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Excessive use of alcohol can induce neurobiological and neuropathological alterations in the brain, including the hippocampus and forebrain, through changes in neurotransmitter systems, hormonal systems, and neuroimmune processes. We aimed to investigate the effects of ethanol on the expression of coding and noncoding RNAs in a brain-derived cell line exposed to ethanol. After exposing Neuro2a cells, a neuroblastoma cell line, to ethanol for 24 and 72 h, we observed cell proliferation and analyzed up- and downregulated mRNAs and long noncoding RNAs (lncRNAs) using total RNA-Seq technology. We validated the differential expression of some mRNAs and lncRNAs by RT-qPCR and analyzed the expression of and through knock-down of . Cell proliferation was significantly reduced in cells exposed to 100 mM ethanol for 72 h, with 1773 transcripts up- or downregulated by greater than three-fold in ethanol-treated cells compared to controls. Of these, 514 were identified as lncRNAs. Differentially expressed mRNAs and lncRNAs were mainly observed in cells exposed to ethanol for 72 h, in which and decreased, but , , and increased. On the other hand, lncRNAs , , and were changed by ethanol, and in particular was greatly increased by chronic ethanol treatment through inhibition of . Our results increase the understanding of cellular and molecular mechanisms related to coding and noncoding RNAs in an in vitro model of acute and chronic exposure to ethanol.
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http://dx.doi.org/10.3390/ijms23137294 | DOI Listing |
Mutat Res Rev Mutat Res
September 2025
Institute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China. Electronic address:
To maintain genomic stability, cells have evolved complex mechanisms collectively known as the DNA damage response (DDR), which includes DNA repair, cell cycle checkpoints, apoptosis, and gene expression regulation. Recent studies have revealed that long non-coding RNAs (lncRNAs) are pivotal regulators of the DDR. Beyond their established roles in recruiting repair proteins and modulating gene expression, emerging evidence highlights two particularly intriguing functions.
View Article and Find Full Text PDFActa Diabetol
September 2025
Department of Endocrinology & Metabolism, Medical College & Hospital, Kolkata, 88, College St. College Square, Kolkata, West Bengal, 700073, India.
Background And Aims: Gestational diabetes mellitus (GDM) is defined as glucose intolerance first identified during pregnancy that does not meet the criteria for overt diabetes. Its pathophysiology shares key features with type 2 diabetes mellitus (T2D), including insulin resistance and inflammation. Emerging evidence suggests that long non-coding RNAs (lncRNAs) are implicated in T2D.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Phytoveda Pvt. Ltd, Mumbai, 400022, India.
Background: The dysregulation of long-chain noncoding RNAs (lncRNAs) causes several complex human diseases including neurodegenerative disorders across the globe.
Methods And Results: This study aimed to investigate lncRNA expression profiles of Withania somnifera (WS)-treated human neuroblastoma SK-N-SH cells at different timepoints (3 & 9 h) and concentrations (50 & 100 µg/mL) using RNA sequencing. Differential gene expression analysis showed a total of 4772 differentially expressed lncRNAs, out of which 3971 were upregulated and 801 were downregulated compared to controls.
Inflamm Res
September 2025
Department of General Surgery, Beijing Anzhen Hospital, Capital Medical University, No.2 Anzhen Road, Chaoyang District, Beijing, 100029, China.
Background: The roles of long non-coding RNAs (lncRNAs) in the progression of various human tumors have been extensively studied. However, their specific mechanisms and therapeutic potential in Triple-Negative Breast Cancer (TNBC) remain to be fully elucidated.
Materials And Methods: The qRT-PCR assay was utilized to assess the relative mRNA levels of TFAP2A-AS1, PHGDH, and miR-6892.
JACC Basic Transl Sci
September 2025
BHF Centre for Cardiovascular Science, Queens Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom; Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre, Maastricht, the Netherlands. Electronic address: andy.bak
Coronary artery bypass graft (CABG) surgery remains the gold standard of care to prevent myocardial ischemia in patients with advanced atherosclerosis; however, poor long-term graft patency remains a considerable and long-standing problem. Excessive vascular smooth muscle cell (SMC) proliferation in the grafted tissue is recognized as central to late CABG failure. We previously identified SMILR, a human-specific SMC-enriched long noncoding RNA that drives SMC proliferation, suggesting that targeting SMILR expression could be a novel way to prevent neointima formation, and thus CABG failure.
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