期刊文献+

细胞黏附分子在先天性巨结肠症中的表达 被引量:2

Expression of CAMs in Hirschsprung disease
原文传递
导出
摘要 目的 观察先天性巨结肠症 (HD)患者细胞黏附分子 (CAMs)在神经节正常肠段和神经节缺如肠段的表达情况。探讨CAM 成纤维细胞生长因子 (FGFR)信号传导在HD致病机制中的作用。方法 应用链酶抗生素蛋白 生物素 过氧化酶复合体法 (SABC) ,检测 16例HD患者中神经节正常和缺如肠段中CAMs的表达。结果 神经节细胞黏附分子 (NCAM )和神经元细胞钙黏素(N cadherin)在神经组织和平滑肌组织中都有表达 ,但在神经节正常肠段 (NG )肠组织中NCAM和N cadherin染色的神经纤维的数量明显多于神经节缺如肠段 (AG)。结论 CAMs在AG肠段的明显减少说明HD患者中CAM FGFR信号传导发生了异常 ,可能是导致肠神经母细胞移行障碍的原因之一。 Objective To investigate the expression of cell adhesion molecule (CAMs) in ganglionic (NG) and aganglionic (AG) segments of Hirschsprung disease (HD) in order to understand the role of CAM-FGFR signaling in the pathogenesis of HD.Methods The SABC immunohistochemical method was used in the experiment to detect the expression of CAMs both in 16 NG and AG segments of HD.Results NCAM and N-cadherin were detected both in nerve tissue and myenteric plexus,but numerous NCAM-positive and N-cadherin-positive fine fibres were present in NG segment,only a few were present in AG segment.Conclusion The markedly decreased expression of CAMs on nerve fibres within the muscle of AG segment suggests that CAM-FGFR signaling is altered in HD,resulting in failure of enteric neuroblast migration.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2004年第2期218-219,共2页 Chinese Journal of Experimental Surgery
关键词 细胞黏附分子 先天性巨结肠症 表达 成纤维细胞生长因子受体 Hirschsprung disease Adhesion molecule Fibroblast growth factors receptors
  • 相关文献

参考文献5

  • 1Kato S,Sekine K.FGF-FGFR signaling in vertebrate organogenesis[].Cellular and Molecular Neurobiology.1999
  • 2Bolande RP.The neurocristopathies;a unifying concept of disease arising in neural crest maldevelopment[].Human Pathology.1973
  • 3Touraine R,Attie-Bitach T,Manceau E,et al.Neurological phenotype in Waardenburg syndrome type 4 correlates with novel SOX10 truncating mutations and expression in developing brain[].The American Journal of Human Genetics.2000
  • 4Jeanne A,Stanislas L.Hirschsprung disease, associated syndromes, and genetics: a review[].Journal of Medical Genetics.2001
  • 5Baynash AG,Hosoda K,Giaid A,et al.Interaction of endothelin-3 with endothelin-B receptor is essential for development of epidermal melanocytes and enteric neurons[].Cell.1994

同被引文献22

  • 1师迎旭,韩艳秋,谢印良,杜华.人诱导性多潜能干细胞系的建立[J].中国组织工程研究,2015,19(6):868-875. 被引量:3
  • 2黄姗,易斌,魏明发.先天性巨结肠内皮素B受体基因的研究[J].中华实验外科杂志,2004,21(12):1565-1565. 被引量:4
  • 3Young HM,Hearn CJ,Newgreen DF.Embryology and development of the enteric nervous system.Gut,2000,26:2-4.
  • 4Walzem RL,Cliford AJ.Fohte deficiency in rats fed diets containing free amino acids or intact poteins.J Nutr,1988,118:1089-1096.
  • 5Gath R,Goessling A,Keller K M,et al.Analysis of the RET,GDNF,EDN3,and EDNRB genes in patients with intestinal neuronal dysplasia and Hirsehsprung disease[J].Gut,2001,48(5):671-675.
  • 6Moore S W.The contribution of associated congenital anomalies in understanding Hirsehsprung’s disease[J].Pediatr Surg Int,2006,22(4):305-315.
  • 7Botstein D,Riseh N.Discovering genotypes underlying human phenotypes:past successes for mendelian disease,future approaches for eomplex disease[J].Nat Genet,2003,33(Suppl):228-237.
  • 8Wu T T,Tsai T W,Chu C T,et al.Low RET mutation frequency and Polymorphism Analysis of the RET and EDNRBgenes in patients with Hirsehsprung disease in Taiwan[J].J Hum Genet,2005,50(4):168-174.
  • 9Sham M H,Lui V C,Fu M,et al.SOX10 is abnormally expressed in aganglionic bowel of Hirsehsprung’s disease infants[J].Gut,2001,49(2):220-226.
  • 10郑桁,陈育民,魏明发,郭志义,赵时宇,李平.肥大细胞在先天性巨结肠症中的分布及其在发病机制中的作用[J].中华胃肠外科杂志,2009,12(5):507-510. 被引量:2

引证文献2

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部