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Expression and Cpg Island Methylation Pattern of Mmp-2 and Mmp-9 Genes in Patients With Congenital Factor Xiii Deficiency and Intracranial Hemorrhage Publisher Pubmed



Norooziaghideh A1, 2 ; Kashani Khatib Z3 ; Naderi M4 ; Dorgalaleh A5 ; Yaghmaie M6 ; Paryan M7 ; Alizadeh S1
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Authors Affiliations
  1. 1. Hematology Department, Allied Medical School, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Hematology Department, AJA University of Medical Sciences, Tehran, Iran
  3. 3. Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine (IBTO), Tehran, Iran
  4. 4. Ali-Ebne Abitaleb Hospital, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran
  5. 5. Hematology Department, Allied Medical School, Iran University of Medical Sciences, Tehran, Iran
  6. 6. Hematology-Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. Department of Research and Development, Production and Research Complex, Pasteur Institute of Iran, Tehran, Iran

Source: Hematology (United Kingdom) Published:2019


Abstract

Objectives: Congenital factor XIII (FXIII) deficiency is a rare severe bleeding disorder. Intracranial hemorrhage (ICH) is the leading cause of mortality and morbidity in FXIII deficiency. However, its pathogenesis is not well understood yet. In this study, we investigated the expression and CpG island methylation status of matrix metalloproteinase-2 (MMP-2) and MMP-9 in patients with FXIII deficiency and ICH. Methods: Forty patients with FXIII deficiency including twenty patients with ICH, and twenty without ICH were recruited as case and control groups, respectively. Methylation status was determined by bisulfite sequencing polymerase chain reaction (PCR), and gene expression was assessed by quantitative real-time PCR. Results and discussion: We found an unmethylated pattern for both MMP-2 and MMP-9 genes in the case group. Both genes were partially methylated in the control group, while the percentage of methylated CpGs was significantly higher in MMP-9 than MMP-2 (P = 0.001). Furthermore, higher expression of MMP-9 (in both the mRNA and protein levels) was found in the case than control group (P = 0.008 and P = 0.009, respectively). On the other hand, there was no significant difference in MMP-2 expression level (neither mRNA nor protein) between the two groups (P = 0.12 and P = 0.25, respectively). Conclusion: Our findings indicated that MMP-9 over-expression might be related to ICH in FXIII deficiency, and gene methylation effectively regulates its expression. Future researches will expand our understanding of the pathogenesis of ICH in congenital FXIII deficiency. © 2019, © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
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