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机构地区:[1]重庆医科大学附属第一医院普外科,400016 [2]第三军医大学大坪医院普外科
出 处:《中华实验外科杂志》2012年第5期888-890,共3页Chinese Journal of Experimental Surgery
基 金:国家自然科学基金资助项目(30300156)
摘 要:目的观察阻断c—Kit信号通路致cajal间质细胞(ICC)缺失,而c.Kit的配体干细胞因子(SCF)能否促进其恢复。方法将新出生的小鼠于腹腔内隔天注射c—Kit抗体(ACK2)100μg,共5次,建立ICC缺失模型,再于第10天腹腔内注射SCF,连续注射5d后观察空肠电节律并通过免疫组织化学法观察Cajal间质细胞的恢复;采用逆转录-聚合酶链反应(RT-PCR)、Westernblot法检测c—Kit基因转录和表达。结果当c—Kit受体被阻断后,空肠ICC几乎缺失且慢波消失;SCF腹腔注射给药可使ICC缺失小鼠空肠慢波频率明显增快(7.83±1.34)次/min(P〈0.01),振幅也有加大(0.044±0.009)mV(P〈0.05);而且肌间神经丛区ICC增多,c—KitmRNA及c—Kit蛋白表达也上调。结论c-Kit与其配体SCF结合所启动的信号途径对ICC的生存及表型维持至关重要。阻断c-Kit的作用后,ICC会出现缺失。通过给予外源性SCF刺激后,缺失的ICC部分恢复,且这种恢复与C—Kit表达水平的上调有关。Objective To observe interstitial cells of Cajal (ICC) loss by blocking the c-Kit re- ceptors and determine whether exogenous stem cell factor (SCF) can promote ICC restoration following the blockade of c-Kit signaling. Methods New-born mice were injected intraperitoneally with antibody of c-Kit ( ACK2 ), 100μg every two days for 5 times. Secondly, the mice with ICC loss were injected intraperitone-ally with SCF for 5 days continuously, and control groups were given saline. The activities of slow waves, the distribution of ICC, and the mRNA and protein expression of c-Kit were determined in the jejunum. Re- suits When c-Kit receptors were blocked, ICC nearly disappeared from the jejunum accompanied by the loss of electrical slow waves. After intraperitoneal injection of SCF, the amplitude of slow waves in ICC loss mice was restored to (0. 044±0. 009) mV ( P 〈 0. 05 ) , whereas the frequency recovered to (7. 83±1.34)/min (P 〈0. 01 ). Furthermore, labeling for c-Kit+ cells in the myenteric plexus was increased, and c-Kit mRNA and protein expression was up-regulated compared to that of controls. Conclusion The cell signaling via c-Kit and its ligand SCF is the critical pathway associated with the control of ICC survival and maintenance. The restoration of ICC number and jejunal electrical rhythm, resulting from blockade of the c-Kit signaling pathway, could be promoted by exogenous SCF administration.
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