本文選題：Connexin43(Cx43) + 嚴(yán)重膿毒癥��； 參考：《第三軍醫(yī)大學(xué)》2015年博士論文

【摘要】：休克為戰(zhàn)創(chuàng)傷最常見的并發(fā)癥,其發(fā)生率和死亡率都很高。嚴(yán)重創(chuàng)傷/休克病人廣泛存在血管功能下降,主要包括兩個(gè)方面:一是休克后血管反應(yīng)性下降,即是全身血管對(duì)內(nèi)源性和外源性血管舒縮物質(zhì)反應(yīng)性降低或是不反應(yīng)。這種血管的低反應(yīng)性嚴(yán)重影響休克的發(fā)生發(fā)展及治療,是導(dǎo)致休克晚期血壓難以回升和致死的主要原因之一。二是休克后血管屏障功能下降,即血管滲漏,也叫血管通透性升高,特別是創(chuàng)傷失血休克繼發(fā)的嚴(yán)重膿毒癥、膿毒性休克。血管滲漏可使血管內(nèi)液體外滲,導(dǎo)致組織水腫和有效循環(huán)量的進(jìn)一步下降,影響組織和器官功能,并最終發(fā)展為多器官功能障礙(MODS),其死亡率高達(dá)40-70%。目前研究證實(shí)血管低反應(yīng)性的發(fā)生機(jī)制主要有:血管平滑肌細(xì)胞膜受體失敏機(jī)制、膜超極化及我們實(shí)驗(yàn)室提出的鈣失敏學(xué)說。血管滲漏的機(jī)制主要包括兩種途徑:跨內(nèi)皮細(xì)胞途徑和內(nèi)皮細(xì)胞旁途徑。這兩種途徑在休克血管滲漏中發(fā)揮著主要作用,血管內(nèi)皮生長因子(VEGF),凝血酶(thrombin),TNF-α等多種細(xì)胞因子主要也是通過這兩條通路來影響血管的屏障功能�？p隙連接是一種細(xì)胞間的重要結(jié)構(gòu),在血管中呈現(xiàn)高表達(dá),可介導(dǎo)細(xì)胞間多種電化學(xué)信號(hào)的傳導(dǎo),參與多種血管功能的調(diào)控。Cx43是細(xì)胞間縫隙連接的主要構(gòu)成蛋白,研究發(fā)現(xiàn)Cx43在多種血管疾病中發(fā)揮重要的作用,如:動(dòng)脈粥樣硬化,高血壓等。我們前期研究發(fā)現(xiàn)Cx43參與休克后血管反應(yīng)性的調(diào)控,但其機(jī)制不清。最近有研究顯示在酸吸入所導(dǎo)致的急性肺損傷中,Cx43的表達(dá)在肺血管的通透性變化中發(fā)揮重要作用,那么縫隙連接蛋白Cx43是否會(huì)參與在休克后血管滲漏的調(diào)節(jié),機(jī)制如何?目前尚不清楚。研究已證實(shí)Rho激酶信號(hào)通路和PKC信號(hào)通路在調(diào)節(jié)細(xì)胞骨架、引起細(xì)胞收縮和細(xì)胞遷移等方面發(fā)揮關(guān)鍵的作用。我們前期的研究證實(shí)Rho激酶通路和PKC信號(hào)通路在休克后血管低反應(yīng)性的調(diào)節(jié)中發(fā)揮重要的作用。另外也有研究發(fā)現(xiàn)在血管滲漏方面,Rho激酶通路也起著關(guān)鍵的作用,如Rho A/Rock通路介導(dǎo)了凝血酶引起的血管內(nèi)皮通透性的增加。研究證實(shí)骨橋蛋白可作為一種信號(hào)分子參與與血管相關(guān)的多種病理生理變化的調(diào)節(jié):如細(xì)胞粘附,血管生成和細(xì)胞遷移。例如OPN通過改變內(nèi)皮屏障功能介導(dǎo)了由VEGF誘導(dǎo)的細(xì)胞遷移。此外,OPN可激活FAK和ERK信號(hào)通路,而這些信號(hào)通路可導(dǎo)致細(xì)胞的剛度變化和細(xì)胞骨架重排。這些生理和病理事件都提示OPN可能與血管內(nèi)皮屏障功能有密切的關(guān)系,但具體的機(jī)制不清楚。那么Rho激酶通路和OPN是否參與休克后Cx43對(duì)血管滲漏和血管反應(yīng)性的調(diào)節(jié)呢,尚不清楚。據(jù)此,我們首先利用嚴(yán)重膿毒癥大鼠模型和體外LPS刺激肺靜脈血管內(nèi)皮細(xì)胞,研究了Cx43在嚴(yán)重膿毒癥血管滲漏中的作用及其與Rho激酶,PKC和OPN的關(guān)系;第二,利用大鼠出血性休克模型,以及缺血缺氧處理的血管環(huán)和血管平滑肌細(xì)胞研究了Cx43在休克血管反應(yīng)性調(diào)節(jié)中的作用及其與Rho激酶和PKC的關(guān)系。研究內(nèi)容與方法:第一部分Cx43在調(diào)節(jié)嚴(yán)重膿毒癥大鼠血管滲漏中的作用及機(jī)制。1.初步探討Cx43在嚴(yán)重膿毒癥血管滲漏中的作用:利用嚴(yán)重膿毒癥大鼠及LPS刺激的肺靜脈血管內(nèi)皮細(xì)胞(VEC),觀察血管滲漏情況和血管Cx43蛋白表達(dá)變化;利用慢病毒轉(zhuǎn)染肺靜脈血管內(nèi)皮細(xì)胞,改變Cx43的表達(dá),測(cè)定了單層VECs的TER和對(duì)熒光白蛋白(FITC-BSA)透過率的變化。2.Rho激酶在Cx43調(diào)節(jié)血管滲漏中的作用及機(jī)制研究:利用Cx43高表達(dá)和正常的肺靜脈血管內(nèi)皮細(xì)胞,觀察Rho激酶抑制劑對(duì)Cx43調(diào)節(jié)休克血管滲漏的影響及Cx43對(duì)Rho激酶表達(dá)的影響。3.OPN/緊密連接蛋白在Cx43調(diào)節(jié)休克血管滲漏中的作用及機(jī)制研究:利用嚴(yán)重膿毒癥大鼠和LPS刺激的肺靜脈血管內(nèi)皮細(xì)胞,測(cè)定OPN,zo-1,claudin-5表達(dá)變化及血管滲漏的變化,及OPN的RNA干擾對(duì)血管滲漏及zo-1和claudin-5表達(dá)的影響;及利用Cx43轉(zhuǎn)染的肺靜脈血管內(nèi)皮細(xì)胞,觀察Cx43對(duì)OPN表達(dá)的影響及Cx43對(duì)OPN上游轉(zhuǎn)錄因子表達(dá)的影響。第二部分Cx43在調(diào)節(jié)失血性休克大鼠血管低反應(yīng)性中的作用及機(jī)制。1.Cx43在PDGF調(diào)節(jié)血管反應(yīng)性中的作用及與PKC和Rho激酶的關(guān)系:利用失血性休克大鼠及缺氧血管環(huán),觀察MEGJ阻斷劑和Cx43AODN對(duì)休克血管鈣敏感性和反應(yīng)性的影響;利用血管平滑肌細(xì)胞,觀察了Rho激酶和PKC的抑制劑在PDGF調(diào)節(jié)血管反應(yīng)性中的作用,及Cx43AODN在PDGF調(diào)節(jié)Rho激酶和PKC活性中的作用。2.Cx43在BK調(diào)節(jié)血管反應(yīng)性中的作用及機(jī)制:利用失血性休克大鼠缺氧處理的血管環(huán),觀察MEGJ阻斷劑18α-GA對(duì)血管反應(yīng)性的影響,及Rho激酶和PKC抑制劑在Cx43介導(dǎo)BK調(diào)節(jié)休克血管反應(yīng)性中的作用及機(jī)制。實(shí)驗(yàn)結(jié)果第一部分Cx43對(duì)嚴(yán)重膿毒癥血管滲漏的調(diào)節(jié)作用及機(jī)制(一)Cx43在嚴(yán)重膿毒癥血管滲漏中的作用Cx43參與了嚴(yán)重膿毒癥血管血管滲漏的發(fā)生,Cx43表達(dá)變化與通透性變化呈正相關(guān),改變Cx43的表達(dá)可顯著調(diào)節(jié)血管滲漏。提示Cx43在嚴(yán)重膿毒癥血管滲漏中發(fā)揮重要的作用。(二)Rho激酶-MLC20在Cx43調(diào)節(jié)血管滲漏中的作用及機(jī)制研究LPS刺激和Cx43高表達(dá)可顯著升高白蛋白的透過率和降低TER值,改變內(nèi)皮細(xì)胞應(yīng)激纖維的形態(tài),使細(xì)胞呈現(xiàn)向中心收縮。Rho激酶抑制劑Y-27632可減輕透過率的升高和TER值的降低及抑制細(xì)胞向心收縮。LPS刺激和Cx43高表達(dá)可顯著性升高Rho激酶的表達(dá),Cx43RNAi可降低了Rho激酶的表達(dá)。LPS刺激和Cx43高表達(dá)可顯著升高的MLC20的磷酸化水平,Rho激酶抑制劑可抑制MLC20磷酸化升高。Cx43的高表達(dá)可上調(diào)Rho激酶蛋白表達(dá)水平。提示Rho激酶-MLC20通路參與了Cx43對(duì)休克血管滲漏的調(diào)節(jié)(三)OPN/緊密連接蛋白在Cx43調(diào)節(jié)血管滲漏中的作用及機(jī)制研究嚴(yán)重膿毒癥大鼠和LPS刺激內(nèi)皮細(xì)胞后,OPN的表達(dá)顯著升高,zo-1和claudin-5的表達(dá)逐漸降低。Cx43高表達(dá)顯著性地降低了zo-1和claudin-5的表達(dá)。Cx43干擾對(duì)zo-1和claudin-5的表達(dá)沒影響,但能阻止LPS刺激引起的zo-1和claudin-5表達(dá)的下降。OPN干擾可抑制Cx43對(duì)zo-1和claudin-5表達(dá)的下調(diào)。提示,OPN介導(dǎo)了Cx43對(duì)休克血管滲漏的調(diào)節(jié)。Cx43高表達(dá)顯著性地升高了Tcf-4和β-catenin的m RNA水平及上調(diào)了OPN的表達(dá),β-catenin和Tcf-4的RNA干擾可抑制Cx43對(duì)OPN表達(dá)的上調(diào)。證實(shí)了Cx43對(duì)OPN的調(diào)節(jié)是通過轉(zhuǎn)錄因子Tcf-4/β-catenin來實(shí)現(xiàn)的。第二部分Cx43調(diào)節(jié)失血性休克大鼠血管反應(yīng)性及其機(jī)制(一)Cx43介導(dǎo)PDGF調(diào)節(jié)血管反應(yīng)性及與PKC和Rho激酶的關(guān)系PDGF可明顯改善休克后血管的反應(yīng)性,MEGJ的阻斷劑18-GA和Cx43AODN抑制了PDGF對(duì)休克血管反應(yīng)性的改善作用。PKC抑制劑和Rho激酶抑制劑可顯著抑制PDGF對(duì)休克血管反應(yīng)性和鈣敏感性的的改善作用。PDGF可明顯升高缺氧血管中Rho激酶底物MYPT和PKC底物Peptag C1的磷酸化,Cx43AODN明顯抑制了PDGF對(duì)缺氧血管MYPT和Peptag C1的磷酸化改善作用。提示Cx43通過激活PKC和Rho激酶通路,介導(dǎo)了PDGF對(duì)休克血管反應(yīng)性的調(diào)節(jié)。(二)Cx43在BK調(diào)節(jié)血管反應(yīng)性中的作用及機(jī)制BK顯著改善休克后血管的反應(yīng)性,MEGJ阻斷劑18-GA和Cx43AODN顯著性的降低了血管對(duì)BK的反應(yīng)性。BK可磷酸化Cx43的ser368位點(diǎn)及激活Rho激酶,PKC-α和PKC-ε的活性,BK對(duì)休克血管的改善作用可被Rho激酶抑制劑和PKC抑制劑所阻斷。PKC和Rho激酶的激動(dòng)劑可改善休克血管對(duì)BK的反應(yīng)性,這種作用可被Cx43AODN所阻斷。提示,Cx43通過其ser368位點(diǎn)磷酸化和PKC,Rho激酶通路,參與了BK對(duì)休克血管反應(yīng)性的調(diào)節(jié)。結(jié)論1.Cx43參與了休克后血管通透性的調(diào)節(jié),一方面Cx43通過激活Rock1-MLC20通路,使細(xì)胞骨架發(fā)生改變,細(xì)胞出現(xiàn)向心收縮,增大內(nèi)皮細(xì)胞間的縫隙;另一方面,Cx43通過轉(zhuǎn)錄因子Tcf-4/β-catenin通路,上調(diào)OPN的表達(dá)。OPN表達(dá)的上調(diào)會(huì)抑制緊密連接蛋白zo-1和claudin-5的表達(dá),使細(xì)胞間緊密連接減少,增大通透性。2.Cx43參與了PDGF和BK對(duì)休克血管反應(yīng)性的調(diào)節(jié),通過磷酸化Cx43的ser368位點(diǎn),調(diào)節(jié)Rho激酶和PKC的活性,改善休克血管的鈣敏感性和反應(yīng)性。
[Abstract]:Shock is the most common complication of war trauma, its incidence and mortality are very high. Severe trauma / shock patients have extensive vascular function decline, mainly including two aspects: one is the decrease of vascular reactivity after shock, that is, the systemic vascular reactivity to endogenous and exogenous vasomotor substances is reduced or not reacted. Low reactivity seriously affects the development and treatment of shock, which is one of the main causes of the difficult to recover and death of the blood pressure in the late shock. Two is the decrease of blood vessel barrier function after shock, that is, vascular leakage, also called blood vessel permeability, especially the severe sepsis secondary to traumatic hemorrhagic shock, septic shock. Blood vessel leakage can cause blood to cause blood. Fluid extravasation in the tube leads to a further decline in tissue edema and effective circulation, affecting the function of tissue and organs and eventually developing multiple organ dysfunction (MODS). The mortality rate is up to 40-70%.. The mechanism of vascular smooth muscle cell membrane receptor desensitization, membrane hyperpolarization and us The mechanism of calcium desensitization proposed by the laboratory. The mechanism of vascular leakage mainly consists of two pathways: the cross endothelial cell pathway and the endothelial cell side pathway. These two pathways play a major role in shock vascular leakage, and the vascular endothelial growth factor (VEGF), thrombin (thrombin), TNF- alpha and many other cytokines are mainly through these two pathways To affect the barrier function of blood vessels, gap junction is an important structure of intercellular, high expression in the blood vessels, mediating the transmission of multiple electrochemical signals between cells, and participating in the regulation of various vascular functions,.Cx43 is the main constituent of intercellular gap junction, and Cx43 plays an important role in a variety of vascular diseases. For example, atherosclerosis, hypertension, and so on. We have found that Cx43 is involved in the regulation of vascular reactivity after shock, but its mechanism is not clear. Recent studies have shown that in acute lung injury caused by acid inhalation, the expression of Cx43 plays a vital role in the permeability changes of the pulmonary vessels, and whether the gap connexin Cx43 will be involved in the acute lung injury. How is the regulation of vascular leakage after shock? It is not clear now. It has been confirmed that the Rho kinase signaling pathway and the PKC signaling pathway play a key role in regulating the cytoskeleton, causing cell contraction and cell migration. Our previous study confirmed that the Rho kinase pathway and the PKC signaling pathway were in the modulation of vascular hypo response after shock. The Rho kinase pathway also plays a key role in vascular leakage, such as the Rho A/Rock pathway that mediates the increase in vascular endothelial permeability caused by thrombin. The study confirms that osteopontin can be used as a signal molecule to regulate a variety of vascular related pathophysiological changes. Such as cell adhesion, angiogenesis and cell migration. For example, OPN mediated cell migration induced by VEGF by changing the endothelial barrier function. In addition, OPN activates the FAK and ERK signaling pathways, which can lead to cell stiffness changes and cytoskeleton rearrangement. These biological and pathological events suggest that OPN may be associated with vascular endothelial screen. There is a close relationship between the barrier function, but the specific mechanisms are not clear. Then, it is not clear whether the Rho kinase pathway and OPN are involved in the regulation of vascular leakage and vascular reactivity after shock. Accordingly, we first used the rat model of severe sepsis and the external LPS stimulation of the pulmonary venous blood tube endothelial cells to study the blood of Cx43 in severe sepsis. The role of tube leakage and its relationship with Rho kinase, PKC and OPN; second. Using rat hemorrhagic shock model, vascular rings and vascular smooth muscle cells treated by ischemia and anoxia, the role of Cx43 in the regulation of shock vascular reactivity and the relationship with Rho kinase and PKC are studied. The contents and methods of the study are: the first part of Cx43 is regulated strictly. Role and mechanism of vascular leakage in rats with severe sepsis.1. preliminary study of the role of Cx43 in vascular leakage of severe sepsis: the use of severe sepsis rats and LPS stimulated pulmonary venous endothelial cells (VEC) to observe vascular leakage and changes in the expression of vascular Cx43 protein; transfection of the pulmonary vein endothelial cells by lentivirus The expression of Cx43, the TER of single layer VECs and the changes in the transmittance of fluorescent albumin (FITC-BSA), the role and mechanism of.2.Rho kinase in Cx43 regulation of vascular leakage: the effect of Cx43 high expression and normal pulmonary vein endothelial cells, the effect of Rho kinase inhibitor on the regulation of the leakage of shock vessels by Cx43 and Cx43 to Rho kinase Effect and mechanism of.3.OPN/ close connexin in Cx43 regulation of shock vascular leakage: the use of severe sepsis rats and LPS stimulated pulmonary venous endothelial cells to determine the changes of OPN, ZO-1, claudin-5 expression and vascular leakage, and the effect of RNA interference on vascular leakage and expression of ZO-1 and claudin-5 in OPN; and The effects of Cx43 on the expression of OPN and the effect of Cx43 on the expression of transcription factors in the upstream of OPN were observed by Cx43 transfected vascular endothelial cells. Second the role of Cx43 in regulating vascular hyporesponsiveness in rats with hemorrhagic shock and the mechanism of.1.Cx43 in regulating vascular reactivity by PDGF and the relationship with PKC and Rho kinase The effects of MEGJ blockers and Cx43AODN on the calcium sensitivity and reactivity of shock vessels were observed and the effects of Rho kinase and PKC inhibitors on PDGF regulation of vascular reactivity were observed with vascular smooth muscle cells, and the role of Cx43AODN in PDGF regulation of Rho kinase and PKC activity was observed in BK regulating blood. The role and mechanism of tube responsiveness: the effect of MEGJ blocker 18 alpha -GA on vascular reactivity and the role and mechanism of Rho kinase and PKC inhibitor in regulating the reactivity of shock vessels by Cx43 mediated BK in hemorrhagic shock rats, and the regulation of Cx43 on vascular leakage of severe sepsis in the first part of the experiment Role and mechanism (1) the role of Cx43 in severe sepsis vascular leakage Cx43 participates in the occurrence of vascular leakage in severe sepsis. The change of Cx43 expression is positively correlated with the change of permeability, and the expression of Cx43 can significantly regulate vascular leakage. It suggests that Cx43 plays an important role in the leakage of severe sepsis blood tube. (two) Rho kinase -MLC 20 the role and mechanism of Cx43 in regulating vascular leakage, LPS stimulation and high expression of Cx43 can significantly increase the transmittance of albumin and reduce the value of TER, change the morphology of stress fibers in endothelial cells, and make the cells present a central contraction of.Rho kinase inhibitor Y-27632 to reduce the rise of the transmittance and decrease the TER value and inhibit the centripetal contraction of the cells. .LPS stimulation and high expression of Cx43 can significantly increase the expression of Rho kinase, and Cx43RNAi can reduce the phosphorylation level of Rho kinase expression.LPS stimulation and Cx43 high expression of MLC20. Rho kinase inhibitors can inhibit the high expression of.Cx43 phosphorylation and up regulation of the expression of Rho kinase protein. The effect of Cx43 on shock vascular leakage (three) the role and mechanism of OPN/ tight connexin in Cx43 regulation of vascular leakage, the expression of OPN was significantly increased after severe sepsis rats and LPS stimulation of endothelial cells. The expression of ZO-1 and claudin-5 gradually reduced the high expression of.Cx43 and reduced the.Cx43 expression of ZO-1 and claudin-5. Interference has no effect on the expression of ZO-1 and claudin-5, but the decrease of.OPN interference from the expression of ZO-1 and claudin-5 induced by LPS stimulation inhibits the downregulation of ZO-1 and claudin-5 expression by Cx43. It suggests that OPN mediated Cx43 on shock vascular leakage. The expression of RNA in beta -catenin and Tcf-4 inhibits the up regulation of Cx43 on OPN expression. It is confirmed that the regulation of Cx43 to OPN is realized through the transcription factor Tcf-4/ beta -catenin. Second part Cx43 regulates the vascular reactivity and its mechanism in hemorrhagic shock rats. Significantly improved vascular reactivity after shock, MEGJ blockers 18-GA and Cx43AODN inhibit the improvement of PDGF to shock vascular reactivity,.PKC inhibitors and Rho kinase inhibitors can significantly inhibit the improvement of PDGF on shock vascular reactivity and calcium sensitivity..PDGF can significantly increase the MYPT and PKC of Rho kinase substrate in anoxic blood vessels The phosphorylation of substrate Peptag C1, Cx43AODN significantly inhibits the effect of PDGF on the phosphorylation of MYPT and Peptag C1 in anoxic blood vessels. It is suggested that Cx43 is mediated by the activation of PKC and Rho kinase pathway, which mediates the regulation of PDGF on the reactivity of the shock vessels. (two) the role of Cx43 in regulating vascular reactivity and the mechanism of angiogenesis significantly improve the reactivity of blood vessels after shock. MEGJ blockers, 18-GA and Cx43AODN, significantly reduced the ser368 site of the vascular reactive.BK phosphorylated Cx43 and the activation of the Rho kinase, PKC- alpha and PKC- epsilon, and the BK on the shock of the shock vessels could be modified by the inhibitors and inhibitors of the Rho kinase and the activator of the kinase to improve the response to the shock vessel. This effect can be blocked by Cx43AODN. It is suggested that Cx43 participates in the regulation of BK on the vascular reactivity of shock through its phosphorylation of ser368 site and PKC, Rho kinase pathway. Conclusion 1.Cx43 is involved in the regulation of vascular permeability after shock. On the one hand, Cx43 changes the cytoskeleton by activating the Rock1-MLC20 pathway, and the cell appears centripetal contraction. On the other hand, the up regulation of Cx43 through the transcription factor Tcf-4/ beta -catenin pathway up-regulation the expression of.OPN expression of OPN inhibits the expression of tight connexin ZO-1 and claudin-5, reduces the close connection between cells and increases the permeability.2.Cx43 involved in the regulation of PDGF and BK on the reactivity of shock vessels and through phosphorylation Cx4 3 of the ser368 locus regulates the activity of Rho kinase and PKC, and improves calcium sensitivity and responsiveness of shock vessels.

【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2015
【分類號(hào)】：R605.971

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