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العنوان
The role of microRNA-31 and microRNA-21 as regulator biomarkers in the activation of T-lymphocytes /
الناشر
Eman Eissa Ateya Mohammed ,
المؤلف
Eman Eissa Ateya Mohammed
هيئة الاعداد
باحث / Eman Eissa Ateya Mohammed
مشرف / Sanaa Osman Abdallah
مشرف / Faten Sayed Bayoumi
مشرف / Khalda Said Amr
تاريخ النشر
2016
عدد الصفحات
168 P. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
Biochemistry
تاريخ الإجازة
11/6/2017
مكان الإجازة
جامعة القاهرة - كلية العلوم - Biochemistry
الفهرس
Only 14 pages are availabe for public view

from 198

from 198

Abstract

The present study aimed to evaluate the possibility of using miR-31 and miR- 21 as regulatory biomarkers in the activation of T-lymphocytes of Egyptian lupus patients through estimating the correlation of miR-31 and miR-21 with IL- 2 in SLE patients and investigating the association of miR-31 and miR-21 expressions with the systemic lupus erythematosus disease activity index (SLEDAI) and proteinuria of patients. Quantitative RT-PCR was used to estimate the expression patterns of miR-31 and miR-21, and IL-2 levels were determined using ELISA in plasma of 40 patients with SLE, 20 of their first degree relatives and 20 healthy controls. This study also determined SLEDAI score and proteinuria in SLE patients. The results revealed that miR-31 expression was lower while miR-21 was higher in SLE patients than that of their first degree relatives and normal controls. MiR-31was negatively correlated with SLEDAI and proteinuria in lupus patients while miR-21 showed positively correlation with both of which in those patients. Also the present study found that there is a significant positive correlation between miR-31 and IL-2 in SLE patients while miR-21 was negatively correlated with IL-2 level in those patients. In conclusion, the study disclosed a significant association between miR-31 and miR-21 expressions with IL-2 level in SLE patients. Therefore, both of miR-31 and miR-21 may play an important role as regulatory biomarkers and might have an impact on regulating IL-2 expression and in turn the activation of T-lymphocytes in SLE