作為一類病因復(fù)雜且缺乏有效治療手段的中樞神經(jīng)系統(tǒng)自身免疫疾病,，多發(fā)性硬化癥多年來(lái)一直困擾著國(guó)際醫(yī)療界,。我國(guó)科學(xué)家最新的一項(xiàng)研究揭示了非編碼小RNA在多發(fā)性硬化癥發(fā)生過(guò)程中的新機(jī)制,。
由中國(guó)科學(xué)院上海生命科學(xué)研究院生物化學(xué)與細(xì)胞生物學(xué)研究所裴鋼院士領(lǐng)導(dǎo)的研究組及他們的合作者,，在研究中發(fā)現(xiàn)一種非編碼小RNA (miR-326)在多發(fā)性硬化癥病人的CD4+T細(xì)胞亞群中特異性上調(diào),。而近年來(lái)免疫學(xué)家發(fā)現(xiàn),，人體中的CD4+T細(xì)胞亞群的大量誘導(dǎo)及其對(duì)病灶部位的主動(dòng)入侵,，能加速誘發(fā)組織損傷,。
研究人員通過(guò)多發(fā)性硬化癥的小鼠模型研究進(jìn)一步證實(shí)，人為提高非編碼小RNA (miR-326)的水平,，會(huì)加重小鼠的病情,，而抑制非編碼小RNA (miR-326)的水平，則能顯著減輕小鼠的病情,。
這一研究成果已于10月19日在線發(fā)表在國(guó)際著名學(xué)術(shù)期刊《自然·免疫》網(wǎng)絡(luò)版上,。業(yè)內(nèi)專家認(rèn)為，該項(xiàng)研究不僅揭示了非編碼小RNA在多發(fā)性硬化癥發(fā)生過(guò)程中的新機(jī)制,，并且為包括多發(fā)性硬化癥在內(nèi)的自身免疫疾病的治療,，提供了可借鑒的新策略。
我國(guó)科學(xué)家進(jìn)行的這項(xiàng)研究,，得到了科技部,、國(guó)家自然科學(xué)基金、上海市科委和中國(guó)科學(xué)院的資金資助,，相關(guān)研究成果已申請(qǐng)專利,。（生物谷Bioon.com）
裴剛院士近期研究成果：
Nature：胰島素耐受/II型糖尿病發(fā)病機(jī)制研究
生物谷推薦原始出處：
Nature Immunology 18 October 2009 | doi:10.1038/ni.1798
MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis
Changsheng Du1,5, Chang Liu1,5, Jiuhong Kang1,2, Guixian Zhao3, Zhiqiang Ye4, Shichao Huang1, Zhenxin Li3, Zhiying Wu3 & Gang Pei1,2
Interleukin 17 (IL-17)-producing T helper cells (TH-17 cells) are increasingly recognized as key participants in various autoimmune diseases, including multiple sclerosis. Although sets of transcription factors and cytokines are known to regulate TH-17 differentiation, the role of noncoding RNA is poorly understood. Here we identify a TH-17 cell–associated microRNA, miR-326, whose expression was highly correlated with disease severity in patients with multiple sclerosis and mice with experimental autoimmune encephalomyelitis (EAE). In vivo silencing of miR-326 resulted in fewer TH-17 cells and mild EAE, and its overexpression led to more TH-17 cells and severe EAE. We also found that miR-326 promoted TH-17 differentiation by targeting Ets-1, a negative regulator of TH-17 differentiation. Our data show a critical role for microRNA in TH-17 differentiation and the pathogenesis of multiple sclerosis.
1 Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
2 School of Life Science and Technology, Tongji University, Shanghai, China.
3 Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Shanghai, China.
4 Key Laboratory of Systems Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
5 These authors contributed equally to this work.
