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      gga-miR-101-3p Plays a Key Role in Mycoplasma gallisepticum ( HS Strain) Infection of Chicken

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          Abstract

          Mycoplasma gallisepticum (MG), one of the most pathogenic Mycoplasma, has caused tremendous economic loss in the poultry industry. Recently, increasing evidence has suggested that micro ribonucleic acids (miRNAs) are involved in microbial pathogenesis. However, little is known about potential roles of miRNAs in MG infection of chicken. In the present study, using miRNA Solexa sequencing we have found that gga-miR-101-3p was up-regulated in the lungs of MG-infected chicken embryos. Moreover, gga-miR-101-3p regulated expression of the host enhancer of zeste homolog 2 (EZH2) through binding to the 3’ un-translated region (3’-UTR) of EZH2 gene. Over-expression of gga-miR-101-3p significantly inhibited EZH2 expression and hence inhibited proliferation of chicken embryonic fibroblast (DF-1 cells) by blocking the G1-to-S phase transition. Similar results were obtained in MG-infected chicken embryos and DF-1 cells, where gga-miR-101-3p was significantly up-regulated, while EZH2 was significantly down-regulated. This study reveals that gga-miR-101-3p plays an important role in MG infection through regulation of EZH2 expression and provides a new insight into the mechanisms of MG pathogenesis.

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          The Toll-like receptors (TLRs) are the key proteins that allow mammals--whether immunologically naive or experienced--to detect microbes. They lie at the core of our inherited resistance to disease, initiating most of the phenomena that occur in the course of infection. Quasi-infectious stimuli that have been used for decades to study inflammatory mechanisms can activate the TLR family of proteins. And it now seems that many inflammatory processes, both sterile and infectious, may depend on TLR signalling. We are in a good position to apply our understanding of TLR signalling to a range of challenges in immunology and medicine.
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              Members of the Toll-like receptor (TLR) family recognize conserved microbial structures, such as bacterial lipopolysaccharide and viral double-stranded RNA, and activate signaling pathways that result in immune responses against microbial infections. All TLRs activate MyD88-dependent pathways to induce a core set of stereotyped responses, such as inflammation. However, individual TLRs can also induce immune responses that are tailored to a given microbial infection. Thus, these receptors are involved in both innate and adaptive immune responses. The mechanisms and components of these varied responses are only partly understood. Given the importance of TLRs in host defense, dissection of the pathways they activate has become an important emerging research focus. TLRs and their pathways are numerous; Science's Signal Transduction Knowledge Environment's TLR Connections Map provides an immediate, clear overview of the known components and relations of this complex system.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                02 December 2015
                December 2015
                : 16
                : 12
                : 28669-28682
                Affiliations
                [1 ]Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Ministry of Education, Huazhong Agricultural University, Wuhan 430070, China; chenjiao123@ 123456webmail.hzau.edu.cn (J.C.); wangzaiwei@ 123456webmail.hzau.edu.cn (Z.W.); houyue@ 123456webmail.hzau.edu.cn (Y.H.); zyb@ 123456webmail.hzau.edu.cn (Y.Z.)
                [2 ]China National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan 430070, China; bidingren@ 123456mail.hzau.edu.cn
                [3 ]Department of Biological Sciences and Border Biomedical Research Center, University of Texas at El Paso, El Paso, TX 79968, USA
                Author notes
                [* ]Correspondence: jsun@ 123456utep.edu (J.S.); xlpengsishun@ 123456mail.hzau.edu.cn (X.P.); Tel.: +915-747-8905 (J.S.); +86-27-8728-1396 (X.P.); Fax: +915-747-5808 (J.S.); +86-27-8728-0408 (X.P.)
                Article
                ijms-16-26121
                10.3390/ijms161226121
                4691068
                26633386
                1b8fd9fd-d7c3-4ce6-a805-2b19838e29d7
                © 2015 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 28 October 2015
                : 24 November 2015
                Categories
                Article

                Molecular biology
                chicken,mycoplasma gallisepticum (hs strain),gga-mir-101-3p,ezh2
                Molecular biology
                chicken, mycoplasma gallisepticum (hs strain), gga-mir-101-3p, ezh2

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