本文選題：冷誘導(dǎo)RNA結(jié)合蛋白 + H1N1流感病毒��； 參考：《西南民族大學(xué)》2015年碩士論文

【摘要】：冷誘導(dǎo)RNA結(jié)合蛋白(Cirbp)是在哺乳動(dòng)物體內(nèi)鑒定的首個(gè)與冷應(yīng)激相關(guān)的蛋白,廣泛表達(dá)于多種組織與細(xì)胞中,在脊椎動(dòng)物間高度保守。在多種應(yīng)激條件下Cirbp表達(dá)升高,并發(fā)揮細(xì)胞保護(hù)作用。此外,Cirbp在胚胎發(fā)育,神經(jīng)發(fā)育,生物鐘調(diào)節(jié),腫瘤發(fā)生等過程中發(fā)揮重要的調(diào)節(jié)作用;近期研究表明Cirbp介導(dǎo)了多種病理?xiàng)l件下的炎癥反應(yīng),如LPS刺激,腦缺血性休克,膿毒血癥,酒精刺激等。本實(shí)驗(yàn)室前期研究結(jié)果表明,H1N1 PR-8流感病毒感染SPF小鼠后,各組織器官中Cirbp在mRNA和蛋白水平上都有不同程度的升高;過表達(dá)的Cirbp能通過上調(diào)NF-Kappa B信號通路顯著促進(jìn)H1N1甲型流感病毒的復(fù)制,但Cirbp對病毒復(fù)制過程的影響還不清楚。為了進(jìn)一步探討Cirbp在病毒復(fù)制過程中的作用及機(jī)制,篩選Cirbp相互作用的靶蛋白,我們進(jìn)行了以下研究,主要取得了以下成果:1 H1N1流感病毒感染細(xì)胞后Cirbp表達(dá)升高并發(fā)生核質(zhì)穿梭為了搞清楚Cirbp在H1N1感染的細(xì)胞內(nèi)的表達(dá)規(guī)律,本試驗(yàn)將H1N1流感病毒以MOI=1分別接種三種細(xì)胞,其中BHK-21(敘利亞倉鼠腎細(xì)胞),和MH-S(小鼠肺泡巨噬細(xì)胞)接種人A/Puerto Rico/8/1934 H1N1,PUVEC(豬血管內(nèi)皮細(xì)胞)接種豬A/Swine/GD/2/12 H1N1。分別于感染后0 h,4 h,8 h,16 h,24 h取樣,用免疫組化法檢測各細(xì)胞各時(shí)間點(diǎn)Cirbp的表達(dá)情況并用IPP6.0軟件進(jìn)行半定量分析。結(jié)果顯示:感染PR-8 H1N1甲型流感病毒后8 h~24 h,BHK-21細(xì)胞中Cirbp的表達(dá)水平升高,達(dá)到了差異顯著水平;感染PR-8 H1N1甲型流感后4 h~24 h,MH-S細(xì)胞中Cirbp的表達(dá)水平顯著升高;感染豬H1N1流感病毒后8 h~24 h,PUVEC細(xì)胞中Cirbp的表達(dá)水平顯著升高。為了探討H1N1流感病毒感染下Cirbp在細(xì)胞內(nèi)的亞定位,本試驗(yàn)將H1N1流感病毒以MOI=1感染BHK-21細(xì)胞,分別在感染后2 h,4 h,6 h,8 h對樣品進(jìn)行間接免疫熒光染色,并在激光共聚焦顯微鏡下觀察結(jié)果。結(jié)果顯示,H1N1流感病毒感染后2 h,Cirbp定位于細(xì)胞核與細(xì)胞漿中;感染后4 h Cirbp主要定位于細(xì)胞核中;感染后6 h Cirbp定位于細(xì)胞核與細(xì)胞漿中;感染后8 h,Cirbp主要定位于細(xì)胞核中。鑒于Cirbp在生理?xiàng)l件下存在于細(xì)胞核中,因此此結(jié)果表明在h1n1病毒感染條件下,cirbp可反復(fù)穿梭于細(xì)胞核和細(xì)胞漿之間。上述結(jié)果表明,h1n1流感病毒感染情況下,細(xì)胞中cirbp表達(dá)上調(diào),并且發(fā)生了核質(zhì)穿梭,為進(jìn)一步研究cirbp在流感病毒復(fù)制過程中的最用奠定了基礎(chǔ)。2敲低cirbp降低了h1n1流感病毒mrna的穩(wěn)定性從而抑制病毒的復(fù)制為了證實(shí)cirbp對h1n1病毒mrna穩(wěn)定性、rna合成以及蛋白合成的影響,本試驗(yàn)用real-timepcr方法檢測了敲低cirbp的bhk21細(xì)胞(cirbp-bhk-21)感染h1n1病毒(moi=1)后病毒m和np基因mrna的半衰期,結(jié)果表明,敲低cirbp后h1n1病毒np基因和m基因mrna的相對半衰期分別約為7.5h和8h,對照組中m基因和np基因mrna的相對半衰期都超過了12h;同時(shí)用real-timepcr分析了h1n1流感病毒感染(moi=1)后3h,9h,15h,21h敲低cirbp對病毒m基因mrna合成的影響,結(jié)果顯示,敲低cirbp顯著(p0.05)抑制了h1n1病毒m基因mrna的合成,試驗(yàn)組分別是對照組的21.3%,18.6%,12.4%,7.6%,感染后15h和21h,其抑制作用達(dá)到了極顯著(p0.01)水平;用real-timepcr分析了h1n1流感病毒感染(moi=1)后8h敲低cirbp對病毒m和np基因mrna,crna,vrna合成的影響,結(jié)果顯示,敲低cirbp極顯著(p0.01)抑制了病毒m基因crna和vrna1、vrna2的合成,試驗(yàn)組分別是對照組的16.9%、5.3%、11.3%;敲低cirbp極顯著(p0.01)抑制了病毒np基因crna和vrna1、vrna2的合成,試驗(yàn)組分別是對照組的5.1%、2.2%、2.6%。進(jìn)一步用間接免疫熒光技術(shù)分析了感染h1n1(moi=1)后3h和6h敲低cirbp對病毒np蛋白合成的影響,結(jié)果顯示敲低cirbp抑制了病毒np蛋白的合成。最后在bhk-21和cirbp-bhk-21細(xì)胞上測定了h1n1病毒的tcid50效價(jià)。檢測結(jié)果顯示敲低cirbp后h1n1的tcid50效價(jià)顯著高于正常bhk-21細(xì)胞的tcid50效價(jià),試驗(yàn)組為對照組的57.54倍。上述結(jié)果表明,敲低cirbp降低了流感病毒np和m基因mrna的穩(wěn)定性,進(jìn)而抑制了病毒蛋白的合成,并影響了病毒crna和vrna的合成,最終抑制病毒的復(fù)制。分析上述結(jié)果表明敲低cirbp通過降低病毒mrna的穩(wěn)定性抑制病毒的復(fù)制。本試驗(yàn)首次證實(shí)cirbp通過影響病毒mrna穩(wěn)定性來影響病毒復(fù)制,豐富了機(jī)體因子與流感病毒互作的網(wǎng)絡(luò),為深入研究流感病毒的復(fù)制機(jī)理提供了資料。3過表達(dá)cirbp提高了h1n1病毒的復(fù)制效率cirbp在病毒感染情況下表達(dá)升高,為了探討cirbp過表達(dá)對病毒復(fù)制的影響,本試驗(yàn)分別在bhk-21對照細(xì)胞和過表達(dá)cirbp細(xì)胞(cirbp+bhk-21細(xì)胞)上同時(shí)接種moi為0.001,0.01,2的h1n1病毒;分別在感染后3h,8h,16h,24h提取總rna,用熒光定量pcr檢測h1n1m基因mrna的絕對表達(dá)量。結(jié)果顯示,moi=0.001時(shí),感染后3h,8h,16h,24h試驗(yàn)組m基因mrna的絕對表達(dá)量分別是對照組的1.28,30.78,79.05,26.89倍;moi=0.01時(shí),試驗(yàn)組分別是對照組的0.85,26.95,83.84,47.88倍;moi=2時(shí),試驗(yàn)組分別是對照組的4.07,6.46,5.01,3.98倍。結(jié)果表明過表達(dá)cirbp提高了h1n1病毒的復(fù)制效率,moi越低時(shí),過表達(dá)cirbp使病毒復(fù)制效率的提高越明顯。4過表達(dá)cirbp促進(jìn)了h1n1病毒vrnp的出核轉(zhuǎn)運(yùn)cirbp在h1n1病毒感染情況下穿梭于細(xì)胞核和細(xì)胞漿之間,為了探討cirbp在h1n1病毒轉(zhuǎn)運(yùn)過程中的作用,本試驗(yàn)利用間接免疫熒光技術(shù)研究了cirbp過表達(dá)對病毒粘附,穿入,入核轉(zhuǎn)運(yùn)和出核轉(zhuǎn)運(yùn)的影響。在研究cirbp過表達(dá)對病毒粘附和穿入時(shí),以moi=50的感染量分別接種于試驗(yàn)組和對照組,以病毒感作后1h的時(shí)間點(diǎn)為0h,0h為病毒粘附和穿入的最佳時(shí)間,在此時(shí)間點(diǎn)固定樣本,并進(jìn)行間接免疫熒光染色,在激光共聚焦顯微鏡下觀察,結(jié)果顯示:感染后0h試驗(yàn)組和對照組細(xì)胞膜和細(xì)胞質(zhì)內(nèi)的病毒顆粒無明顯差異,表明cirbp過表達(dá)對h1n1病毒的粘附和穿入無明顯影響。研究對vrnp入核轉(zhuǎn)運(yùn)和出核轉(zhuǎn)運(yùn)時(shí)感染量為moi=1。分別在4h,6h,8h固定樣本,并進(jìn)行間接免疫熒光染色,在激光共聚焦顯微鏡下觀察,結(jié)果顯示:感染后4h,少量病毒vrnp已經(jīng)由細(xì)胞漿進(jìn)入細(xì)胞核中,且試驗(yàn)組和對照組無差異;感染后6h,病毒vrnp依然存在于細(xì)胞漿和細(xì)胞核中,且試驗(yàn)組和對照組無差異;感染后8h,試驗(yàn)組病毒vrnp完全由細(xì)胞核轉(zhuǎn)運(yùn)至細(xì)胞漿中,而對照組病毒vrnp正在從細(xì)胞核向細(xì)胞漿內(nèi)轉(zhuǎn)運(yùn),因此此結(jié)果表明過表達(dá)cirbp促進(jìn)了病毒vrnp的出核轉(zhuǎn)運(yùn)。上述結(jié)果表明,過表達(dá)cirbp促進(jìn)了病毒vrnp的出核轉(zhuǎn)運(yùn),而對其它過程無明顯影響。為深入研究流感病毒vrnp出核轉(zhuǎn)運(yùn)的機(jī)制提供了線索。5h1n1流感病毒感染條件下cirbp靶蛋白的篩選與初步驗(yàn)證為了篩選H1N1病毒感染情況下Cirbp的靶蛋白,本試驗(yàn)利用免疫共沉淀(Co-IP)結(jié)合質(zhì)譜的方法,在病毒感染BHK-21細(xì)胞24h后,對Cirbp結(jié)合的靶蛋白進(jìn)行了篩選,結(jié)果共沉淀下來了29種Cirbp的候選靶蛋白,其中27種為宿主靶蛋白,2種為病毒靶蛋白;Pathway注釋結(jié)果顯示候選的宿主靶蛋白主要參與了核酸代謝和蛋白質(zhì)翻譯信號通路,神經(jīng)調(diào)節(jié)相關(guān)信號通路,感染與免疫相關(guān)的信號通路。27種候選靶蛋白中質(zhì)譜得分前5的蛋白,分別為Hsp90,hnRNP R,D1Pas1,Ddx17,Cttn,質(zhì)譜得分分別為1122.72,381.43,230.4,186.49,185.49。其中Hsp90和Ddx17與流感病毒的復(fù)制密切相關(guān)。Hsp90的質(zhì)譜得分最高并在流感病毒復(fù)制過程中發(fā)揮重要的作用,因此我們進(jìn)一步用間接免疫熒光驗(yàn)證Hsp90與Cirbp發(fā)生了共定位,表明Hsp90與Cirbp至少是以復(fù)合體的形式發(fā)生了結(jié)合。Hsp90與Cirbp是否直接物理結(jié)合還需要進(jìn)一步的試驗(yàn)驗(yàn)證。此外,western-blot結(jié)果顯示過表達(dá)Cirbp上調(diào)了Hsp90蛋白的表達(dá),表明Cirbp對Hsp90具有調(diào)節(jié)作用。2種候選的病毒靶蛋白中,NP的質(zhì)譜得分最高,為108.68。流感病毒NP蛋白在復(fù)制過程中發(fā)揮重要的作用,它與病毒RNA,其他病毒蛋白及宿主細(xì)胞的某些大分子相互作用,影響病毒的轉(zhuǎn)錄、復(fù)制、裝配及轉(zhuǎn)運(yùn)功能。進(jìn)一步用間接免疫熒光驗(yàn)證NP與Cirbp發(fā)生了共定位,表明NP與Cirbp至少以復(fù)合體的形式發(fā)生了結(jié)合。此結(jié)果為進(jìn)一步研究Cirbp與H1N1互作的分子機(jī)制提供了線索。
[Abstract]:Cold induced RNA binding protein (Cirbp) is the first protein associated with cold stress in mammals. It is widely expressed in a variety of tissues and cells, highly conserved among vertebrates. The expression of Cirbp is elevated in a variety of stressful conditions and cell protection is played. In addition, Cirbp is in embryo development, neural development, clock regulation, and swelling. The recent study showed that Cirbp mediated the inflammatory response under various pathological conditions, such as LPS stimulation, cerebral ischemic shock, sepsis, and alcohol stimulation. The results of the early study in this laboratory showed that after the H1N1 PR-8 influenza virus was infected with SPF mice, Cirbp was in mRNA and protein water in various tissues and organs. The overexpressed Cirbp can promote the replication of H1N1 influenza A virus by up regulation of the NF-Kappa B signaling pathway, but the effect of Cirbp on the replication process of the virus is not clear. In order to further explore the role and mechanism of Cirbp in the replication process of the virus and to screen the target protein of Cirbp interaction, we enter the Cirbp. Following the following research, the following results were obtained: 1 H1N1 influenza virus infected cells increased Cirbp expression and occurred nuclear shuttle in order to understand the expression of Cirbp in H1N1 infected cells. This experiment inoculated the H1N1 influenza virus with three cells respectively, including BHK-21 (Syria hamster kidney cells), and MH-S (mouse alveolus). Macrophages were inoculated with A/Puerto Rico/8/1934 H1N1, and PUVEC (porcine vascular endothelial cells) inoculated swine A/Swine/GD/2/12 H1N1. were sampled at 0 h, 4 h, 8 h, 16 h, 24 h respectively. The expression of each cell at each time point was detected by immunohistochemistry and semi quantitative analysis was performed with the software. The expression level of Cirbp increased in 8 h~24 h after the virus, and the level of Cirbp was significantly different. The expression level of Cirbp in MH-S cells was significantly increased after the infection of PR-8 H1N1 A influenza A, and 8 of the infected pigs H1N1 influenza virus. In the subcellular localization, the H1N1 influenza virus was infected with MOI=1 in BHK-21 cells, 2 h, 4 h, 6 h, 8 h after infection, and the results were observed under the laser confocal microscope. The results showed that H1N1 influenza virus infection was 2 h after infection, Cirbp was located in the nucleus and cytoplasm; 4 h Cirbp was after infection. 6 h Cirbp was located in the nucleus and cytoplasm after infection; after infection, 8 h, Cirbp was located mainly in the nucleus. Since Cirbp exists in the nucleus under physiological conditions, this result indicates that cirbp can repeatedly shuttle between the nucleus and cytoplasm under the condition of H1N1 virus infection. The above results show that H1 In the case of N1 influenza virus infection, the expression of cirbp in the cells was up-regulated, and the nuclear shuttle was taken, which laid the foundation for the most use of cirbp in the replication process of influenza virus to reduce the stability of the H1N1 influenza virus mRNA and inhibit the replication of the virus, so as to verify the stability of cirbp against H1N1 virus mRNA, and to synthesize the RNA synthesis. The real-timepcr method was used to detect the half-life of M and NP gene mRNA after cirbp BHK21 cells (cirbp-bhk-21) infected with H1N1 virus (moi=1). The relative half-life was more than 12h, and the effect of 3H, 9h, 15h and 21h on mRNA synthesis of the virus M gene after H1N1 influenza virus infection (moi=1) was analyzed with real-timepcr. The results showed that the knock down cirbp significantly inhibited the synthesis of the virus, and the experimental group was 21.3%, 18.6%, 12.4%, 7.6% of the control group, respectively. And 21h, the inhibitory effect reached very significant (P0.01) level; the effect of 8h knockout cirbp on M and NP gene mRNA, cRNA, vRNA synthesis after H1N1 influenza virus infection (moi=1) was analyzed with real-timepcr. 5.3%, 11.3%; the knock low cirbp extremely significant (P0.01) inhibited the virus NP gene cRNA and vrna1, vrna2 synthesis, the test group was 5.1%, 2.2% of the control group, respectively, 2.6%. further used indirect immunofluorescence technique to analyze the effect of H1N1 (moi=1) 3H and 6h cirbp on the synthesis of egg white. The TCID50 titer of H1N1 virus was finally measured on BHK-21 and cirbp-bhk-21 cells. The test results showed that the TCID50 titer of H1N1 was significantly higher than the TCID50 titer of normal BHK-21 cells after the knock low cirbp, and the test group was 57.54 times as high as that of the control group. The results showed that the knock low cirbp reduced the stability of the influenza virus NP and the M gene. It inhibits the synthesis of viral proteins and affects the synthesis of virus cRNA and vRNA, and eventually inhibits the replication of the virus. Analysis of the above results shows that knocking low cirbp by reducing the stability of the virus mRNA inhibits the replication of the virus. It is the first time that cirbp has been proved to affect the replication of the virus by affecting the stability of the virus mRNA and enriching the body factor and flow. The network of virus interacting with each other provides information on the replication mechanism of influenza virus,.3 overexpression cirbp enhances the replication efficiency of H1N1 virus, cirbp increases in virus infection. In order to explore the effect of cirbp overexpression on virus replication, this experiment is in BHK-21 control cells and over expressed cirbp cells (cirbp+bhk-21), respectively. Cells were inoculated with H1N1 virus of 0.001,0.01,2 at the same time, and the total RNA was extracted from 3h, 8h, 16h, 24h after infection, and the absolute expression of h1n1m gene mRNA was detected by fluorescence quantitative PCR. The results showed that when moi=0.001, the absolute expression of MOI was twice as much as that of the control group; When the test group was 0.85,26.95,83.84,47.88 times of the control group, the test group was 4.07,6.46,5.01,3.98 times of the control group respectively. The results showed that the overexpression of cirbp increased the replication efficiency of the H1N1 virus, the lower the MOI, the more the overexpressed cirbp enhanced the replication efficiency of the virus, the more obvious the.4 overexpressed cirbp promoted the nucleation of H1N1 virus vrnp. In order to explore the role of cirbp in the process of H1N1 virus transport, the transshipment cirbp was shuttle between the nucleus and cytoplasm of H1N1 virus infection. The effect of cirbp overexpression on the adhesion, penetration, nuclear transfer and nuclear transfer of the virus was studied by indirect immunofluorescence. In the study of cirbp overexpression, the adhesion and penetration of the virus to the virus was studied. At the time of entry, the infection of moi=50 was inoculated in the experimental group and the control group respectively. The time point of 1h after the virus feeling was 0h, and the 0h was the best time for the adhesion and penetration of the virus. The samples were fixed at this time point, and the indirect immunofluorescence staining was carried out under the laser confocal microscope. The results showed that the cell membrane of the 0h test group and the control group after infection was revealed. There is no obvious difference between the virus particles in the cytoplasm, indicating that the overexpression of cirbp has no obvious effect on the adhesion and penetration of H1N1 virus. The infection amount of vrnp in nuclear transfer and nuclear transfer was moi=1. in 4h, 6h, 8h fixed samples, and the indirect immunofluorescence staining was carried out under the light confocal microscope. The results showed: 4h after infection. A small amount of virus vrnp has come into the nucleus from the cytoplasm, and there is no difference between the test group and the control group. After infection 6h, the virus vrnp still exists in the cytoplasm and nucleus, and there is no difference between the test group and the control group. After infection, the test group of virus vrnp is completely transferred from the nucleus to the cytoplasm, and the control group of the virus vrnp is from the nucleus to the nucleus. Intracellular transport, therefore, the results showed that overexpression of cirbp promoted the nuclear transfer of viral vrnp. The above results showed that overexpression of cirbp promoted the nuclear transfer of viral vrnp, but had no obvious effect on other processes. It provided a clue to the mechanism of.5h1n1 influenza virus infection in cirbp targets for further study of the mechanism of nucleation and transport of influenza virus vrnp. Screening and preliminary verification of protein in order to screen the target protein of Cirbp in H1N1 virus infection, this experiment uses immunoprecipitation (Co-IP) binding mass spectrometry. After the virus infected BHK-21 cell 24h, the target protein of Cirbp binding is screened. The results have precipitated 29 candidate target proteins of Cirbp, of which 27 are the host target eggs. The 2 species are virus target proteins; the Pathway annotation results show that the candidate host target proteins are mainly involved in nucleic acid metabolism and protein translation signal pathway, neuromodulation related signaling pathway, and the first 5 egg white of the candidate target proteins of the signal pathway related to the immune related signaling pathway, which are Hsp90, hnRNP R, D1Pas1, Ddx17, Cttn, mass spectrometry, respectively. The scores were 1122.72381.43230.4186.49185.49. and Hsp90 and Ddx17 were closely related to the replication of influenza virus and the.Hsp90 score was highest and played an important role in the replication process of influenza virus. Therefore, we further demonstrated that Hsp90 and Cirbp were Co located by indirect immunofluorescence, indicating that Hsp90 and Cirbp are at least the same. Further experimental verification was needed in the form of a combination of.Hsp90 and Cirbp directly. In addition, the Western-blot results showed that overexpression Cirbp increased the expression of Hsp90 protein, indicating that Cirbp has the highest score of the NP mass spectrum in the viral target protein of the.2 candidate for Hsp90, which is 108.68. influenza virus NP. Protein plays an important role in the process of replication. It interacts with the virus RNA, other viral proteins and some large molecules of the host cell. It affects the transcription, replication, assembly and transport functions of the virus. Further indirect immunofluorescence is used to verify the co localization of NP and Cirbp, indicating that NP and Cirbp are at least in the form of complex complexes. These results provide clues for further studying the molecular mechanism of Cirbp and H1N1 interactions.
【學(xué)位授予單位】：西南民族大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：S852.65

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