DNA and cell biology最新文献

{"title":"Genome-Wide Association Studies to Drug: Identifying Retinoic Acid Metabolism Blocking Agents to Suppress Mechanoflammation in Osteoarthritis.","authors":"Linyi Zhu, Tonia L Vincent","doi":"10.1089/dna.2023.0197","DOIUrl":"10.1089/dna.2023.0197","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a highly prevalent debilitating joint disease for which there are currently no licensed disease-modifying treatments. The pathogenesis of OA is complex, involving genetic, mechanical, biochemical, and environmental factors. Cartilage injury, arguably the most important driving factor in OA development, is able to activate both protective and inflammatory pathways within the tissue. Recently, >100 genetic risk variants for OA have been identified through Genome Wide Association Studies, which provide a powerful tool to validate existing putative disease pathways and discover new ones. Using such an approach, hypomorphic variants within the aldehyde dehydrogenase 1 family member A2 (<i>ALDH1A2</i>) gene were shown to be associated with increased risk of severe hand OA. <i>ALDH1A2</i> encodes the enzyme that synthesizes all-trans retinoic acid (atRA), an intracellular signaling molecule. This review summarizes the influence of the genetic variants on expression and function of <i>ALDH1A2</i> in OA cartilage, its role in the mechanical injury response of cartilage, and its potent anti-inflammatory effect after cartilage injury. In doing so it identifies atRA metabolism-blocking agents as potential treatments for suppressing mechanoflammation in OA.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10185460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genotypic Analysis of <i>COL4A1</i> Gene in Diabetic Nephropathy and Type 2 Diabetes Mellitus Patients: A Comparative Genetic Study.","authors":"Neha Shukla,&nbsp;Shivani Kumari,&nbsp;Poornima Verma,&nbsp;Atar Singh Kushwah,&nbsp;Monisha Banarjee,&nbsp;S N Sankhwar,&nbsp;Aneesh Srivastava,&nbsp;M S Ansari,&nbsp;Naveen Kumar Gautam","doi":"10.1089/dna.2023.0125","DOIUrl":"https://doi.org/10.1089/dna.2023.0125","url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is specified by microalbuminuria, glomerular lesions, and renal fibrosis leading to end-stage renal disease. The pathophysiology of DN is multifactorial as a result of gene-environment interaction. Clinical studies suggested that gene mutations affect various pathways involved in DN, including extracellular matrix (ECM). During chronic hyperglycemia, collagen type-4-mediated ECM overproduction occurs, leading to renal fibrosis and DN development. In this study, <i>COL4A1</i> gene variant rs605143 (G/A) was analyzed in diabetes and DN patients from the study population. We genotyped 386 study subjects, comprising 120 type 2 diabetes mellitus (T2DM) patients, 120 DN, and 146 healthy controls. All study subjects were analyzed for biochemical assays by commercially available kits and genotypic analysis by polymerase chain reaction-restriction fragment length polymorphism and confirmed by Sanger sequencing. Statistical analyses were done using SPSS and GraphPad. Anthroclinicopathological parameters showed a significant association between T2DM and DN. Genotype AA of <i>COL4A1</i> gene variant rs605143 (G/A) showed a significant association with T2DM and DN compared with controls with 5.87- and 8.01-folds risk, respectively. Mutant allele A also significantly associated with T2DM and DN independently compared with healthy controls with 2.29- and 2.81-time risk in the study population. This study's findings suggested that <i>COL4A1</i> gene variant rs605143 (G/A) can be used as predictive biomarkers for T2DM and DN independently. However, this gene variant needs to be analyzed in a large sample to explore the shared genetic association between T2DM and DN.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10221200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of miR-92a in Decidual Stromal Cells Suppresses Migration Ability of Trophoblasts by Promoting Macrophage Polarization.","authors":"Huansheng Zhou,&nbsp;Hui Wang,&nbsp;Xiaohan Liu,&nbsp;Bei Liu,&nbsp;Yanci Che,&nbsp;Rendong Han","doi":"10.1089/dna.2022.0510","DOIUrl":"https://doi.org/10.1089/dna.2022.0510","url":null,"abstract":"<p><p>Preeclampsia (PE) is a severe pregnancy complication that accounts for about 14% of maternal deaths. Its clinical manifestations commonly include hypertension and proteinuria. However, it is largely limited in understanding its pathogenetic mechanism. In this study, we used bioinformatics to compare differential gene expressions in decidual stromal cells from PE patients and healthy donors. The result indicated that higher levels of CCL5 and CXCL2 were expressed in decidual stromal cells of PE patients compared with healthy pregnancy. The bioinformatics analysis confirmed that decidual stromal cells derived from PE patients expressed significantly lower miR-92a compared with those derived from healthy donors. Transfection of miR-92a inhibitors upregulated IL-6, CXCL2, CXCL3, CCL5, and CXCL8 expressions in decidual stromal cells. Luciferase activity assay confirmed that miR-92a directly targeted the mRNA of IRF3 whose overexpression could promote the secretion of cytokines. The flow cytometric analysis demonstrated that M1 macrophage infiltration was higher in the placentas of PE patients than in those of healthy donors. We also observed that after transfection of miR-92a inhibitor, condition medium (CM) derived from decidual stromal cells significantly promoted M1 polarization of macrophages. In addition, the transwell migration assay and flow cytometric analysis together showed that decidual stromal cell-derived CM induced macrophages to suppress the trophoblast migration and proliferation. Taken together, our result indicates that downregulation of miR-92a in decidual stromal cells promotes the macrophage polarization and suppresses the trophoblast migration and proliferation.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10025854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Low Dietary Folate on Mouse Spermatogenesis and Spindle Assembly Checkpoint Dysfunction May Contribute to Folate Deficiency-Induced Chromosomal Instability in Cultured Mouse Spermatogonia.","authors":"Huanhuan Ren,&nbsp;Kaixian Wang,&nbsp;Zirui Liu,&nbsp;Xuansheng Zhong,&nbsp;Meng Liang,&nbsp;Yaping Liao","doi":"10.1089/dna.2023.0035","DOIUrl":"https://doi.org/10.1089/dna.2023.0035","url":null,"abstract":"<p><p>Folate, as the initial substrate in one-carbon metabolism, is involved in the synthesis of important substances such as DNA, RNA, and protein. Folate deficiency (FD) is associated with male subfertility and impaired spermatogenesis, yet the underlying mechanisms are poorly understood. In the present study, we established an animal model of FD to investigate the effect of FD on spermatogenesis. GC-1 spermatogonia were used as a model to investigate the effect of FD on proliferation, viability, and chromosomal instability (CIN). Furthermore, we explored the expression of core genes and proteins of spindle assembly checkpoint (SAC), a signaling cascade ensuring accurate chromosome segregation and preventing CIN during mitosis. Cells were maintained in medium containing 0, 20, 200, or 2000 nM folate for 14 days. CIN was measured by using a cytokinesis-blocked micronucleus cytome assay. We found that sperm counts decreased significantly (<i>p</i> < 0.001) and the rate of sperm with defects in the head increased significantly (<i>p</i> < 0.05) in FD diet mice. We also found, relative to the folate-sufficient conditions (2000 nM), cells cultured with 0, 20, or 200 nM folate exhibited delayed growth and increased apoptosis in an inverse dose-dependent manner. FD (0, 20, or 200 nM) significantly induced CIN (<i>p</i> < 0.001, <i>p</i> < 0.001, and <i>p</i> < 0.05, respectively). Moreover, FD significantly and inverse dose dependently increased the mRNA and protein expression of several key SAC-related genes. The results indicate that FD impairs SAC activity, which contributes to mitotic aberrations and CIN. These findings establish a novel association between FD and SAC dysfunction. Thus, FD-impaired spermatogenesis may be partly due to genomic instability and proliferation inhibition of spermatogonia.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9975023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of Properties of the Mitochondrial Permeability Transition Pore Using Whole-Mitoplast Patch-Clamp Technique.","authors":"Maria A Neginskaya, Evgeny V Pavlov","doi":"10.1089/dna.2023.0171","DOIUrl":"10.1089/dna.2023.0171","url":null,"abstract":"<p><p>The mitochondrial permeability transition pore (mPTP) is a channel in the mitochondrial inner membrane that is activated by excessive calcium uptake. In this study, we used a whole-mitoplast patch-clamp approach to investigate the ionic currents associated with mPTP at the level of the whole single mitochondrion. The whole-mitoplast conductance was at the level of 5 to 7 nS, which is consistent with the presence of three to six single mPTP channels per mitochondrion. We found that mPTP currents are voltage dependent and inactivate at negative potential. The currents were inhibited by cyclosporine A and adenosine diphosphate. When mPTP was induced by oxidative stress, currents were partially blocked by the adenine nucleotide translocase inhibitor bongkrekic acid. Our data suggest that the whole-mitoplast patch-clamp approach is a useful method for investigating the biophysical properties and regulation of the mPTP.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10460960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10099733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid Metabolic Regulatory Crosstalk Between Cancer Cells and Tumor-Associated Macrophages.","authors":"Shu Liu,&nbsp;Ying Ying Shen,&nbsp;Li Yang Yin,&nbsp;Jianghua Liu,&nbsp;Xuyu Zu","doi":"10.1089/dna.2023.0071","DOIUrl":"https://doi.org/10.1089/dna.2023.0071","url":null,"abstract":"<p><p>In the tumor microenvironment, tumor-associated macrophages (TAMs) are one of the most abundant cell populations, playing key roles in tumorigenesis, chemoresistance, immune evasion, and metastasis. There is an important interaction between TAMs and cancer cells: on the one hand, tumors control the function of infiltrating macrophages, contributing to reprogramming of TAMs, and on the other hand, TAMs affect the growth of cancer cells. This review focuses on lipid metabolism changes in the complex relationship between cancer cells and TAMs. We discuss how lipid metabolism in cancer cells affects macrophage phenotypic and metabolic changes and, subsequently, how altered lipid metabolism of TAMs influences tumor progression. Identifying the metabolic changes that influence the complex interaction between tumor cells and TAMs is also an important step in exploring new therapeutic approaches that target metabolic reprogramming of immune cells to enhance their tumoricidal potential and bypass therapy resistance. Our work may provide new targets for antitumor therapies.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10339133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Hub Genes Involved in Muscle Injury Induced by Jumping Load Based on Transcriptomics.","authors":"Xiaolan Shi,&nbsp;Yijie Wang,&nbsp;Haitao Liu,&nbsp;Rui Han","doi":"10.1089/dna.2022.0285","DOIUrl":"https://doi.org/10.1089/dna.2022.0285","url":null,"abstract":"The purpose of this study was to find hub genes that may play key roles in skeletal muscle injury induced by jumping load. Twelve female Sprague Dawley rats were divided into the normal control (NC) group and the jumping-induced muscle injury (JI) group. After 6 weeks of jumping, transmission electron microscopy, hematoxylin-eosin staining, transcriptomics sequencing and genes analysis, interaction network prediction of multiple proteins, real-time PCR detection, and Western blotting were performed on gastrocnemius muscles from NC and JI groups. As compared with NC rats, excessive jumping can result in notable structural damage and inflammatory infiltration in JI rats. A total of 112 differentially expressed genes were confirmed in NC rats versus JI rats, with 59 genes upregulated and 53 genes downregulated. Using the online String database, four hub genes in the transcriptional regulatory network were targeted, including FOS, EGR1, ATF3, and NR4A3. All expression levels of FOS, EGR1, ATF3, and NR4A3 mRNAs were decreased in JI rats compared with NC rats (p < 0.05 or p < 0.01). All expression levels of c-Fos, EGR1, ATF3, and NOR1 proteins were upregulated in JI rats (p < 0.01, p < 0.05, p > 0.05, and p < 0.01, respectively). Collectively, these findings indicate that FOS, EGR1, ATF3, and NR4A3 genes may be functionally important in jumping-induced muscle injury.","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9975577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Long Noncoding RNAs, <i>LINC01093</i> and <i>MYLK-AS1</i>, Serve as Potential Diagnostic and Prognostic Biomarkers or Hepatocellular Carcinoma.","authors":"Yanming Qin,&nbsp;Xin Tu,&nbsp;Meifang Huang,&nbsp;Caifang Ma,&nbsp;Qiongqing Huang,&nbsp;Qiqi Huang,&nbsp;Hong Shu,&nbsp;Chao Ou","doi":"10.1089/dna.2022.0566","DOIUrl":"https://doi.org/10.1089/dna.2022.0566","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the most fatal human malignancies worldwide. In this research, we aimed to identify long noncoding RNAs (lncRNAs) as biomarkers for HCC diagnosis and prognosis. lncRNA expression profiles were obtained from Gene Expression Omnibus and The Cancer Genome Atlas databases. The differentially expressed lncRNAs between HCC and adjacent tissues were analyzed with bioinformatic tools. Four lncRNAs with area under the curve of the receiver operating characteristic curve >0.9 were selected from both datasets. Univariate and Kaplan-Meier analyses were performed to obtain <i>LINC01093</i>, <i>MYLK-AS1</i>, and <i>MCM3AP-AS1</i> as the optimal diagnostic and prognostic biomarkers. Finally, qPCR confirmed that <i>LINC01093</i> and <i>MYLK-AS1</i> were significantly differentially expressed in HCC and adjacent normal tissues. In general, we demonstrated that novel lncRNAs, <i>LINC01093</i> and <i>MYLK-AS1</i>, could be used as potential diagnostic and prognostic biomarkers for HCC.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10339132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aquaporin 1 Facilitates Ferroptosis, M1 Polarization, Mitochondrial Dysfunction, and Autophagy Damage on Lipopolysaccharide-Induced Macrophage Through Down-Regulation of P53 Signaling Pathway.","authors":"Wuyang Lv, Lei Liang, Dongyang Liu, Cuicui Li, Liao Jia, Yingyu Jin","doi":"10.1089/dna.2023.0016","DOIUrl":"10.1089/dna.2023.0016","url":null,"abstract":"<p><p>This study was designed to investigate the role of aquaporin 1 (AQP1) in ferroptosis, macrophage polarization, mitochondrial dysfunction, and impaired autophagy of lipopolysaccharide (LPS)-stimulated RAW264.7 cells and explored the underlying mechanisms. Si-AQP1-mediated AQP1 silencing RAW264.7 cells was constructed. Si-P53-mediated P53 silencing or pcDNA-P53 overexpression RAW264.7 cells was constructed. Assays of ATP, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Mitochondrial membrane potential (JC-1) staining were performed to evaluate mitochondrial biological function. Assays of flow cytometry, reactive oxygen species (ROS) staining, western blot (WB), RT-qPCR, malondialdehyde (MDA), glutathione (GSH), and total superoxide dismutase (SOD) were performed to detect cell ferroptosis, macrophage polarization, and impaired autophagy. The involvement of the P53 pathway was revealed by WB. The results showed that LPS (30 μg/mL) could induce ferroptosis, M1 polarization, mitochondrial dysfunction, and autophagy damage in RAW264.7 cells. Meanwhile, the expression of AQP1 was increased and the expression of P53 was decreased. In addition, Pifithrin-α (PIF; 15 μM), a P53 inhibitor, significantly aggravated ferroptosis, M1 polarization, mitochondrial dysfunction, and autophagy damage as well as up-regulation of AQP1 protein expression in LPS-induced RAW264.7 cells. Interestingly, this phenomenon was markedly alleviated by Kevetrin hydrochloride (70 μM), a P53 agonist. Mechanistically, silencing AQP1 significantly alleviated ferroptosis, M1 polarization, mitochondrial dysfunction, and autophagy damage by up-regulating the expression of P53 in LPS-stimulated RAW264.7 cells. Indeed, inhibition of P53 expression by PIF treatment dramatically reversed this effect on the basis of LPS+si-AQP1. Therefore, we concluded for the first time that AQP1 can promote ferroptosis, M1 polarization, mitochondrial dysfunction, and autophagy impairment by inhibiting the expression of P53 in LPS-stimulated RAW264.7 cells, and AQP1 or P53 may be considered as a crucial determiner that can regulate the biological behavior of RAW264.7 cells stimulated by LPS.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10457627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10474384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypomethylation of Long Interspersed Nucleotide Elements and Aldehyde Dehydrogenase in Patients of Alcohol Use Disorder with Cirrhosis.","authors":"Bhagyalakshmi Shankarappa,&nbsp;Jayant Mahadevan,&nbsp;Pratima Murthy,&nbsp;Meera Purushottam,&nbsp;Biju Viswanath,&nbsp;Sanjeev Jain,&nbsp;Harshad Devarbhavi,&nbsp;Ashok Mysore Visweswariah","doi":"10.1089/dna.2022.0669","DOIUrl":"https://doi.org/10.1089/dna.2022.0669","url":null,"abstract":"<p><p>Alcohol use disorder (AUD) and cirrhosis are key outcomes of excessive alcohol use, and a genetic influence in these outcomes is increasingly recognized. While 80-90% of heavy alcohol users show evidence of fatty liver, only 10-20% progress to cirrhosis. There is currently no clear understanding of the causes of this difference in progression. The aim of this study is to evaluate genetics and epigenetics at the aldehyde dehydrogenase (<i>ALDH2)</i> locus in patients with AUD and liver complications. Study participants were inpatients from the clinical services of Gastroenterology and Psychiatry at St. John's Medical College Hospital (SJMCH) and the National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India. Men diagnosed as having AUD with cirrhosis (AUDC+ve, <i>N</i> = 136) and AUD without cirrhosis (AUDC-ve, <i>N</i> = 107) were assessed. FibroScan/sonographic evidence was used to rule out fibrosis in the AUDC-ve group. Genomic DNA was used for genotyping at the <i>ALDH2</i> (rs2238151) locus. A subset of 89 samples was used for DNA methylation (AUDC+ve, <i>N</i> = 44; and AUDC-ve, <i>N</i> = 45) analysis at long interspersed nucleotide element 1 (<i>LINE-1</i>) and <i>ALDH2</i> cytosine-phosphate-guanine (CpG) loci by pyrosequencing. <i>ALDH2</i> DNA methylation was significantly lower in the AUDC+ve group compared with the AUDC-ve group (<i>p</i> < 0.001). Lower methylation was associated with a risk allele (T) of the <i>ALDH2</i> locus (rs2238151) (<i>p</i> = 0.01). Global (<i>LINE-1</i>) DNA methylation levels were also significantly lower in the AUDC+ve group compared with the AUDC-ve group (<i>p</i> = 0.01). Compromised global methylation (<i>LINE-1)</i> and hypomethylation at the <i>ALDH2</i> gene was observed in patients with cirrhosis compared with those without cirrhosis. DNA methylation could be explored as a biomarker for cirrhosis and liver complications.</p>","PeriodicalId":11248,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":3.1,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9803092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}