本文關(guān)鍵詞：非基因毒應激對小G蛋白RhoB表達的誘導作用、機制及生物學意義　出處：《第二軍醫(yī)大學》2008年博士論文　論文類型：學位論文

  更多相關(guān)文章： 熱應激 燙傷 缺氧 小G蛋白RhoB 細胞凋亡 p38 MAPK

【摘要】： 應激是機體處于不利環(huán)境和遇到有害刺激時所產(chǎn)生的防御或適應性反應,應激反應發(fā)生在整體和細胞層面,后者也稱為細胞應激。糖皮質(zhì)激素(GC)是體內(nèi)最重要的應激激素,其作用主要是由糖皮質(zhì)激素受體(GR)介導的,應激時GC分泌增多對機體抵抗有害刺激起著極為重要的作用。動物實驗表明,切除雙側(cè)腎上腺后,極小的有害刺激即可導致動物死亡,動物幾乎不能適應任何應激環(huán)境。除了在整體應激中發(fā)揮重要作用(如調(diào)節(jié)代謝、通過允許作用調(diào)節(jié)血壓等)外,已有較多體外實驗顯示,GC能夠保護多種細胞免受應激原所致的損傷和凋亡,受GC/GR調(diào)節(jié)的蛋白在此過程中可能發(fā)揮了重要作用,如已證明一些能被細胞應激誘導、并在細胞應激中發(fā)揮重要作用的應激蛋白,如熱休克蛋白70,也能被GC/GR誘導。小G蛋白RhoB是近年來我們發(fā)現(xiàn)的一個新的GC/GR誘導蛋白。國外近年來的研究表明,RhoB是一個早期反應基因,能夠被多種基因毒應激原(致DNA損傷),如放射線、紫外線、抗癌藥(如5-氟脲嘧啶、順鉑)等誘導或使其激活,并有報道RhoB上調(diào)能夠促進細胞存活。但是非基因毒應激是否也影響RhoB的表達尚不十分清楚�？紤]到RhoB是GR調(diào)節(jié)蛋白,因此推測該蛋白有可能也在非基因毒應激中起作用,本課題從在體和離體兩個水平觀察了熱應激和低氧應激這兩種常見的非基因毒應激對RhoB表達的影響,并進一步研究了熱應激影響RhoB表達的機制以及可能的生物學意義,以期為臨床燒傷、休克等疾病的救治提供新的靶點。 一、熱應激對RhoB表達的誘導作用、機制及生物學意義 (一)熱應激能誘導RhoB的表達 我們首先制備了30%體表面積Ⅲ度燙傷大鼠模型,采用半定量RT-PCR、Real-time PCR及Western blot方法檢測了大鼠肝和肺組織中RhoB mRNA及蛋白的表達情況。結(jié)果發(fā)現(xiàn),大鼠肝,肺組織中RhoB mRNA在燙傷后2h時即上調(diào),4h時達到最大值,分別為對照組的7.5及5.7倍(p＜0.01);RhoB蛋白在燙傷后8h表達量最高。 由于燙傷后體內(nèi)會產(chǎn)生一系列的神經(jīng)內(nèi)分泌反應,而我們以往的實驗也證實GC可以誘導RhoB的表達。為排除體內(nèi)的神經(jīng)內(nèi)分泌因素的影響,確定熱應激本身是否可直接上調(diào)RhoB,我們進一步觀察了熱應激對體外培養(yǎng)的細胞中RhoB表達的影響。與整體實驗采取肝、肺組織作為研究對象相對應,體外實驗中選用了人肝癌HepG2細胞及人肺腺癌A549細胞;同時考慮肝、肺組織中除了實質(zhì)細胞以外,還含有大量的組織巨噬細胞,因此我們還選取了小鼠巨噬細胞系RAW264.7作為研究對象。結(jié)果顯示,熱應激本身能以時間依賴性的方式快速地誘導這三種體外培養(yǎng)細胞中RhoBmRNA和蛋白的表達。上述實驗表明,熱刺激在體內(nèi)和體外都可以上調(diào)RhoB的表達,且這種誘導作用無明顯的組織細胞特異性。 (二)熱應激誘導RhoB表達的機制研究 1.熱應激上調(diào)RhoB mRNA的表達與增強其穩(wěn)定性有關(guān) 我們首先采用放線菌素D(5μg/ml)抑制基因的轉(zhuǎn)錄,觀察了熱應激對RhoBmRNA穩(wěn)定性的影響,以明確熱應激誘導RhoB的表達是發(fā)生在轉(zhuǎn)錄水平,還是在轉(zhuǎn)錄后水平。結(jié)果顯示,在A549細胞中熱應激能使RhoB的半衰期由3.95h增加至7.1h(p＜0.01),在RAW264.7細胞中RhoB的半衰期則由3.98h增至7.6h(p＜0.01),表明熱應激誘導RhoB mRNA的表達主要由RhoB的穩(wěn)定性增加所致。 2.應激激活的p38 MAPK通路參與了熱應激對RhoB的誘導作用。 已證實p38 MAPK信號通路能被包括熱應激在內(nèi)的多種應激原激活,我們因而觀察了p38 MAPK的抑制劑SB203580對熱應激誘導RhoB表達的影響。結(jié)果顯示,于A549細胞的培養(yǎng)液中加入SB203580(10μM)抑制p38 MAPK的激活后,再將細胞進行熱應激處理,RhoB的誘導水平比未經(jīng)SB203580處理的細胞降低了約40%(p＜0.01);在RAW264.7細胞中RhoB的誘導水平降低了約50%(p＜0.01),表明p38 MAPK通路的激活參與了熱應激對RhoB的誘導作用。 (三)熱應激誘導RhoB表達的生物學意義及可能的機制 1.RhoB上調(diào)能夠抑制熱應激誘導的細胞凋亡 應激雖然是防御性反應,但嚴重的應激也可導致細胞凋亡。因此,我們觀察了RhoB表達改變對A549細胞凋亡的影響,以探討熱應激時RhoB上調(diào)的生物學意義。結(jié)果顯示,轉(zhuǎn)染RhoB野生型質(zhì)粒使RhoB過表達后,熱應激引起的細胞凋亡比率由64.1%降至49.5%(p＜0.01),caspase3的活化也明顯降低;而利用RNA干擾的方法減少RhoB表達后,熱應激引起的細胞凋亡比率以及caspase3的活化明顯增加,在RAW264.7細胞中也得到類似的結(jié)果,表明RhoB的上調(diào)能夠抑制熱應激誘導的細胞凋亡。 2.RhoB上調(diào)抑制熱應激誘導細胞凋亡的可能機制 (1)RhoB的上調(diào)能夠增強NF-κB的轉(zhuǎn)錄激活活性 已證明多種應激原可激活轉(zhuǎn)錄因子NF-κB,激活的NF-κB通過調(diào)節(jié)多種基因的轉(zhuǎn)錄,調(diào)節(jié)細胞的生長、分化、免疫和炎癥反應,并在應激反應中發(fā)揮重要作用,如已證明NF-κB在多種細胞中能抵抗多種應激原導致的細胞凋亡。由此,我們進一步觀察了RhoB對NF-κB轉(zhuǎn)錄激活活性的影響。結(jié)果顯示,在A549細胞及RAW264.7細胞中,瞬時轉(zhuǎn)染RhoB-wt質(zhì)粒使RhoB過表達后既可增加NF-κB的基礎轉(zhuǎn)錄激活活性,也可提高熱應激時NF-κB的轉(zhuǎn)錄激活活性;而通過RNA干擾方法抑制RhoB表達后,則可明顯抑制NF-κB的轉(zhuǎn)錄激活活性。提示,RhoB的上調(diào)可能通過增強NF-κB的轉(zhuǎn)錄激活活性發(fā)揮抗凋亡的作用。 (2)熱應激時RhoB的上調(diào)不影響熱休克蛋白70(HSPT0)的表達 HSP70是一種可由熱及其他應激原誘導產(chǎn)生的非特異性細胞保護蛋白,可以增強機體對應激的耐受性,提高細胞生存率。大量研究表明,HSP70對射線(如γ-射線)、TNF-α等多種刺激誘導的細胞凋亡有抑制作用。因此,我們也觀察了RhoB表達的改變對HSP70表達的影響。在對A549細胞和RAW264.7細胞的研究中均發(fā)現(xiàn),無論是RhoB過表達還是通過RNA干擾方法使其表達受抑制,均不影響HSP70的表達,表明HSP70并未參與RhoB對熱應激誘導的細胞凋亡的抑制作用。 二、低氧對RhoB表達的誘導作用 我們首先將SD大鼠放入含8%O_2、92%N_2的混合氣體的低氧艙內(nèi)復制急性缺氧大鼠模型,采用Real-time PCR及Western blot方法檢測了大鼠脾臟和肺組織中RhoBmRNA及蛋白的表達情況。結(jié)果發(fā)現(xiàn),低氧能夠以時間依賴性方式誘導大鼠脾,肺組織中RhoB mRNA和蛋白的表達。繼而,我們又觀察了低氧對體外培養(yǎng)的人肺腺癌A549細胸及小鼠巨噬細胞系RAW264.7細胞中RhoB表達的影響。結(jié)果顯示,低氧本身也能夠以時間依賴性方式上調(diào)兩種細胞中RhoB mRNA和蛋白的表達。以上結(jié)果表明,低氧這個非基因毒應激原也能夠在體內(nèi)和體外實驗中誘導RhoB的表達,且這種誘導作用沒有組織和細胞特異性。 綜上所述,本實驗首次發(fā)現(xiàn),熱應激、低氧這兩個非基因毒應激原均能夠在整體水平和細胞水平誘導RhoB的表達,且這種誘導沒有明顯的組織和細胞的特異性。熱應激誘導RhoB的表達主要與其明顯提高RhoB mRNA的穩(wěn)定性有關(guān),而熱應激時p38 MAPK通路激活參與了RhoB表達的上調(diào)。RhoB的上調(diào)能夠抑制熱應激誘導的細胞凋亡,其機制并不是由HSP70介導的,而可能與RhoB增強NF-κB的轉(zhuǎn)錄激活活性有關(guān)。本課題所得的結(jié)果提示,RhoB具有細胞應激蛋白的特征。
[Abstract]:Stress is the body in the unfavorable environment and have encountered harmful stimuli of defense or adaptive response, stress response and cell in the overall level, the latter is also known as cell stress. Glucocorticoid (GC) is the most important body of stress hormones, which is mainly composed of glucocorticoid receptor (GR) mediated when the stress, the increase of GC secretion of the body against harmful stimuli plays a very important role. The animal experiment showed that adrenalectomy, minimal harmful stimulation can lead to the death of the animal, the animal can hardly adapt to any environmental stress. In addition to play an important role in the overall stress (such as regulating metabolism, by allowing the effect of regulating blood pressure there have been many shows, etc.) in vitro, GC can protect cells from a variety of stressors caused by injury and apoptosis may play an important role in this process by regulating protein GC/GR, such as It have been proved that some cells can be induced by stress, and play an important role in stress protein in cell stress, such as heat shock protein 70, can also be induced by GC/GR. The small G protein RhoB is a new GC/GR in recent years, we found that the induced protein. Recent studies abroad show that RhoB is an early response genes can be a variety of genotoxic stress (original induced DNA damage), such as radiation, ultraviolet radiation, anti-cancer drugs (such as 5- fluorouracil, cisplatin) or induced the activation of RhoB has been reported to increase and promote cell survival. But non genotoxic stress also affect the expression of RhoB is not very clear considering RhoB is GR regulatory protein, therefore speculated that this protein may also play a role in non genotoxic stress, the effects of heat stress and hypoxia of the two kinds of non genotoxic stress on the expression of RhoB in vivo and in vitro from two levels, We further studied the mechanism of heat stress affecting the expression of RhoB and its possible biological significance, in order to provide new targets for the treatment of clinical burn and shock.
The inducement, mechanism and biological significance of heat stress on RhoB expression
(1) heat stress can induce the expression of RhoB
We first made scald rat model of 30% body surface area were prepared by semi quantitative RT-PCR, Real-time PCR and Western blot method to detect the expression of mRNA protein and RhoB in liver and lung tissues of rats. The results showed that rat liver and lung tissue in RhoB mRNA in 2h after scald is raised to the maximum value of 4h, the control group respectively 7.5 and 5.7 times (P < 0.01); RhoB protein in rats after the expression of 8h was highest.
Because the body will produce a series of neuroendocrine responses after scald, and our previous experiments also confirmed the expression of GC can induce RhoB. Effects of neuroendocrine factors from the body, to determine whether the heat stress itself can be directly up-regulated RhoB, we further examined the effects of heat stress on the expression of RhoB in cultured cells. And the whole experiment to the liver, lung tissue as the research object corresponding to human hepatoma HepG2 cells and lung adenocarcinoma A549 cells were selected in vitro; considering the liver and lung tissues in addition to parenchymal cells, but also contains a large number of tissue macrophages, so we also selected a mouse macrophage cell line RAW264.7 as the research object. The results showed that heat stress itself in a time-dependent manner rapidly induced by these three kinds of in vitro expression of RhoBmRNA and protein in the cell. The experimental results show that the heat The expression of RhoB can be up-regulated in both in vivo and in vitro, and there is no obvious tissue cell specificity in this induction.
(two) study on the mechanism of heat stress induced RhoB expression
1. the expression of RhoB mRNA up regulated by heat stress is related to the enhancement of its stability
We used actinomycin D (5 g/ml) transcription suppressor gene, to observe the effect of heat stress on the stability of RhoBmRNA, the expression of RhoB induced by heat stress is clear at the transcription level, or at the post transcriptional level. The results showed that heat stress in A549 cells can make the half-life of RhoB by 3.95h increased to 7.1h (P < 0.01), RhoB in RAW264.7 cells the half-life increases from 3.98h to 7.6h (P < 0.01), showed that the expression of RhoB mRNA induced by heat stress mainly by the stability of RhoB increased.
2. the p38 MAPK pathway activated by stress participates in the induction of heat stress on RhoB.
It has been confirmed that p38 MAPK signaling pathway can be a variety of stress including heat stress, the original activation, we observed the effect of p38 MAPK inhibitor SB203580 induced expression of RhoB in heat stress. The results showed that SB203580 culture solution was added to A549 cells in p38 (10 M) inhibited the activation of MAPK, then the cells were heat stress, induced level of RhoB than the untreated SB203580 cells was reduced by 40% (P < 0.01); the level of RhoB induced in RAW264.7 cells was decreased by about 50% (P < 0.01), p38 showed that the activation of MAPK pathway involved in the induction of heat stress on RhoB.
(three) the biological significance and possible mechanism of heat stress induced RhoB expression
1.RhoB up regulation can inhibit the apoptosis induced by heat stress
Although the stress is a defensive reaction, but severe stress can lead to apoptosis. Therefore, we observed the changes of expression of RhoB effect on apoptosis of A549 cells, the biological significance of RhoB increase of heat stress. The results showed that the transfection of wild-type RhoB plasmid RhoB expression, apoptosis rate induced by heat stress 64.1% to 49.5% (P < 0.01), the activation of Caspase3 also decreased significantly; while using RNA interference to reduce the expression of RhoB after activation of heat stress induced apoptosis and the ratio of Caspase3 increased obviously, similar results are also obtained in RAW264.7 cells showed that the upregulation of RhoB can inhibit apoptosis induced by heat stress.
2.RhoB up-regulated the possible mechanism of inhibiting apoptosis induced by heat stress
(1) up regulation of RhoB can enhance the transcriptional activation activity of NF- kappa B
It has been proved that many stressors can activate NF- transcription factor kappa B, activation of NF- kappa B by transcriptional regulation of many genes that regulate cell growth, differentiation, immune and inflammatory responses, and play an important role in stress responses, such as the NF- kappa B has been shown in many kinds of cells can lead to apoptosis resistance to various stressors. Therefore, we further examined the effect of RhoB on activation of NF- kappa B transcription activity. The results showed that in A549 cells and RAW264.7 cells, transfected RhoB-wt plasmid that overexpression of RhoB can increase the basal transcription NF- kappa B activation activity, can also be the transcription of NF- kappa B activation activity increased during heat stress; and the inhibition of RhoB expression by RNA interference method, transcription is inhibited NF- kappa B activation activity. Suggest that upregulation of RhoB may enhance the transcription of NF- kappa B activation play anti apoptotic effect.
(2) the up-regulation of RhoB did not affect the expression of heat shock protein 70 (HSPT0) during heat stress
HSP70 is a nonspecific cell protect protein by heat and other stressors induce, can enhance tolerance to stress, improve the survival rate of cells. Many studies showed that HSP70 of radiation (such as gamma rays), TNF- alpha and other stimulation induced apoptosis is inhibited. Therefore, we also observed the effect of RhoB expression on the expression of HSP70 were found in a study of A549 cells and RAW264.7 cells, whether overexpression of RhoB or by RNA interference method to make the inhibition of the expression, did not affect the expression of HSP70 showed that the inhibitory effect of HSP70 was not involved in RhoB on apoptosis induced by heat stress.
Two, the induction of hypoxia on the expression of RhoB
We first copy the rat model of acute hypoxic hypoxia cabin SD rats in the mixed gas containing 8%O_2,92%N_2 in the detection of the expression of RhoBmRNA and protein in spleen and lung tissue in rats with Real-time PCR and Western blot method. The results showed that hypoxia can be time dependent manner to induce rat spleen, the expression of RhoB mRNA and protein in the lung tissue. Then, we also observed the effect of hypoxia on the expression of RhoB RAW264.7 cells in cultured human lung adenocarcinoma A549 cells and mouse macrophage cell line. The results showed that the expression of hypoxia itself in a time dependent manner by two kinds of cells in RhoB mRNA and protein. The above results this indicates that hypoxia non genotoxic stress is able to induce RhoB expression in vivo and in vitro, no specific tissues and cells and this effect.
To sum up, for the first time found that the experimental heat stress, hypoxia of the two non genotoxic stress were able to induce RhoB expression in the overall level and cell level, and the inducible no obvious tissue and cell specificity. The expression stability of heat stress induced by RhoB and RhoB mRNA mainly is higher, while the heat the stress of p38 MAPK activation is involved in the upregulation of.RhoB RhoB expression upregulation can inhibit apoptosis induced by heat stress, the mechanism is not mediated by HSP70 and RhoB, which may enhance transcription of NF- kappa B activation activity related to this topic. The results suggest that RhoB has the character of cell stress proteins.

【學位授予單位】：第二軍醫(yī)大學
【學位級別】：博士
【學位授予年份】：2008
【分類號】：R363

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