[1]韩鹃,梅峰,乔着意,等.Kit信号通路调控成年小鼠Cajal间质细胞的表型改变[J].第三军医大学学报,2014,36(12):1268-1272.
 Han Juan,Mei Feng,Qiao Zhuoyi,et al.Kit signaling regulates phenotype of interstitial cells of Cajal in adult mice[J].J Third Mil Med Univ,2014,36(12):1268-1272.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
36卷
期数:
2014年第12期
页码:
1268-1272
栏目:
论著
出版日期:
2014-06-30

文章信息/Info

Title:
Kit signaling regulates phenotype of interstitial cells of Cajal in adult mice
作者:
韩鹃梅峰乔着意王梅任慧琴赵庆波刘剑
解放军第324医院急诊科;第三军医大学基础医学部组织与胚胎学教研室,重庆市神经科学研究所
Author(s):
Han Juan Mei Feng Qiao Zhuoyi Wang Mei Ren Huiqin Zhao Qingbo Liu Jian
Department of Emergency, No. 324 Hospital of PLA, Chongqing, 400020, Department of Histology and Embryology, Chongqing Institute of Neurosciences, College of Basic Medical Sciences, Third Military Medical University, Chongqing, 400038, China
关键词:
Cajal间质细胞Kit受体CD44受体干细胞生长因子伊马替尼
Keywords:
interstitial cells of Cajal Kit CD44 stem cell factor imatinib
分类号:
R322.45;R329.24;R329.26
文献标志码:
A
摘要:
目的      通过构建阻断Kit信号的动物模型,观察结肠壁内Cajal间质细胞(interstitial cells of cajal,ICC)数量与网络的变化,探讨调控ICC可塑性的分子机制。      方法      选取45只4周龄健康BALB/c小鼠,体质量18~20 g,酪氨酸激酶特异性抑制剂伊马替尼(imatinib,STI571)灌胃制作动物模型,全层铺片Kit/CD44双重荧光标记观察造模后0、8、16 d及停药8、16 d,各亚型Kit+和CD44+ICC数量和形态的变化,Western blot和实时定量荧光RT-PCR分别从蛋白水平和基因水平检测Kit和CD44量的变化。      结果      ①以近端结肠为例,Imatinib可致结肠壁内Kit+ICC-IM、ICC-MY数量明显减少,用药16 d其数量下降至对照组的50%左右[ICC-MY:(136.17±3.56)vs(66.74±1.47),P<0.05],停药后逐渐恢复正常。②ICC-SM的数量及网络在整个实验过程中没有明显变化。③用药后,Kit蛋白水平和基因水平均明显下降,停药后恢复正常。④用药后各亚型CD44+ICC的数量及网络没有变化,且CD44在蛋白和基因水平均没有变化。      结论      Kit信号通路可调节结肠ICC的可塑性。抑制Kit信号通路后,ICC并没有消失,只是丢失了其Kit表型。
Abstract:
Objective      To investigate the regulatory mechanisms of the plasticity of interstitial cells of Cajal (ICC) in the colon of adult mice with imatinib (STI571)-mediated Kit signaling blockage.       Methods      Forty-five 4-week-old healthy BALB/c mice (18 to 20 g) were divided into 5 groups including a control group (treated with identical doses of normal saline), an 8 d group and a 16 d group after imatinib treatment, and an 8 d group and a 16 d group after imatinib withdrawal. The number and shape changes of Kit+ and CD44+ICC subtypes (ICC-MY, ICC-SM, ICC-IM, and ICC-SS) were revealed by fluorescence immunoassay with anti-Kit antibody and CD44 antibody. The protein and mRNA changes of Kit and CD44 were measured by Western blotting and real time RT-PCR, respectively.       Results      (1) Imatinib treatment led to a gradual reduction of Kit+ ICC-IM and ICC-MY numbers to almost 50% that of the control group in day 16 (ICC-MY: 136.17±3.56 vs 66.74±1.47, P<0.05), and the numbers recovered to normal within 16 d after imatinib withdrawal. (2) The number and network of Kit+ ICC-SM did not change during the whole process. (3) Kit protein and mRNA also decreased in a time-dependent manner and recovered to normal after imatinib withdrawal. (4) The CD44+ ICC did not change significantly in amount during the process, and neither did CD44 protein and mRNA.       Conclusion      Kit signaling regulates ICC plasticity in the colon of adult mice. ICC loses Kit phenotype after blockage of Kit signal pathway, while CD44 expression is not affected.

参考文献/References:

韩鹃, 梅峰, 乔着意, 等. Kit信号通路调控成年小鼠Cajal间质细胞的表型改变[J].第三军医大学学报,2014,36(12):1268-1272.

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更新日期/Last Update: 2014-06-20