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Zakeri S, Rahimi Z, Jalilian N, Vaisi-Raygani A, Rezvani A, Dastafkan Z. Aberrant Methylation of the SOD1 GENE, its Expression and Enzyme Activity in the Placenta of Patients with Preeclampsia. rbmb.net 2023; 12 (1) :112-119
URL: http://rbmb.net/article-1-1113-en.html
Department of Clinical Biochemistry, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran & Medical Biology Research Center, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran. And Department of Clinical Biochemistry, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Abstract:   (1086 Views)
Background: Oxidative stress is involved in the pathogenesis of preeclampsia (PE). Dysregulation of SOD1 may be involved in the pathogenesis of PE. We examined and compared the methylation level of the promoter region (PMR) of the SOD1, gene expression, and enzyme activity of superoxide dismutase (SOD) in both placenta and maternal blood in PE women.

Methods: A total of 140 blood samples and 40 placental tissue samples from PE and healthy pregnant controls were studied. The PMR of the SOD1 (Methylight PCR method), the expression (Real-time PCR), and its enzyme activity were investigated and compared in two groups.

Results: The PMR of the SOD1 gene in the placental tissue of the patients was significantly increased compared to the control group (P= 0.008); this result was accompanied by a decrease in the expression of the gene and a decrease in the activity of the SOD enzyme. Meanwhile, the PMR of the SOD1 gene did not significantly change in the blood samples of the patients (P= 0.95), while a significant decrease in the expression of SOD1 (without a significant change in the SOD activity) was observed.

Conclusions: The results showed significant changes in the PMR of the SOD1 gene and gene expression in placenta tissue. The results highlight the role of the placenta in complications during pregnancy and also revealed epigenetics as an important regulatory pathway in the pathogenesis of preeclampsia.
Full-Text [PDF 269 kb]   (977 Downloads)    
Type of Article: Original Article | Subject: Molecular Biology
Received: 2022/12/15 | Accepted: 2023/01/2 | Published: 2023/08/15

References
1. Agrawal S, Walia G. Prevalence and risk factors for symptoms suggestive of pre-eclampsia in Indian women. J Women's Health. 2014;3(6):2-9. [DOI:10.4172/2325-9795.1000169]
2. Fikadu K, Getahun F, Chufamo N, Misiker D. Family history of chronic illness, preterm gestational age and smoking exposure before pregnancy increases the probability of preeclampsia in Omo district in southern Ethiopia: a case-control study. Clinical Hypertension. 2020;26(1):1-12. [DOI:10.1186/s40885-020-00149-9] [PMID] [PMCID]
3. Zerón HM, Parada-Flores A, Chávez AA, García MVD. Oxidative stress in preeclampsia, more than enzymes. Revista Latinoamericana de Hipertensión. 2013;8(2):25-8.
4. Burton GJ, Redman CW, Roberts JM, Moffett A. Pre-eclampsia: pathophysiology and clinical implications. BMJ (Clinical research ed). 2019;366:l2381. [DOI:10.1136/bmj.l2381] [PMID]
5. Phipps E, Prasanna D, Brima W, Jim B. Preeclampsia: Updates in Pathogenesis, Definitions, and Guidelines. Clinical journal of the American Society of Nephrology : CJASN. 2016;11(6):1102-13. [DOI:10.2215/CJN.12081115] [PMID] [PMCID]
6. Aouache R, Biquard L, Vaiman D. Oxidative Stress in Preeclampsia and Placental Diseases. 2018;19(5). P [DOI:10.3390/ijms19051496] [PMID] [PMCID]
7. Namdari S, Saadat M. Susceptibility to preeclampsia is associated with a 50-bp insertion/deletion polymorphism at the promoter region of the SOD1 gene. 2021;22(4):268-72. [DOI:10.4274/jtgga.galenos.2021.2021.0005] [PMID] [PMCID]
8. Cheng Y, Chen H. Aberrance of Zinc Metalloenzymes-Induced Human Diseases and Its Potential Mechanisms. Nutrients. 2021;13(12). [DOI:10.3390/nu13124456] [PMID] [PMCID]
9. Irizarry RA, Ladd-Acosta C, Wen B, Wu Z, Montano C, Onyango P, et al. The human colon cancer methylome shows similar hypo- and hypermethylation at conserved tissue-specific CpG island shores. Nature genetics. 2009;41(2):178-86. [DOI:10.1038/ng.298] [PMID] [PMCID]
10. Javadi A, Shamaei M, Mohammadi Ziazi L, Pourabdollah M, Dorudinia A, Seyedmehdi SM, et al. Qualification study of two genomic DNA extraction methods in different clinical samples. Tanaffos. 2014;13(4):41-7.
11. Rahimi Z, Ghorbani Z, Motamed H, Jalilian N. Aberrant expression profile of miR-32, miR-98 and miR-374 in chronic lymphocytic leukemia. Leukemia research. 2021;111:106691. [DOI:10.1016/j.leukres.2021.106691] [PMID]
12. Sant KE, Nahar MS, Dolinoy DC. DNA methylation screening and analysis. Methods in molecular biology (Clifton, NJ). 2012;889:385-406. [DOI:10.1007/978-1-61779-867-2_24] [PMID] [PMCID]
13. Cai Z, Jia X, Liu M, Yang X, Cui L. Epigenome-wide DNA methylation study of whole blood in patients with sporadic amyotrophic lateral sclerosis. Chinese medical journal. 2022;135(12):1466-73. [DOI:10.1097/CM9.0000000000002090] [PMID] [PMCID]
14. Rezvani N, Alibakhshi R, Vaisi-Raygani A, Bashiri H, Saidijam M. Detection of SPG20 gene promoter-methylated DNA, as a novel epigenetic biomarker, in plasma for colorectal cancer diagnosis using the MethyLight method. Oncology letters. 2017;13(5):3277-84. [DOI:10.3892/ol.2017.5815] [PMID] [PMCID]
15. Rakyan VK, Down TA, Balding DJ, Beck S. Epigenome-wide association studies for common human diseases. Nature reviews Genetics. 2011;12(8):529-41. [DOI:10.1038/nrg3000] [PMID] [PMCID]
16. Cirkovic A, Garovic V, Milin Lazovic J, Milicevic O, Savic M, Rajovic N, et al. Systematic review supports the role of DNA methylation in the pathophysiology of preeclampsia: a call for analytical and methodological standardization. 2020;11(1):36. [DOI:10.1186/s13293-020-00313-8] [PMID] [PMCID]
17. Lind GE, Danielsen SA, Ahlquist T, Merok MA, Andresen K, Skotheim RI, et al. Identification of an epigenetic biomarker panel with high sensitivity and specificity for colorectal cancer and adenomas. Molecular cancer. 2011;10:85. [DOI:10.1186/1476-4598-10-85] [PMID] [PMCID]
18. Mayne BT, Leemaqz SY, Smith AK, Breen J, Roberts CT, Bianco-Miotto T. Accelerated placental aging in early onset preeclampsia pregnancies identified by DNA methylation. Epigenomics. 2017;9(3):279-89. [DOI:10.2217/epi-2016-0103] [PMID] [PMCID]
19. Martinez-Fierro ML, Garza-Veloz I, Carrillo-Sanchez K, Martinez-Gaytan V, Cortes-Flores R, Ochoa-Torres MA, et al. Expression levels of seven candidate genes in human peripheral blood mononuclear cells and their association with preeclampsia. Hypertension in pregnancy. 2014;33(2):191-203. [DOI:10.3109/10641955.2013.853777] [PMID] [PMCID]
20. Ching T, Song MA, Tiirikainen M, Molnar J, Berry M, Towner D, et al. Genome-wide hypermethylation coupled with promoter hypomethylation in the chorioamniotic membranes of early onset pre-eclampsia. Molecular human reproduction. 2014;20(9):885-904. [DOI:10.1093/molehr/gau046] [PMID] [PMCID]
21. Feng C, Lu Q. Dysregulation of endogenous anti-oxidants in placentae of preeclampsia via epigenetic variation. Fertility and Sterility. 2015;104(3):e147-e8. [DOI:10.1016/j.fertnstert.2015.07.455]
22. Jin X, Xu Z, Cao J, Shao P, Zhou M, Qin Z, et al. Proteomics analysis of human placenta reveals glutathione metabolism dysfunction as the underlying pathogenesis for preeclampsia. Biochimica et Biophysica Acta (BBA)-Proteins and Proteomics. 2017;1865(9):1207-14. [DOI:10.1016/j.bbapap.2017.07.003] [PMID]
23. Jin X, Xu Z, Cao J, Shao P, Zhou M, Qin Z, et al. Proteomics analysis of human placenta reveals glutathione metabolism dysfunction as the underlying pathogenesis for preeclampsia. Biochimica et biophysica acta Proteins and proteomics. 2017;1865(9):1207-14. [DOI:10.1016/j.bbapap.2017.07.003] [PMID]

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