Identification and Characterization of mRNA Biomarkers for Sodium Cyanide Exposure

Kim, Min; Jee, Seung-Cheol; Kim, Soee; Hwang, Karam; Sung, Jung‐Suk

doi:10.3390/toxics9110288

Cited by 4 publications

(3 citation statements)

References 40 publications

(43 reference statements)

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“…PPI networks provide comprehensive overviews of sub-cellular interactions [ 24 ]. Therefore, by using the Cytoscape program according to the STRING database, we constructed a PPI network of the 31 DEGs involved in DNA-repair mechanisms.…”

Section: Resultsmentioning

confidence: 99%

Quercetin and Isorhamnetin Reduce Benzo[a]pyrene-Induced Genotoxicity by Inducing RAD51 Expression through Downregulation of miR−34a

Kim

Jee

Shin

et al. 2022

IJMS

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Benzo[a]pyrene (B[a]P) is metabolized in the liver into highly reactive mutagenic and genotoxic metabolites, which induce carcinogenesis. The mutagenic factors, including B[a]P-7,8-dihydrodiol-9,10-epoxide (BPDE) and reactive oxygen species, generated during B[a]P metabolism can cause DNA damage, such as BPDE-DNA adducts, 8-oxo-dG, and double-strand breaks (DSBs). In this study, we mechanistically investigated the effects of quercetin and its major metabolite isorhamnetin on the repair of B[a]P-induced DNA DSBs. Whole−transcriptome analysis showed that quercetin and isorhamnetin each modulate the expression levels of genes involved in DNA repair, especially those in homologous recombination. RAD51 was identified as a key gene whose expression level was decreased in B[a]P−treated cells and increased by quercetin or isorhamnetin treatment. Furthermore, the number of γH2AX foci induced by B[a]P was significantly decreased by quercetin or isorhamnetin, whereas RAD51 mRNA and protein levels were increased. Additionally, among the five microRNAs (miRs) known to downregulate RAD51, miR−34a level was significantly downregulated by quercetin or isorhamnetin. The protective effect of quercetin or isorhamnetin was lower in cells transfected with a miR−34a mimic than in non−transfected cells, and the B[a]P-induced DNA DSBs remained unrepaired. Our results show that quercetin and isorhamnetin each upregulates RAD51 by downregulating miR−34a and thereby suppresses B[a]P-induced DNA damage.

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Section: Resultsmentioning

confidence: 99%

Quercetin and Isorhamnetin Reduce Benzo[a]pyrene-Induced Genotoxicity by Inducing RAD51 Expression through Downregulation of miR−34a

Kim

Jee

Shin

et al. 2022

IJMS

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“…CD9 is upregulated in the mouse and human brains infected with transmissible spongiform encephalopathy [ 58 ]. In addition, CD9 has been reported as a biomarker of sodium cyanide exposure [ 59 ], a hazardous chemical linked to neurodegeneration [ 60 ], and PD [ 61 ]. HIP1 is associated with Huntington’s disease and neuronal cell death through the intrinsic apoptotic pathway [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

Physical Activity Rewires the Human Brain against Neurodegeneration

Santiago¹,

Quinn

Potashkin

2022

IJMS

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Physical activity may offset cognitive decline and dementia, but the molecular mechanisms by which it promotes neuroprotection remain elusive. In the absence of disease-modifying therapies, understanding the molecular effects of physical activity in the brain may be useful for identifying novel targets for disease management. Here we employed several bioinformatic methods to dissect the molecular underpinnings of physical activity in brain health. Network analysis identified ‘switch genes’ associated with drastic hippocampal transcriptional changes in aged cognitively intact individuals. Switch genes are key genes associated with dramatic transcriptional changes and thus may play a fundamental role in disease pathogenesis. Switch genes are associated with protein processing pathways and the metabolic control of glucose, lipids, and fatty acids. Correlation analysis showed that transcriptional patterns associated with physical activity significantly overlapped and negatively correlated with those of neurodegenerative diseases. Functional analysis revealed that physical activity might confer neuroprotection in Alzheimer’s (AD), Parkinson’s (PD), and Huntington’s (HD) diseases via the upregulation of synaptic signaling pathways. In contrast, in frontotemporal dementia (FTD) its effects are mediated by restoring mitochondrial function and energy precursors. Additionally, physical activity is associated with the downregulation of genes involved in inflammation in AD, neurogenesis in FTD, regulation of growth and transcriptional repression in PD, and glial cell differentiation in HD. Collectively, these findings suggest that physical activity directs transcriptional changes in the brain through different pathways across the broad spectrum of neurodegenerative diseases. These results provide new evidence on the unique and shared mechanisms between physical activity and neurodegenerative diseases.

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“…Transcriptome analyses were performed adhering to previous research [ 51 , 52 ]. Gene ontology (GO) analysis of DEGs (fold change ≥ 2; normalized log 2 ≥ 5) was performed.…”

Section: Methodsmentioning

confidence: 99%

Chronic Exposure to TDI Induces Cell Migration and Invasion via TGF-β1 Signal Transduction

Han

Shin

et al. 2023

IJMS

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Toluene diisocyanate (TDI) is commonly used in manufacturing, and it is highly reactive and causes respiratory damage. This study aims to identify the mechanism of tumorigenesis in bronchial epithelial cells induced by chronic TDI exposure. In addition, transcriptome analysis results confirmed that TDI increases transforming growth factor-beta 1 (TGF-β1) expression and regulates genes associated with cancerous characteristics in bronchial cells. Our chronically TDI-exposed model exhibited elongated spindle-like morphology, a mesenchymal characteristic. Epithelial-mesenchymal transition (EMT) was evaluated following chronic TDI exposure, and EMT biomarkers increased concentration-dependently. Furthermore, our results indicated diminished cell adhesion molecules and intensified cell migration and invasion. In order to investigate the cellular regulatory mechanisms resulting from chronic TDI exposure, we focused on TGF-β1, a key factor regulated by TDI exposure. As predicted, TGF-β1 was significantly up-regulated and secreted in chronically TDI-exposed cells. In addition, SMAD2/3 was also activated considerably as it is the direct target of TGF-β1 and TGF-β1 receptors. Inhibiting TGF-β1 signaling through blocking of the TGF-β receptor attenuated EMT and cell migration in chronically TDI-exposed cells. Our results corroborate that chronic TDI exposure upregulates TGF-β1 secretion, activates TGF-β1 signal transduction, and leads to EMT and other cancer properties.

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Identification and Characterization of mRNA Biomarkers for Sodium Cyanide Exposure

Cited by 4 publications

References 40 publications

Quercetin and Isorhamnetin Reduce Benzo[a]pyrene-Induced Genotoxicity by Inducing RAD51 Expression through Downregulation of miR−34a

Quercetin and Isorhamnetin Reduce Benzo[a]pyrene-Induced Genotoxicity by Inducing RAD51 Expression through Downregulation of miR−34a

Physical Activity Rewires the Human Brain against Neurodegeneration

Chronic Exposure to TDI Induces Cell Migration and Invasion via TGF-β1 Signal Transduction

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