GW25-e5121 Role of DNA Methylation in NET Gene Promoter Region on the Association between Depression and Hypertension

2014 ◽  
Vol 64 (16) ◽  
pp. C222-C223
Author(s):  
Meng Lin ◽  
Chen Jingzhou ◽  
Wang Jizheng ◽  
Pei Fei ◽  
Hui Rutai ◽  
...  
Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4386-4386
Author(s):  
Ye Zhao ◽  
Zi-xing Chen ◽  
Shao-yan Hu ◽  
Jian-nong Cen

Abstract The methylation at CpG island in the promoter region of a gene is one of the important epigenetic mechanism which regulates the gene activity. To study the DNA methylation pattern of WT1 gene promoter region within hematologic neoplastic cell lines and its correlation with WT1 gene expression by using the PCR-based methods. RT-PCR and Methylation-specific PCR were performed to study the WT1 gene expression in 8226, HL-60, Jurkat, K562, KG-1, NB4, Raji, SHI-1, U266 and U937 cell lines and the DNA methylation status in promoter region of WT1 gene. After treatment of U937 cell line by 5-aza-CdR, a demethylation inducing agent, the changes of WT1 gene expression level and the methylation status in its promter region in U937 cells was determined. Our Results showed that HL-60, K562, KG-1, NB4, SHI-1 cell lines demonstrated higher level of WT1 expression, while extremely low level was found in 8226, Jurkat, Raji, U266 and U937. The DNA hypermethylation in WT1 gene promoter region was identified in 8226, Jurkat, Raji, U266 and U937 cell lines. The WT1 gene expression in U937 was markedly enhanced after treatment with 5-aza-CdR in company with the decrease of methylated level and the increase of unmethylated level in its promoter region. These results indicate that modulation of the DNA methylation in WT1 promoter region is one of the epigenetic mechanisms to regulate its expression.


The Prostate ◽  
2002 ◽  
Vol 52 (1) ◽  
pp. 82-88 ◽  
Author(s):  
Satoru Takahashi ◽  
Shingo Inaguma ◽  
Michihisa Sakakibara ◽  
Young-Man Cho ◽  
Shugo Suzuki ◽  
...  

Author(s):  
Si-Qiang Zheng ◽  
Huan-Xin Chen ◽  
Xiao-Cheng Liu ◽  
Qin Yang ◽  
Guo-Wei He

Ventricular septal defects (VSD) are the most common congenital heart defects (CHD). Studies have documented that ISL1 has a crucial impact on cardiac growth, but the role of variants in the ISL1 gene promoter in patients with VSD has not been explored. In 400 subjects (200 isolated and sporadic VSD patients: 200 healthy controls), we investigated the ISL1 gene promoter variant and performed cellular functional experiments by using the dual-luciferase reporter assay to verify the impact on gene expression. In the ISL1 promoter, 5 variants were found only in VSD patients by sequencing. Cellular functional experiments demonstrated that three variants decreased the transcriptional activity of the ISL1 promoter (P < 0.05). Further analysis with the online JASPAR database demonstrated that a cluster of putative binding sites for transcription factors may be altered by these variants, possibly resulting in change of ISL1 protein expression and VSD formation. Our study has for the first time identified novel variants in the ISL1 gene promoter region in the Han Chinese patients with isolated and sporadic VSD. Additionally, the cellular functional experiments, electrophoretic mobility shift assay, and bioinformatic analysis have demonstrated that these variants significantly alter the expression of the ISL1 gene and affect the binding of transcription factors, likely resulting in VSD. Therefore, this study may provide new insights into the role of the gene promoter region for a better understanding of genetic basis of the formation of CHD and may promote further investigations on mechanism of the formation of CHD.


2009 ◽  
Vol 61 (6) ◽  
pp. 1243-1244
Author(s):  
Habich Aleksandra ◽  
Golan Maciej ◽  
Klimczak-Jajor Edyta ◽  
Bany-Laszewicz Urszula ◽  
Domańska-Janik Krystyna

2019 ◽  
Vol 38 (8) ◽  
pp. 2161-2169 ◽  
Author(s):  
Mengya Chen ◽  
Meng Wu ◽  
Xingxing Hu ◽  
Jiajia Yang ◽  
Renfang Han ◽  
...  

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1742-1742 ◽  
Author(s):  
Mahipal Singh ◽  
Kestas Vaitkus ◽  
Maria Hankewych ◽  
Donald Lavelle ◽  
Nadim Mahmud ◽  
...  

Abstract The role of epigenetic modifications, which represent a second layer of genetic regulation, appear to play an important role during hematopoiesis. How the chromatin structure changes from a preprogrammed hematopoietic stem cell to progressively differentiated cells and how the cell’s inner and surrounding environment affects orchestrating the epigenetic modifications is not clearly understood. This investigation was initiated to determine the pattern of DNA methylation in the γ-globin gene promoter region in the cells isolated from different stages of erythroid development in baboon (P. anubis). Baboon fetal liver hematopoietic stem progenitor cells (HSPC) were purified by passage through a Miltenyi magnetic column (to deplete mature erythroblasts) followed by flow cytometric cell sorting of erythroblast depleted cells into various sub populations depending upon the expression of CD36 antigen. Three types of cell populations i.e. CD34+CD36−, CD34+CD36+ and CD34−CD36+ were collected. Clonal analysis was performed to verify the degree of differentiation of CD34+ cells based on their co-expression of CD36. CFC assays of CD34+CD36−, CD34+CD36+ and CD34−CD36+ cells revealed a cloning efficiency of 89%, 38.5% and 12% respectively, after 12 days of culture using methylcellulose media supplemented with a cocktail of growth factors and serum. Only CD34−CD36+ cells produced detectable CFU-E colonies while CD34+CD36− and CD34+CD36+ generated mostly BFU-Es. CD34+CD36− cells produced about 2 fold more BFU-Es as compared to CD34+CD36+ cell population. Moreover, the colony size also decreased as the cells progressed towards maturation. Our data suggest that CD34+CD36−cells are most primitive erythroid progenitors while CD34−CD36+ cells are the most committed mature erythroid progenitors and the CD34+CD36+ cells represent the intermediate stage. The methylation pattern of 5 CpG sites in the γ-globin promoter region in the above purified cell populations along with erythroblast fraction was assayed using bisulfite sequencing. Two independent fetuses, 56 and 58 days post conception (dpc) were analysed. Bisulfite treated genomic DNA was used to amplify the γ-globin promoter region and the PCR products were subcloned into pCR-TOPO vector. Sequences of fifteen independent clones per sample were analysed. Our results indicated almost complete methylation of the γ-globin promoter region in earlier stages of differentiation and a progressive decrease in methylation as the cells progress towards maturation. The methylation pattern observed was 98.3%, 63.3%, 28.3% and 7.4 % in 58d fetus and 92.6%, 69.2%, 26.3% and 0.0% in 56d fetus in CD34+CD36−, CD34+CD36+, CD34−CD36+ and erythroblast cell populations respectively. Only the −54 CpG site exhibited hypomethylation in the most primitive CD34+CD36− cell population. In conclusion, our results show a progressive decrease in methylation as the HSPC mature into erythroblasts and progressively accumulate more hemoglobin indicating a direct role of DNA methylation in regulation of hemoglobin production. Status of histone methylation and acetylation along with DNA methylation pattern of ε- and β-globin gene promoters in hematopoietic progenitors at various differentiated stages should enhance our understanding of γ-globin gene regulation in a non-human primate model which closely mimics human beings.


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