本文選題：經(jīng)典型瞬時感受器電位通道 + 鼻息肉　； 參考：《山東大學(xué)》2013年博士論文

【摘要】：背景 鼻息肉(nasal polyps)是上呼吸道常見疾病,發(fā)病率約為1-2%�，F(xiàn)有的研究發(fā)現(xiàn)鼻息肉的病理生理基礎(chǔ)是重度鼻粘膜組織水腫和慢性炎癥反應(yīng),但其具體機(jī)制至今仍未闡明。 近年來人們發(fā)現(xiàn)細(xì)胞內(nèi)鈣離子在免疫細(xì)胞的活化、增殖、分泌細(xì)胞因子和脫顆粒反應(yīng)等功能中起關(guān)鍵作用,但是其具體調(diào)節(jié)機(jī)制尚未清楚。經(jīng)典型瞬時感受器電位(canonical transient receptor potential, TRPC)通道是果蠅TRP蛋白的哺乳動物同系物。TRPC通道能被IP3激活而產(chǎn)生持續(xù)的鈣內(nèi)流。研究發(fā)現(xiàn)TRPC通道表達(dá)于中性粒細(xì)胞、嗜酸性細(xì)胞和T淋巴細(xì)胞等免疫細(xì)胞,介導(dǎo)免疫細(xì)胞鈣庫操縱性鈣內(nèi)流機(jī)制；而在TRPC6敲基因鼠研究發(fā)現(xiàn)TRPC6的缺失減少了由卵清蛋白激發(fā)的支氣管嗜酸性細(xì)胞數(shù)量。然而TRPC通道在鼻息肉發(fā)生發(fā)展中的的作用及分子機(jī)制尚未深入研究。因此我們提出如下假說：鼻息肉組織中TRPC通道以TRPC5通道表達(dá)增高為主,高表達(dá)的TRPC5通道可能通過激活NF-κB信號轉(zhuǎn)導(dǎo)通路增加嗜酸性粒細(xì)胞浸潤和致炎介質(zhì)的增加,從而在鼻息肉的發(fā)病機(jī)制中發(fā)揮重要作用。 目的 1.觀察鼻息肉組織中經(jīng)典型瞬時型感受器電位通道家族表達(dá)情況； 2.探討經(jīng)典型瞬時型感受器電位通道與鼻息肉嗜酸性粒細(xì)胞浸潤和炎癥反應(yīng)的關(guān)系； 3.探討經(jīng)典型瞬時型感受器電位通道與核轉(zhuǎn)錄因子NF-κB的關(guān)系。 方法 1.鼻息肉患者的入選及標(biāo)本收集：從2011年5月至2011年12月在山東大學(xué)齊魯醫(yī)院耳鼻咽喉科隨機(jī)收集行息肉切除術(shù)患者58例和接受鼻中隔偏曲矯正術(shù)的患者的下鼻甲黏膜35例做正常對照。 2.應(yīng)用實(shí)時熒光定量逆轉(zhuǎn)錄聚合酶鏈反應(yīng)(real time RT-PCR)檢測鼻息肉患者組織中經(jīng)典型瞬時型感受器電位通道m(xù)RNA表達(dá)水平。 3.應(yīng)用病理組織學(xué)和免疫組織化學(xué)技術(shù)檢測鼻息肉組織標(biāo)本中經(jīng)典型瞬時型感受器電位通道的分布和嗜酸性粒細(xì)胞數(shù)量,分析它們之間的關(guān)系。 4.應(yīng)用蛋白免疫印跡(Western Blot)技術(shù)檢測鼻息肉患者組織中經(jīng)典型瞬時型感受器電位通道的蛋白表達(dá)、炎癥因子IL-6和核轉(zhuǎn)錄因子NF-κB表達(dá),分析他們之間的關(guān)系。 結(jié)果 2.1一般臨床資料分析 鼻息肉患者和鼻中隔偏曲患者在年齡和性別方面無顯著性差異(P＞0.05)。 2.2TRPC通道m(xù)RNA和蛋白表達(dá)水平 鼻.息肉組織中TRPC5通道m(xù)RNA表達(dá)水平明顯高于正常對照組(P＜0.05),其他成員表達(dá)變化不明顯。鼻息肉組織TRPC5通道蛋白表達(dá)水平明顯高于對照組(P＜0.05)。 2.3鼻息肉組織中嗜酸性粒細(xì)胞數(shù)量 嗜酸性粒細(xì)胞在HE染色成明顯的嗜伊紅特性,顯示為胞漿內(nèi)呈反光強(qiáng) 的鮮紅色。鼻息肉組織中嗜酸性粒細(xì)胞數(shù)量明顯高于正常鼻甲粘膜(P＜0.01)。 2.4鼻息肉組織IL-6的蛋白表達(dá)水平 鼻息肉患者IL-6蛋白表達(dá)水平明顯高于正常鼻甲粘膜(P＜0.05)。免疫 組化顯示鼻息肉組織中IL-6蛋白陽性產(chǎn)物主要位于細(xì)胞漿和細(xì)胞間質(zhì),陽性 區(qū)域所占面積也明顯增高(P＜0.05)。 2.5鼻息肉組織NF-κB的蛋白表達(dá)水平 Western blot結(jié)果顯示：鼻息肉組織NF-κB的非活性形式p65表達(dá)量與正常鼻甲粘膜無顯著差別(P＞0.05),但是NF-κB的活性形式磷酸化水平的p65(p-p65)表達(dá)量比正常鼻黏膜顯著增高(P＜0.05)。 2.6TRPC通道表達(dá)量與鼻息肉組織中各項(xiàng)指標(biāo)的相關(guān)分析 鼻息肉組織中TRPC5通道表達(dá)水平與嗜酸性粒細(xì)胞數(shù)量、致炎因子IL-6表達(dá)量和NF-κB的活性形式p-p65表達(dá)量成正相關(guān)(P＜0.01)。 結(jié)論 1.鼻息肉組織中TRPC5通道表達(dá)增高； 2.高表達(dá)的TRPC5通道可能通過激活NF-κB信號轉(zhuǎn)導(dǎo)通路增加嗜酸性粒細(xì)胞浸潤和IL-6的表達(dá),從而在鼻息肉的發(fā)病機(jī)制中發(fā)揮重要作用。 背景 鼻息肉(nasal polyps)是多種致病因素共同作用的結(jié)果,其中以變態(tài)反應(yīng)和鼻粘膜的慢性炎癥為其病理生理基礎(chǔ)。許多炎癥因子、化學(xué)介質(zhì)和趨化因子參與,其中IgE作為主要的介質(zhì)在嗜酸性粒細(xì)胞激活和脫顆粒過程中起關(guān)鍵性作用。本研究第一部分研究發(fā)現(xiàn)：鼻息肉組織中TRPC通道以TRPC5通道表達(dá)增高為主,高表達(dá)的TRPC5通道可影響鼻息肉中嗜酸性粒細(xì)胞浸潤和IL-6,也可影響核轉(zhuǎn)錄因子NF-κB的活性,但是對于其在鼻息肉中的作用機(jī)制尚不明確。 有研究發(fā)現(xiàn)鼻息肉患者外周血和鼻息肉組織中IgE水平增高,IgE可以刺激鼻息肉組織產(chǎn)生更多的組胺、白三烯類、PGD2等早期反應(yīng)介質(zhì),導(dǎo)致鼻黏膜水腫和慢性炎癥反應(yīng)。也有研究發(fā)現(xiàn)IgE可以調(diào)節(jié)多種離子通道和細(xì)胞內(nèi)鈣離子濃度。最近TRPC5通道可以穩(wěn)定表達(dá)于HEK293細(xì)胞,為研究TRPC5通道的功能調(diào)控機(jī)制提供了簡單可行的手段。因此我們推測鼻息肉組織中IgE表達(dá)增高,高表達(dá)IgE引起細(xì)胞內(nèi)鈣離子和鈣庫依賴的鈣內(nèi)流,而TRPC5通道是IgE作用的途徑,這為揭示TRPC5通道在鼻息肉中的作用機(jī)制提供了新的理論依據(jù)。 目的 1.研究鼻息肉組織中IgE表達(dá)改變； 2.體外表達(dá)系統(tǒng)中TRPC5通道的功能； 3.探討TRPC5通道是否介導(dǎo)了IgE誘導(dǎo)的細(xì)胞內(nèi)鈣離子調(diào)控。 方法 1.應(yīng)用免疫組織化學(xué)技術(shù)檢測鼻息肉組織標(biāo)本中IgE的表達(dá)情況。 2.穩(wěn)定表達(dá)TRPC5通道的HEK293細(xì)胞系(HEK-TRPC5)的培養(yǎng)：培養(yǎng)條件：DMEM-F12,含10%胎牛血清、50u/ml青霉素和0.5mg/ml鏈霉素,37℃、5%CO2培養(yǎng)箱中。應(yīng)用5μig/ml blasticidin和400μg/ml zeocin篩選。由于其攜帶tetracycline (Te)轉(zhuǎn)錄抑制子,需要添加1μg/ml Te刺激24h來誘導(dǎo)TRPC5通道表達(dá)。 2.鈣離子成像：Ca2+熒光標(biāo)記物Fura-2AM(2uM)37℃孵育1h,固定發(fā)射波長510nm,固定激發(fā)波長在340nm和380nm作雙波長時間掃描,應(yīng)用TILL Vision軟件包采集圖像,進(jìn)行細(xì)胞內(nèi)鈣成像,340nm和380nm時熒光信號比值反映了鈣離子的濃度。記錄不同濃度IgE對穩(wěn)定表達(dá)的TRPC5通道介導(dǎo)的鈣離子內(nèi)流和鈣庫依賴的鈣內(nèi)流的作用。 3.膜片鉗電生理記錄：室溫下,將細(xì)胞培養(yǎng)在蓋玻片上,置于灌流槽內(nèi),應(yīng)用EPC-10膜片鉗放大器和Pulse軟件進(jìn)行刺激脈沖發(fā)放和數(shù)據(jù)記錄；采用全細(xì)胞膜片鉗技術(shù)記錄TRPC5通道的電流強(qiáng)度的改變及IgE10μg/ml對TRPC5通道電流的作用。 結(jié)果 1.鼻息肉中IgE蛋白表達(dá)：與正常粘膜比較,免疫組織化學(xué)染色顯示鼻息肉中IgE蛋白陽性區(qū)域所占面積明顯增高(P＜0.01)。 2TRPC5通道介導(dǎo)的細(xì)胞內(nèi)鈣離子增加：在Te誘導(dǎo)的細(xì)胞(Te+),鈣離子成像顯示TRPC5通道激活劑Gd3+(100μM)可以誘導(dǎo)細(xì)胞內(nèi)鈣離子的增加(P＜0.05),這種反應(yīng)可以被TRPC通道特異阻斷劑T5E3Ab (50μg/ml)抑制。 3TRPC5通道介導(dǎo)的細(xì)胞內(nèi)鈣庫依賴性鈣內(nèi)流：在Te誘導(dǎo)的細(xì)胞(Te+),首先在無鈣外液中用Tg耗竭細(xì)胞內(nèi)鈣庫,然后將液體換成含2mM Ca2+的標(biāo)準(zhǔn)細(xì)胞浴液(復(fù)鈣),可以引起明顯的鈣離子內(nèi)流,這種現(xiàn)象即鈣庫依賴性鈣內(nèi)流。而在Te未誘導(dǎo)的細(xì)胞(Te-),產(chǎn)生小幅度的鈣庫依賴性鈣內(nèi)流,比Te+細(xì)胞明顯低。證明這種鈣庫依賴性鈣內(nèi)流是過表達(dá)的TRPC5通道介導(dǎo)的。 4.IgE對TRPC5通道介導(dǎo)的細(xì)胞內(nèi)鈣離子增加的影響：在Te誘導(dǎo)的細(xì)胞(Te+),鈣離子成像顯示不同濃度IgE(0.1μg/ml、1μg/ml、10μg/ml)可以誘導(dǎo)細(xì)胞內(nèi)鈣離子的增加(P＜0.05),這種反應(yīng)可以被TRPC通道特異阻斷劑T5E3Ab (50μg/ml)抑制(P＜0.05)。 5.IgE對TRPC5通道介導(dǎo)的細(xì)胞內(nèi)鈣庫依賴性鈣內(nèi)流的影響：在Te誘導(dǎo)的細(xì)胞(Te+),Tg耗竭細(xì)胞內(nèi)鈣庫后再復(fù)鈣可以引起明顯的鈣離子內(nèi)流(P＜0.05)。與未加IgE刺激的細(xì)胞比較,10μg/ml IgE預(yù)刺激30min的細(xì)胞,鈣庫依賴性鈣內(nèi)流明顯增加(P＜0.05)。 6.IgE對TRPC5通道電流強(qiáng)度的影響：膜片鉗記錄顯示TRPC5激活劑Gd3+(100μM)可以使穩(wěn)定表達(dá)TRPC5通道的HEK293細(xì)胞產(chǎn)生明顯的TRPC5通道電流(P＜0.05),10μg/ml IgE也可誘導(dǎo)TRPC5通道電流,TRPC5通道特異性阻斷劑T5E3(50μg/ml)可以抑制IgE引起的TRPC5通道電流。 結(jié)論 1.鼻息肉組織中IgE增高； 2.增高的IgE可以激活TRPC5通道產(chǎn)生細(xì)胞內(nèi)鈣離子增加和增強(qiáng)鈣庫依賴性鈣內(nèi)流,這可能是TRPC5通道在鼻息肉發(fā)生和發(fā)展中的作用機(jī)制。
[Abstract]:background
Nasal polyps (nasal polyps) are common diseases of the upper respiratory tract. The incidence of the disease is about 1-2%.. It is found that the pathophysiological basis of nasal polyps is severe nasal mucous tissue edema and chronic inflammatory response, but its specific mechanism has not been elucidated.
In recent years, the intracellular calcium ions have been found to play a key role in the activation, proliferation, secretion of cytokine and degranulation of immune cells, but the specific regulation mechanism is not clear. The canonical transient receptor potential (TRPC) channel is a mammal homologue of the TRP protein of Drosophila melanogaster The.TRPC channel can be activated by IP3 to produce continuous calcium influx. It was found that the TRPC channel was expressed in neutrophils, eosinophils and T lymphocytes, which mediate the mechanism of calcium influx in the immune cell calcium library. In the TRPC6 knockout mouse study, the deletion of TRPC6 decreased the eosinophilia stimulated by ovalbumin. However, the role of TRPC channel in the development of nasal polyps and its molecular mechanism have not yet been studied. Therefore, we suggest that the TRPC channel in nasal polyps is increased mainly by TRPC5 channel, and the highly expressed TRPC5 channel may increase eosinophil infiltration and cause by activating the NF- kappa B signal transduction pathway. Increased inflammatory mediators play an important role in the pathogenesis of nasal polyps.
objective
1. to observe the expression of classical transient receptor potential pathway in nasal polyps.
2. to explore the relationship between the classical transient receptor potential channel and eosinophil infiltration and inflammatory response in nasal polyps.
3. to explore the relationship between classical transient receptor potential channel and nuclear transcription factor NF- kappa B.
Method
1. patients with nasal polyps were selected and collected: from May 2011 to December 2011, 35 cases of inferior turbinate mucosa of 58 patients with random collection of polyposis in the Department of Otolaryngology, Qilu Hospital, Shandong University, and 35 cases of inferior turbinate mucous membrane were used as normal controls.
2. real time RT-PCR (RT time RT-PCR) was used to detect the expression level of the classical transient receptor potential channel in the tissues of patients with nasal polyps.
3. the distribution of potential channels and the number of eosinophils in the specimens of nasal polyps were detected by histopathological and immunohistochemical techniques, and the relationship between them was analyzed.
4. the protein expression of the classical transient receptor potential channel in the tissues of patients with nasal polyps, the expression of inflammatory factor IL-6 and nuclear factor NF- kappa B were detected by Western Blot, and the relationship between them was analyzed.
Result
2.1 general clinical data analysis
There was no significant difference in age and sex between patients with nasal polyps and deviated nasal septum (P > 0.05).
2.2TRPC channel mRNA and protein expression level
The expression level of TRPC5 channel mRNA in nasal polyps was significantly higher than that in the normal control group (P < 0.05), and the expression of other members was not obvious. The expression level of TRPC5 channel protein in nasal polyps was significantly higher than that of the control group (P < 0.05).
The number of eosinophils in 2.3 nasal polyps
Eosinophils stained with HE showed eosinophilic characteristics, showing strong reflection in the cytoplasm.
The number of eosinophils in nasal polyps was significantly higher than that in normal nasal mucosa (P < 0.01).
Protein expression level of IL-6 in 2.4 nasal polyps
The expression level of IL-6 protein in nasal polyps was significantly higher than that in normal nasal mucosa (P < 0.05).
Histochemical analysis showed that the positive products of IL-6 protein in nasal polyps were mainly located in cytoplasm and intercellular substance.
The area is also significantly increased (P < 0.05).
Protein expression level of NF- kappa B in 2.5 nasal polyps
The results of Western blot showed that the non active p65 expression of NF- kappa B in nasal polyps was not significantly different from that of normal turbinate mucosa (P > 0.05), but the expression of p65 (p-p65) in the activity form of NF- kappa B was significantly higher than that of normal nasal mucosa (P < 0.05).
Correlation analysis between 2.6TRPC channel expression and indicators in nasal polyps
The expression of TRPC5 channel in nasal polyps was positively correlated with the number of eosinophils, the expression of inflammatory factor IL-6 and the p-p65 expression of the active form of NF- kappa B (P < 0.01).
conclusion
The expression of TRPC5 channel was increased in 1. nasal polyps.
2. the high expression of TRPC5 channel may increase eosinophil infiltration and IL-6 expression by activating the NF- kappa B signal transduction pathway, thus playing an important role in the pathogenesis of nasal polyps.
background
Nasal polyps (nasal polyps) are the result of a variety of pathogenic factors, in which the allergic reaction and chronic inflammation of the nasal mucosa are the basis of its pathophysiology. Many inflammatory factors, chemical mediators and chemokines are involved, in which IgE plays a key role in the process of eosinophil activation and degranulation. The first part of the study found that the TRPC channel in nasal polyps is mainly expressed in TRPC5 channel, and the high expression of TRPC5 channel can affect eosinophil infiltration and IL-6 in nasal polyps, and also affect the activity of NF- kappa B in the nuclear transcription factor, but the mechanism of its role in nasal polyps is not clear.
It has been found that the levels of IgE in peripheral blood and nasal polyps in patients with nasal polyps are increased. IgE can stimulate nasal polyps to produce more histamine, leukotrienes, PGD2 and other early reaction mediators, leading to nasal edema and chronic inflammatory response. There are also studies found that IgE can regulate multiple ionic channels and intracellular calcium concentrations. Recently, TRPC The 5 channel can be expressed steadily in HEK293 cells and provides a simple and feasible means to study the functional regulation mechanism of the TRPC5 channel. Therefore, we speculate that the expression of IgE in the nasal polyps is higher and the high expression of IgE causes intracellular calcium and calcium library dependent calcium influx, while the TRPC5 channel is the pathway of IgE action, which is to reveal the TRPC5 channel in the nose. The mechanism of action in meat provides a new theoretical basis.
objective
1. the changes of IgE expression in nasal polyps were studied.
2. the function of TRPC5 channel in the in vitro expression system;
3. to explore whether TRPC5 channels mediate IgE induced intracellular calcium regulation.
Method
1. immunohistochemical staining was used to detect the expression of IgE in nasal polyps.
2. the culture of HEK293 cell line (HEK-TRPC5) that expresses the TRPC5 channel steadily: culture conditions: DMEM-F12, 10% fetal bovine serum, 50u/ml penicillin and 0.5mg/ml streptomycin, 37 C, 5%CO2 culture box. 5 micron blasticidin and 400 micron g/ml zeocin are used. As it carries the transcriptional inhibitor, it needs to add 1 mu to stimulate 24. H is used to induce TRPC5 channel expression.
2. calcium ion imaging: Ca2+ fluorescent labeling Fura-2AM (2uM) was incubated for 1h, fixed emission wavelength 510nm, fixed excitation wavelength in 340nm and 380nm for dual wavelength scanning, using TILL Vision software package to collect images, intracellular calcium imaging, 340nm and 380nm when the ratio of fluorescence signals reflected the concentration of calcium ions. Record different concentrations IgE pairs. Stable expression of TRPC5 channels mediates calcium influx and calcium dependent calcium influx.
The electrophysiological record of 3. patch clamp: at room temperature, the cells were cultured on the cover glass, placed in the irrigation slot, using the EPC-10 patch clamp amplifier and the Pulse software to carry out the stimulation pulse and data recording, and the whole cell patch clamp technique was used to record the changes of the current intensity of the TRPC5 channel and the effect of IgE10 mu g/ml on the TRPC5 channel current.
Result
The expression of IgE protein in 1. nasal polyps: compared with normal mucous membrane, immunohistochemical staining showed that the area of IgE protein positive area in nasal polyps was significantly increased (P < 0.01).
2TRPC5 channel mediated intracellular calcium increased: in Te induced cells (Te+), calcium ion imaging showed that TRPC5 channel activator Gd3+ (100 u M) could induce intracellular calcium increase (P < 0.05). This reaction could be inhibited by T5E3Ab (50 mu g/ ml) of TRPC channel specific blocker.
3TRPC5 channel mediated intracellular calcium library dependent calcium influx: in the Te induced cell (Te+), the calcium Library in the Tg exhausted cells in the calcium free fluid, and then the liquid into a standard cell bath containing 2mM Ca2+ (calcium compound), can cause obvious calcium ion inflow. This phenomenon is calcium library dependent calcium influx. In Te uninduced cells (Te-) a small calcium dependent calcium influx was found, which was significantly lower than that of Te+ cells. It is demonstrated that this calcium dependent calcium influx is mediated by an over expressed TRPC5 channel.
The effect of 4.IgE on intracellular calcium ion increase mediated by TRPC5 channel: in Te induced cells (Te+), calcium ion imaging showed that different concentrations of IgE (0.1 mu g/ml, 1 mu g/ml, 10 u g/ml) could induce intracellular calcium increase (P < 0.05). This reaction could be suppressed by TRPC channel specific blocker T5E3Ab (50 micron g/ml).
The effect of 5.IgE on intracellular calcium dependent calcium influx mediated by TRPC5 channel: in Te induced cells (Te+), and in Tg depleted cells after calcium library, re calcium could cause significant calcium influx (P < 0.05). Compared with those without IgE stimulation, 10 mu g/ml IgE prestimulated 30min cells, and calcium library dependent calcium influx increased significantly (P < 0.05).
The effect of 6.IgE on the current intensity of the TRPC5 channel: the patch clamp recording shows that the TRPC5 activator Gd3+ (100 mu M) can produce a clear TRPC5 channel current (P < 0.05) for the HEK293 cells that stably express the TRPC5 channel (P < 0.05), and the 10 mu g/ml IgE can also induce the TRPC5 channel current. Channel current.
conclusion
The IgE increased in 1. nasal polyps.
2. increased IgE can activate TRPC5 channel to produce intracellular calcium increase and increase calcium library dependent calcium influx, which may be the mechanism of TRPC5 channel in the occurrence and development of nasal polyps.

【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2013
【分類號】：R765.25

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