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microRNAs (miRNAs) play critical roles in many different cellular processes, including metabolism, apoptosis, differentiation and development. We showed miR-181b to be highly expressed in acute myeloid leukemia (AML). Furthermore, miR-181b contributed to proliferation of AML cells by targeting MLK2. Our results demonstrated that miR-181b plays an important role in the biology of AML and may be useful in developing therapies targeting miRNAs.

Authors Iman M Omar, Dina A Fouad, Deena M M Habashy, Doaa G Eissa, Mariam F Abdel-Maksoud Clinical Pathology Department, Hematology Unit, Faculty of Medicine, Ain Shams University, Cairo-Egypt Correspondence Doaa Gamal Eissa MD, Clinical Pathology, Department, Hematology Unit, Faculty of Medicine, Ain Shams University, Cairo, Egypt Address: 20 Nagatysarag Street, Nasr city, Cairo Email: doaaeissa3@yahoo.com Tel: + 02 27772933 Abstract Unique micro RNA (miRNA) expression signatures are aberrantly expressed in acute myeloid leukemia (AML). Certain miRNA signatures have been associated with prognosis of AML, one of these is miR-181b. We aimed to quantify miR-181b in AML Egyptian adult patients and evaluate its prognostic significance in those patients. Eighty newly diagnosed AML patients with 40 age and sex matching healthy volunteers as a control group were studied for the expression of miR-181b by stem-loop quantitative reverse-transcription polymerase chain reaction (qRTPCR).miR-181b expression level was higher in patients’ group than controls (p=0.013). Patients with miR-181b  6.0 were associated with favorable molecular abnormalities and most of them achieved complete remission (CR), whereas most of patients with miR-181b< 6.0 were associated with unfavorable ones and failed to achieve CR. Patients with miR181b values ≥ 6 showed significantly higher mean survival than patients with values

Increased matrix metalloproteinase (MMP) activity, and related collagen and elastin degradation as a result of macrophage accumulation, are key characteristics of abdominal aortic aneurysm (AAA) progression and rupture. Accordingly targeting MMPs or promoting expression of the endogenous tissue inhibitor of metalloproteinases (TIMPs), may represent novel therapeutic strategies to prevent AAA progression and rupture. To closely mimic human AAA, we used an angiotensin II (AngII)-infused, high fat-fed apolipoprotein E knockout mouse model. Sudden death due to aortic dissection/rupture, was significantly increased (30%, p Collectively our data show that miR181b inhibition stabilises AAA through a dual beneficial effect, by promoting collagen preservation via TIMP3 modulation, and through directly increasing elastin production and deposition.