در هنگام جستجو کلمه در قسمت عنوان میتوانید کلمات مورد جستجو را با کاراکتر (-) جدا کنید.
کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: miR-9,miR-7,miR-23a,miR-23b,miR-96,miR-204,miR-211,RGS5
- چکیده:
- چکیده انگلیسی: Objective(s):An earlier meta-analysis on gene expression data derived from four microarray, two cDNA library, and one SAGE experiment had identified RGS5 as one of only ten non-housekeeping genes that were reported to be expressed in human trabecular meshwork (TM) cells by all studies. RGS5 encodes regulator of G-protein signaling-5. The TM tissue is the route of aqueous fluid outflow, and is relevant to the pathology of glaucoma. MicroRNAs constitute the most recently identified components of the cellular machinery for gene regulation in eukaryotic cells. Given our long standing interest in glaucoma, we aimed to identify miRNAs that may target RGS5.
Materials and Methods: Eight miRNAs were selected for study using bioinformatics tools and available data on miRNAs expressed in the eye. Their effects were assessed using the dual luciferase assay. 3'-UTR segments of RGS5 mRNA were cloned downstream of a luciferase coding gene in psiCHECK2 vectors, and these were co-transfected with each of the miRNAs into HEK293 cells.
Results: The outcomes evidenced that one or more of the segments are in fact targeted by miR-7, miR-9, miR-96, miR-23a, miR-23b, miR-204, and miR-211. Down regulations by the miRNAs were statistically significant. The effect of miR-204 is considered particularly important as this miRNA is well known to regulate eye development and to affect multiple ocular functions.
Conclusion: Our results justify further studies on regulation of RGS5 expression and RGS5 downstream functions by these miRNAs.- انتشار مقاله: 06-12-1393
- نویسندگان: Amir Banaei-Esfahani,Hamidreza Moazzeni,Pooya Naseri Nosar,Sadaf Amin,Ehsan Arefian,Masoud Soleimani,Shahin Yazdani,Elahe Elahi
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Biotechnology
- نوع مقاله: Journal Article
- کلمات کلیدی: CD133+ cells,g-globin,Fetal hemoglobin,SCF,TGF-b
- چکیده:
- چکیده انگلیسی: Increased fetal hemoglobin (HbF) in b-globin gene disorders ameliorates the clinical symptoms of the underlying disease. 5-azacytidine, butyrate and hydroxyurea, have been shown to activate g-globin gene expression. It has also been found that hematopoietic growth factors can influence expression of g-globin in erythroid cultures and in animal models. This study was designed to evaluate the in vitro effects of the stem cell factor (SCF) and transforming growth factor-b (TGF-b) on g-globin gene reactivation of erythroid precursors derived from CD133+ cells in vitro. Reverse Transcription-Polymerase Chain Reaction (RT-PCR) analysis showed increased expression of the g-globin transcript in cell culture groups containing either TGF- b or SCF or both as compared to control (2.2-, 2.7- and 5.5-fold, respectively) (p<0.01). Production of HbF in a differentiated population was demonstrated using flow cytometry. The results of this study suggest that SCF and TGF-b warrant further evaluation as potential therapeutic drugs for the treatment of b-globin gene disorders.
- انتشار مقاله: 05-02-1394
- نویسندگان: Amir Atashi,Masoud Soleimani,Saeid Kaviani,Abbas Hajifathali,Ehsan Arefian
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Apoptosis,miRNAs,Glioblastoma,miR-4731
- چکیده:
- چکیده انگلیسی: GBM (Glioblastoma multiforme) is the most prevalent and lethal primary brain tumor. Gene therapy is one of the promising approaches and involves the delivery of genetic therapeutic molecules for specific antitumour response/activity. miRNAs can regulate the cell biology functions including replication, cell growth, and apoptosis by regulating gene expression. In this study, we found that down-regulation of miR-4731 expression occurred in GBM cells. We further determined that miR-4731 behaved as a tumor suppressor by inhibiting GBM cell proliferation. We further investigated the molecular mechanisms of miR-4731 and EGFR, ERK-1,2 and AKT-1,2 in GBM cell lines U87 and U251. The in vitro ectopic expression of miR-4731 affected cell proliferation, migration, and invasion of U87 and U251 cells. Luciferase reporter assays validated that miR-4731 targeted the 3′-untranslated region (3′-UTR) of EGFR. In conclusions, we identified that miR-4731 plays a tumor suppressor role in GBM cell proliferation and migration by targeting EGFR expression, and miR-4731 may act as a novel biomarker for early diagnosis or therapeutic target of GBM.
- انتشار مقاله: 05-10-1398
- نویسندگان: Amir Alahverdi,Ehsan Arefian,Masoud Soleimani,Jafar Ai,Aaliakbar Yousefi-Ahmadipour,Abouzar Babaei,Md Shahidul Islam,Somayeh Ebrahimi-Barough
- مشاهده