scholarly journals Epigenetic regulation mechanism of DNA methylation and miRNAs on the expression of the ALOX5AP gene in patients with ischemic stroke

2021 ◽  
Vol 22 (6) ◽  
Author(s):  
Xiaoshuai Bie ◽  
Huiling Zhao ◽  
Zhaojing Zhang ◽  
Xiaoou Wang ◽  
Yingying Luan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Ischemic Stroke ◽  
Epigenetic Regulation ◽  
Regulation Mechanism ◽  
Alox5ap Gene

scholarly journals Crosstalk of DNA Methylation Triggered by Pathogen in Poplars With Different Resistances

2021 ◽  
Vol 12 ◽  
Author(s):  
Dandan Xiao ◽  
Ke Zhou ◽  
Xiaoqian Yang ◽  
Yuzhang Yang ◽  
Yudie Ma ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Immune Response ◽  
Epigenetic Regulation ◽  
Expression Profiles ◽  
Critical Role ◽  
Infection Process ◽  
Regulation Mechanism ◽  
Post Inoculation ◽  
Pathogen Infection ◽  
Methylation Ratio

DNA methylation plays crucial roles in responses to environmental stimuli. Modification of DNA methylation during development and abiotic stress responses has been confirmed in increasing numbers of plants, mainly annual plants. However, the epigenetic regulation mechanism underlying the immune response to pathogens remains largely unknown in plants, especially trees. To investigate whether DNA methylation is involved in the response to infection process or is related to the resistance differences among poplars, we performed comprehensive whole-genome bisulfite sequencing of the infected stem of the susceptible type Populus × euramerican ‘74/76’ and resistant type Populus tomentosa ‘henan’ upon Lonsdalea populi infection. The results revealed that DNA methylation changed dynamically in poplars during the infection process with a remarkable decrease seen in the DNA methylation ratio. Intriguingly, the resistant P. tomentosa ‘henan’ had a much lower basal DNA methylation ratio than the susceptible P. × euramerican ‘74/76’. Compared to mock-inoculation, both poplar types underwent post-inoculation CHH hypomethylation; however, significant decreases in mC and mCHH proportions were found in resistant poplar. In addition, most differentially CHH-hypomethylated regions were distributed in repeat and promoter regions. Based on comparison of DNA methylation modification with the expression profiles of genes, DNA methylation occurred in resistance genes, pathogenesis-related genes, and phytohormone genes in poplars during pathogen infection. Additionally, transcript levels of genes encoding methylation-related enzymes changed during pathogen infection. Interestingly, small-regulator miRNAs were subject to DNA methylation in poplars experiencing pathogen infection. This investigation highlights the critical role of DNA methylation in the poplar immune response to pathogen infection and provides new insights into epigenetic regulation in perennial plants in response to biotic stress.

SUV39H1-Mediated DNMT1 is Participated in the Epigenetic Regulation of Smad3 in Cervical Cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Li Zhang ◽  
Sijuan Tian ◽  
Minyi Zhao ◽  
Ting Yang ◽  
Shimin Quan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Lines ◽  
Epigenetic Regulation ◽  
Promoter Region ◽  
Methylation Status ◽  
Regulation Mechanism ◽  
Methylation Specific Pcr ◽  
Specific Pcr ◽  
Immune Factor ◽  
Cancer Tissues

Background: Smad3 is a pivotal intracellular mediator for participating in the activation of multiple immune signal pathway. Objective: The epigenetic regulation mechanism of the positive immune factor Smad3 in cervical cancer remains unknown. Therefore, the epigenetic regulation on Smad3 is investigated in this study. Methods: The methylation status of SMAD3 was detected by Methylation-specific PCR (MS-PCR) and Quantitative Methylation-specific PCR (MS-qPCR) in cervical cancer tissues and cell lines. The underlying molecular mechanisms of SUV39H1-DNMT1-Smad3 regulation was elucidated using cervical cancer cell lines containing siRNA or/and overexpression system. Confirmation of the regulation of DNMT1 by SUV39H1 used Chromatin immunoprecipitation-qPCR (ChIP-qPCR). The statistical methods used for comparing samples between groups were paired t tests and one-way ANOVAs. Results: H3K9me3 protein which regulated by SUV39H1 directly interacts with the DNMT1 promoter region to regulate its expression in cervical cancer cells, resulting in the reduce expression of the downstream target gene DNMT1. In addition, DNMT1 mediates the epigenetic modulation of the SMAD3 gene by directly binding to its promoter region. The depletion of DNMT1 effectively restores the expression of Smad3 in vitro. Moreover, in an in vivo assay, the expression profile of SUV39H1-DNMT1 was found to correlate with Smad3 expression in accordance with the expression at the cellular level. Notably, the promoter region of SMAD3 was hypermethylated in cervical cancer tissues, and this hypermethylation inhibits the subsequent gene expression. Conclusion: These results indicate that SUV39H1-DNMT1 is a crucial Smad3 regulatory axis in cervical cancer. SUV39H1-DNMT1 axis may provide a potential therapeutic target for the treatment of cervical cancer.

scholarly journals Altered DNA methylation pattern reveals epigenetic regulation of Hox genes in thoracic aortic dissection and serves as a biomarker in disease diagnosis

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Peiru Liu ◽  
Jing Zhang ◽  
Duo Du ◽  
Dandan Zhang ◽  
Zelin Jin ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Aortic Dissection ◽  
Epigenetic Regulation ◽  
Heart Development ◽  
Type A ◽  
Methylation Pattern ◽  
Healthy Controls ◽  
Global Methylation ◽  
Thoracic Aortic Dissection

Abstract Background Thoracic aortic dissection (TAD) is a severe disease with limited understandings in its pathogenesis. Altered DNA methylation has been revealed to be involved in many diseases etiology. Few studies have examined the role of DNA methylation in the development of TAD. This study explored alterations of the DNA methylation landscape in TAD and examined the potential role of cell-free DNA (cfDNA) methylation as a biomarker in TAD diagnosis. Results Ascending aortic tissues from TAD patients (Stanford type A; n = 6) and healthy controls (n = 6) were first examined via whole-genome bisulfite sequencing (WGBS). While no obvious global methylation shift was observed, numerous differentially methylated regions (DMRs) were identified, with associated genes enriched in the areas of vasculature and heart development. We further confirmed the methylation and expression changes in homeobox (Hox) clusters with 10 independent samples using bisulfite pyrosequencing and quantitative real-time PCR (qPCR). Among these, HOXA5, HOXB6 and HOXC6 were significantly down-regulated in TAD samples relative to controls. To evaluate cfDNA methylation pattern as a biomarker in TAD diagnosis, cfDNA from TAD patients (Stanford type A; n = 7) and healthy controls (n = 4) were examined by WGBS. A prediction model was built using DMRs identified previously from aortic tissues on methylation data from cfDNA. Both high sensitivity (86%) and specificity (75%) were achieved in patient classification (AUC = 0.96). Conclusions These findings showed an altered epigenetic regulation in TAD patients. This altered epigenetic regulation and subsequent altered expression of genes associated with vasculature and heart development, such as Hox family genes, may contribute to the loss of aortic integrity and TAD pathogenesis. Additionally, the cfDNA methylation in TAD was highly disease specific, which can be used as a non-invasive biomarker for disease prediction.

scholarly journals Epigenetic Regulation of Oxidative Stress in Ischemic Stroke

2016 ◽  
Vol 7 (3) ◽  
pp. 295 ◽  
Author(s):  
Haiping Zhao ◽  
Ziping Han ◽  
Xunming Ji ◽  
Yumin Luo
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Epigenetic Regulation

scholarly journals Whole-Blood Methylation Analysis Reveals Respiratory Environmental Functional Pathways Involved in Severity Following SARS-CoV-2 Infection

2021 ◽  
Author(s):  
Guillermo Barturen ◽  
Elena Carnero-Montoro ◽  
Manuel Martínez-Bueno ◽  
Silvia Rojo-Rello ◽  
Beatriz Sobrino ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Immune Response ◽  
Epigenetic Regulation ◽  
Strong Relationship ◽  
Autoimmune Disorder ◽  
Methylation Analysis ◽  
Functional Pathways ◽  
Interferon Responses ◽  
Inflammatory Syndrome ◽  
Dna Genotyping

SARS-CoV-2 causes a severe inflammatory syndrome called COVID-19 that primarily affects the lungs leading, in many cases, to bilateral pneumonia, severe dyspnea and in ~5% of the cases, death. The mechanisms through which this occurs are still being elucidated. A strong relationship between COVID-19 progression and autoimmune disorder pathogenesis has been identified as an exacerbated interferon immune response or an inflammatory condition mediated by an increase of pro-inflammatory cytokine production, among other. DNA methylation is known to regulate immune response processes, thus COVID-19 progression might be also conditioned by DNA methylation changes not studied in depth, yet. Thus, here an epigenome-wide DNA methylation analysis combined with DNA genotyping for 101 and 473 SARS-CoV-2 negative and positive lab tested individuals, respectively, from two different clinical centers is presented in order to evaluate the implications of the epigenetic regulation in the course of COVID-19 disease. The results reveal the existence of an epigenome regulation of functional pathways associated with the COVID-19 progression, such as innate interferon responses, hyperactivation of B and T lymphocytes, phagocytosis and innate C-type lectin DC-SIGN. These DNA methylation changes were found to be regulated by genetic loci associated with COVID-19 susceptibility and autoimmune disease. In mild COVID-19 patients hypomethylation of CpGs regulating genes within the AKT signaling pathway, and the hypermethylation of a group of CpGs related to environmental traits regulating IL-6 expression via the transcription factor CEBP, discriminate these individuals from those who develop the most critical outcomes of the disease. Thus, the analysis points out to an environmental contribution that mediated by DNA methylation changes in SARS-CoV-2 positive patients, might be playing a role in triggering the cytokine storm described in the most severe cases. In addition, important differences were found in terms of epigenetic regulation between severe and mild cases when compared with systemic autoimmune diseases.

scholarly journals Epigenetic regulation of OAS2 shows disease-specific DNA methylation profiles at individual CpG sites

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiaolian Gu ◽  
Linda Boldrup ◽  
Philip J. Coates ◽  
Robin Fahraeus ◽  
Elisabet Nylander ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Epigenetic Regulation ◽  
Cpg Sites ◽  
Disease Specific

Abstract 160: DNA-Methylation and Aging. Contribution of Biological Age to Recovery After Ischemic Stroke

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jordi Jimenez-Conde ◽  
Carolina Soriano-Tarraga ◽  
Eva Giralt-Steinhauer ◽  
Marina Mola ◽  
Rosa Vivanco-Hidalgo ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Ischemic Stroke ◽  
Functional Status ◽  
Biological Age ◽  
Chronological Age ◽  
Bivariate Analysis ◽  
Stroke Severity ◽  
Age Related ◽  
Recovery Capacity ◽  
The Impact

Background: Stroke has a great impact in functional status of patients, although there are substantial interindividual differences in recovery capacity. Apart from stroke severity, age is considered an important predictor of outcome after stroke, but aging is not only due to chronological age. There are age-related DNA-methylation changes in multiple CpG sites across the genome that can be used to estimate the biological age (b-Age), and we seek to analyze the impact of this b-Age in recovery after an ischemic stroke. Methods: We include 600 individuals with acute ischemic stroke assessed in Hospital del Mar (Barcelona). Demographic and clinical data such as chronological age (c-Age), vascular risk factors, NIHSS at admission, recanalization treatment (rtPA or endovascular treatment), previous modified Rankin scale (p-mRS) and 3 months post stroke functional status (3-mRS) were registered. Biological age (b-Age) was estimated with Hannumm algorithm, based on DNA methylation in 71 CpGs. Results: The bivariate analyses for association with 3-mRS showed a significant results of NIHSS, c-Age, b-Age, p-mRS, and current smoking (all with p<0.001). Recanalization treatment showed no significant differences in bivariate analysis. In multivariate ordinal models, b-Age kept its significance (p=0.025) nullifying c-Age (p=0.84). Initial NIHSS, p-mRS and recanalization treatment kept also significant results (p<0.001). Conclusions: Biological Age, estimated by DNA methylation, is an independent predictor of stroke prognosis, irrespective to chronological age. "Healthy aging” affects the capacity of recovering after an ischemic stroke.

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