly downregulated in the amygdala complex based on stringent criteria (p < 0.01). Ingenuity pathway analysis revealed up- or downregulation in the amygdala complex of four signaling networks – one associated with inflammatory and apoptotic pathways, one with immune mediators and metabolism, one with transcriptional factors, and one with chromatin remodeling. Thus, informatics of a neuronal gene array allowed us to determine the expression profile of mitochondrial genes in the amygdala complex of an animal model of PTSD. The result is a further understanding of the metabolic and neuronal signaling mechanisms associated with delayed and exaggerated fear.

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“…The presence of a distinct gene for IDPm has been demonstrated by the biochemical characterization, chromosomal location, and molecular cloning and sequence analyses of IDPm genes in different species (26,(47)(48)(49). Deduced IDPm proteins in various species including human IDPm (GenBank accession number X69433) 2 share highly conserved sequences.…”

Section: Discussionmentioning

confidence: 99%

Control of Mitochondrial Redox Balance and Cellular Defense against Oxidative Damage by Mitochondrial NADP+-dependent Isocitrate Dehydrogenase

Jo¹,

Son²,

Koh³

et al. 2001

Journal of Biological Chemistry

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492

365

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Mitochondria are the major organelles that produce reactive oxygen species (ROS) and the main target of ROS-induced damage as observed in various pathological states including aging. Production of NADPH required for the regeneration of glutathione in the mitochondria is critical for scavenging mitochondrial ROS through glutathione reductase and peroxidase systems. We investigated the role of mitochondrial NADP ؉ -dependent isocitrate dehydrogenase (IDPm) in controlling the mitochondrial redox balance and subsequent cellular defense against oxidative damage. We demonstrate in this report that IDPm is induced by ROS and that decreased expression of IDPm markedly elevates the ROS generation, DNA fragmentation, lipid peroxidation, and concurrent mitochondrial damage with a significant reduction in ATP level. Conversely, overproduction of IDPm protein efficiently protected the cells from ROS-induced damage. The protective role of IDPm against oxidative damage may be attributed to increased levels of a reducing equivalent, NADPH, needed for regeneration of glutathione in the mitochondria. Our results strongly indicate that IDPm is a major NADPH producer in the mitochondria and thus plays a key role in cellular defense against oxidative stress-induced damage.Cell damage induced by oxidative stress and reactive oxygen species (ROS) 1 has been implicated in several human diseases including aging, alcohol-mediated organ damage, neurodegenerative diseases, many types of cancers, cardiovascular diseases, and UV-mediated skin disorders (1). As one of the major sources of ROS (2), mitochondria are highly susceptible to oxidative damage. ROS can damage mitochondrial enzymes directly (3), and they can cause mutation in mitochondrial DNAs (4). At the same time, ROS can change the mitochondrial transmembrane potential (⌬m), which is indicative of mitochondrial membrane integrity (5) and precedes cell death induced by various toxic compounds and cytokines (6). Recent reports indicate that mitochondrial ROS cause apoptosis (7, 8) by activating various apoptotic effectors such as cytochrome c release, procaspase-2, procaspase-9, procaspase-3, and latent apoptosis-inducing factor, which is released from the mitochondria during apoptosis (9 -11). Another report also suggested that mitochondrial ROS directly caused apoptosis of T cells (12). It was also reported that tumor necrosis factor ␣ causes a rapid production of mitochondrial ROS (13) and that ceramide, an apoptotic stimulus, also plays a crucial role in tumor necrosis factor ␣-induced mitochondrial ROS generation (14). Furthermore, several other investigators demonstrated that ROS are involved in the signaling pathway of certain growth factors (15) and cytokines (16). In addition, mitochondrial ROS, under hypoxic conditions, activate the transcription of the genes for glycolytic enzymes as well as erythropoietin and vascular endothelial growth factor by upregulating a transcriptional factor, hypoxia-inducible factor 1 (17), suggesting that mitochondrial ROS mediate cross-talk b...

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Assignment of the Human Mitochondrial NAD+-Specific Isocitrate Dehydrogenase α Subunit (IDH3A) Gene to 15q25.1 → q25.2 byin SituHybridization

Cited by 19 publications

References 0 publications

Proteomic Analysis of Mesenchymal Stem Cells from Normal and Deep Carious Dental Pulp

Proteomic Analysis of Mesenchymal Stem Cells from Normal and Deep Carious Dental Pulp

Mitochondrial Gene Expression Profiles and Metabolic Pathways in the Amygdala Associated with Exaggerated Fear in an Animal Model of PTSD

Control of Mitochondrial Redox Balance and Cellular Defense against Oxidative Damage by Mitochondrial NADP+-dependent Isocitrate Dehydrogenase

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