本文選題：內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng) + 二代RNA測(cè)序��； 參考：《中國(guó)生物化學(xué)與分子生物學(xué)報(bào)》2017年04期

【摘要】：內(nèi)質(zhì)網(wǎng)是真核細(xì)胞的重要細(xì)胞器。某些細(xì)胞內(nèi)外因素如病原體感染等能引起從內(nèi)質(zhì)網(wǎng)到胞漿和胞核的信號(hào)傳導(dǎo)途徑活化,即內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)。但是,目前國(guó)內(nèi)外尚無(wú)針對(duì)內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)的基因表達(dá)譜分析報(bào)道。本研究中,用3種已報(bào)道的內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)誘導(dǎo)劑,包括蛋白質(zhì)糖基化抑制劑衣霉素(tunicamycin)、內(nèi)質(zhì)網(wǎng)Ca~(2+)-ATPases抑制劑毒胡蘿卜素(thapsigargin)和乙腦病毒(Japanese encephalitis virus,JEV),分別處理小鼠顱腔和小鼠腦神經(jīng)瘤細(xì)胞(Neuro-2a),試劑處理組與未處理組的第二代RNA測(cè)序分析發(fā)現(xiàn),衣霉素、毒胡蘿卜素和乙腦病毒在體外和體內(nèi)均引起分子伴侶基因Hsp70表達(dá)上調(diào),誘導(dǎo)內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)。衣霉素、毒胡蘿卜素和乙腦病毒體外處理誘導(dǎo)的內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)信號(hào)通路中,基因差異表達(dá)相似性高于體內(nèi)處理組。乙腦病毒和糖基化抑制劑衣霉素體內(nèi)外處理,主要誘導(dǎo)內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)的非折疊蛋白質(zhì)反應(yīng)信號(hào)通路,引起相關(guān)基因Atf4、Bip、Edem和Perk等表達(dá)上調(diào)。內(nèi)質(zhì)網(wǎng)Ca~(2+)-ATPases抑制劑毒胡蘿卜素主要誘導(dǎo)內(nèi)質(zhì)網(wǎng)超負(fù)荷反應(yīng),激活NF-κB信號(hào)通路。乙腦病毒誘導(dǎo)的內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)相關(guān)差異表達(dá)基因數(shù)量最多,體外與體內(nèi)合計(jì)有40種。乙腦病毒體內(nèi)外處理上調(diào)的基因包括Bax、Casp12、Atf4、Bip、Edem和Perk等,下調(diào)的基因包括Sec23/24、Nef、Svip和Jnk等。糖基化抑制劑衣霉素體內(nèi)外處理上調(diào)基因包括Gadd34、Atf4、Ermani和Bip等,下調(diào)基因包括Grp94、Atf6、Sec23/24和Nef等。內(nèi)質(zhì)網(wǎng)Ca2+-ATPases抑制劑毒胡蘿卜素體內(nèi)外處理上調(diào)的基因包括Sec61、Trap和Ask1等。衣霉素、毒胡蘿卜素和乙腦病毒體內(nèi)外處理也通過(guò)內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng),調(diào)控與炎癥或凋亡相關(guān)的MAPK信號(hào)通路和P53信號(hào)通路。本研究首次通過(guò)使用3種內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)誘導(dǎo)劑分別處理小鼠和細(xì)胞,揭示了體內(nèi)外內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)引起的基因表達(dá)譜變化,為內(nèi)質(zhì)網(wǎng)應(yīng)激反應(yīng)相關(guān)疾病的治療提供了新思路。
[Abstract]:Endoplasmic reticulum is an important organelle of eukaryotic cells. Some internal and external factors, such as pathogen infection, can activate the signal transduction pathway from endoplasmic reticulum to cytoplasm and nucleus, that is, endoplasmic reticulum stress reaction. However, there is no analysis of endoplasmic reticulum stress response gene expression profile at home and abroad. In this study, three reported endoplasmic reticulum stress inducers were used. The protein glycosylation inhibitor, tunicamycin, the endoplasmic reticulum (ER) and the Japanese encephalitis virus (JEV) were used to treat the cranial cavity of mice and the neuro-2aanine of brain neuroma cells, respectively. The second generation RNA sequencing of the reagents treated group and the untreated group was found. In vitro and in vivo, the expression of the molecular chaperone gene Hsp70 was up-regulated and the endoplasmic reticulum stress was induced by itamycin, carotene and Japanese encephalitis virus. The similarity of gene differential expression in the endoplasmic reticulum (ER) stress response signaling pathway induced by itamycin, carotene and encephalitis B virus in vitro was higher than that in vivo treatment group. In vivo and in vitro treatment with Japanese encephalitis B virus and glycosylation inhibitor itamycin mainly induces the signal pathway of non-folded protein reaction in endoplasmic reticulum stress reaction and up-regulates the expression of the related genes Atf4- Bip-Edem and Perk. Endoplasmic reticulum (ER) caprostin-ATPase inhibitor, carotene, mainly induces endoplasmic reticulum overload and activates NF- 魏 B signaling pathway. The number of differentially expressed genes related to endoplasmic reticulum stress induced by encephalitis B virus was the highest, with 40 genes in vitro and in vivo. The up-regulated genes of Japanese encephalitis virus in vivo and in vitro include Baxon Casp12Atf4, BipEdem and Perk, while down-regulated genes include Sec23 / 24 NefSvip and Jnk. The up-regulated genes including Gadd34, Atf4, Ermani and Bip, and down-regulated genes include Grp94, Atf6, Sec23 / 24 and Nef, respectively. Endoplasmic reticulum Ca 2-ATPase inhibitor, carotene, up-regulated genes including Sec61Trap and Ask1 in vitro and in vivo. In vivo and in vitro treatment of itamycin, carotene and encephalitis B virus also regulate MAPK signaling pathway and p53 signaling pathway related to inflammation or apoptosis through endoplasmic reticulum stress. In this study, three endoplasmic reticulum stress inducers were used to treat mice and cells for the first time, which revealed the changes of gene expression profile induced by endoplasmic reticulum stress in vivo and in vitro, and provided a new idea for the treatment of endoplasmic reticulum stress related diseases.
【作者單位】： 江西農(nóng)業(yè)大學(xué)生物科學(xué)與工程學(xué)院;江西省疾病預(yù)防控制中心;南昌大學(xué)生命科學(xué)院人類(lèi)衰老研究所;
【基金】：國(guó)家自然科學(xué)基金項(xiàng)目(No.31460667) 江西省重點(diǎn)項(xiàng)目(No.20161BBF60084)資助~~
【分類(lèi)號(hào)】：R363

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