Inhibition of Micro RNA 219 Expression Protects Synaptic Plasticity via Activating NMDAR1, Ca MKIIγ,and p-CREB after Microwave Radiation

In recent decades,the potential health hazards of microwave exposure have been attracting increasing attention.Our previous studies have demonstrated that microwave exposure impaired learning and memory in experimental animal models[1,2].

Involvement of TLR2-My D88 in Abnormal Expression of mi R-146a in Peripheral Blood Monocytes of Patients with Chronic Hepatitis C

miR-146 a is an immunoregulatory micro RNA closely associated with viral infection. This study investigated the expression changes of mi R-146 a in peripheral blood monocytes of HCV-infected patients and the mechanism by which the THP-1 cells were stimulated with HCV core protein in vitro. It was found that in the peripheral blood monocytes of HCV-infected patients, mi R-146 a expression was upregulated. After treated by interferon/ribavirin, mi R-146 a expression was decreased when HCV RNA became undetectable. HCV core could directly stimulate THP-1 cells to produce mi R-146 a. Silencing TLR2 and My D88 could significantly inhibit the expression of mi R-146 a. It was concluded that the expression of mi R-146 a in peripheral blood monocytes of HCV-infected patients was abnormally increased. The TLR2-My D88 signaling pathway may take part in the overexpression of mi R-146 a in monocytes stimulated with HCV core protein.

Knockdown of Bmi1 Inhibits Bladder Cancer Cell Growth Both In Vitro and In Vivo by Blocking Cell Cycle at G_1 Phase and Inducing Apoptosis

Bmi1 is a member of the polycomb group family of proteins,and it drives the carcinogenesis of various cancers and governs the self-renewal of multiple types of stem cells. However,its role in the initiation and progression of bladder cancer is not clearly known. The present study aimed to investigate the function of Bmi1 in the development of bladder cancer. Bmi1 expression was detected in human bladder cancer tissues and their adjacent normal tissues（n=10） by immunohistochemistry,q RT-PCR and Western blotting,respectively. Bmi1 small interference RNA（si RNA） was synthesized and transfected into human bladder carcinoma cells（EJ） by lipofectamine 2000. The Bmil expression at m RNA and protein levels was measured in EJ cells transfected with Bmil si RNA（0,80,160 nmol/L） by q RT-PCR and Western blotting,respectively. Cell viability and Ki67 expression（a marker of cell proliferation） were determined in Bmi1 si RNA-transfected cells by CCK-8 assay and q RT-PCR,respectively. Cell cycle of transfected cells was flow-cytometrically determined. Immunofluorescence and Western blotting were used to detect the expression levels of cell cycle-associated proteins cyclin D1 and cyclin E in the cells. Pro-apoptotic proteins Bax and caspase 3 and anti-apoptotic protein Bcl-2 were detected by Western blotting as well. Additionally,xenograft tumor models were established by inoculation of EJ cells（infected with Bmil sh RNA/p LKO.1 lentivirus or not） into nude mice. The tumor volumes were measured every other day for 14 days. The results showed that the Bmil expression was significantly increased in bladder tumor tissues when compared with that in normal tissues（P〈0.05）. Perturbation of Bmi1 expression by using si RNA could significantly inhibit the proliferation of EJ cells（P〈0.05）. Bmi1 si RNA-trasnfected EJ cells were accumulated in G1 phase and the expression levels of cyclin D1 and cyclin E were down-regulated. Bax and caspase-3 expression levels were significantly increased and Bcl-2 levels decreased after Bmi1 knockdown. Tumor volume was conspicuously reduced in mice injected with EJ cells with Bmi1 knockdown. Our findings indicate that Bmi1 is a potential driver oncogene of bladder cancer and it may become a potential treatment target for human bladder cancer.

The RNA helicase DDX46 inhibits innate immunity by entrapping m^6 A-demethylated antiviral transcripts in the nucleus

With the support by the National Natural Science Foundation of China,the research team directed by Prof.Cao Xuetao(曹雪涛)at the National Key Laboratory of Medical Molecular Biology&Department of Immunology,Chinese Academy of Medical Sciences,and the National Key Laboratory of Medical Immunology,Second Military Medical University,recently reported that RNA helicase DDX46is