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Iranian Journal of Basic Medical Sciences، جلد ۱۷، شماره ۱۱، صفحات ۸۸۶-۸۹۴
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| عنوان فارسی |
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| چکیده فارسی مقاله |
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| کلیدواژه‌های فارسی مقاله |
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| عنوان انگلیسی |
AKT family and miRNAs expression in IL-2-induced CD4+T cells |
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| چکیده انگلیسی مقاله |
Objective(s): Study of non-coding RNAs is considerable to elucidate principal biological questions or design new therapeutic strategies. miRNAs are a group of non-coding RNAs that their functions in PI3K/AKT signaling and apoptosis pathways after T cell activation is not entirely clear. Herein, miRNAs expression and their putative targets in the mentioned pathways were studied in the activated CD4+T cells. Materials and Methods: Herein, proliferation rate and IL-2 secretion were measured in treated and untreated cells by IL-2. Putative targets of up-regulated miRNAs were predicted by bioinformatics approaches in the apoptotic and PI3K/AKT signaling pathways. Then the expression of two putative targets was evaluated by quantitative RT-PCR. Results: Proliferation rate of treated cells by IL-2 increased in a dose- and time- dependent manner. Naive and activated CD4+T cells induced by different dose of IL-2 secreted abundant amounts of IL-2. Also, in IL-2 un-induced cells (IL-2 depleted cells) after 3 days, decrease of proliferation has been shown. In silico analysis predicted putative targets of up-regulated miRNAs such as AKT1, AKT3 and apoptotic genes in the activated cells induced or un-induced by IL-2. Decrease of AKT3 was shown by Q-RT-PCR as a potential target of miRNAs overexpressed in IL-2 depleted cells. But there was no significant difference in AKT1 expression in two cell groups. Conclusion: Our analysis suggests that decrease of AKT3 was likely controlled via up-regulation of specific miRNAs in IL-2 depleted cells. Also it seems that miRNAs play role in induction of different apoptosis pathways in IL-2 induced and un-induced cells. |
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| کلیدواژه‌های انگلیسی مقاله |
AKT3, IL-2 induction, In silico analysis, miRNAs |
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| نویسندگان مقاله |
نجمه رنجی | najmeh ranji
department of genetics, college of science, rasht branch, islamic azad university, rasht, iran
سازمان اصلی تایید شده: دانشگاه آزاد اسلامی علوم و تحقیقات (Islamic azad university science and research branch)
مجید صادقی زاده | majid sadeghizadeh
department of genetics, school of biological sciences, tarbiat modares university, tehran, iran
سازمان اصلی تایید شده: دانشگاه تربیت مدرس (Tarbiat modares university)
مرتضی کریمی پور | morteza karimipoor
department of molecular medicine, biotechnology research center, pasteur institute of iran, tehran, iran
سازمان اصلی تایید شده: انستیتو پاستور ایران (Pasteur institute of iran)
محمد علی شکرگزار | mohammad ali shokrgozar
national cell bank of iran, pasteur institute of iran, tehran, iran
سازمان اصلی تایید شده: انستیتو پاستور ایران (Pasteur institute of iran)
رضا ابراهیم زاده وصال | reza ebrahimzadeh vesal
department of medical genetics, faculty of medicine, tehran university of medical sciences, tehran, iran
سازمان اصلی تایید شده: دانشگاه علوم پزشکی تهران (Tehran university of medical sciences)
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| نشانی اینترنتی |
http://ijbms.mums.ac.ir/article_3740.html |
| فایل مقاله |
اشکال در دسترسی به فایل - ./files/site1/rds_journals/87/article-87-45351.pdf |
| کد مقاله (doi) |
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| زبان مقاله منتشر شده |
en |
| موضوعات مقاله منتشر شده |
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| نوع مقاله منتشر شده |
Original Article |
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