JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2014, Vol. 52 ›› Issue (9): 15-19.doi: 10.6040/j.issn.1671-7554.0.2014.018

Previous Articles     Next Articles

Expression and significance of Neuroligin2 in children with hirschsprung’s disease

YANG Hongchao, WANG Jian, ZHANG Wentong, LI Aiwu   

  1. Department of Pediatric Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China
  • Received:2014-01-09 Revised:2014-07-02 Online:2014-09-10 Published:2014-09-10
  • Contact: 李爱武。E-mail:liaiwu2012@126.com E-mail:liaiwu2012@126.com

PDF (PC)

162

Abstract: Objective To investigate the expression of Neuroligin2 in normal and spastic segments of colon in children with hirschsprung's disease (HD), and to explore the correlation of Neuroligin2 with pathogenesis of HD. Methods A total of 42 resected colon specimens of HD cases treated during 2012 to 2013 were enrolled. Normal colonic segments were served as control group, while the transitional and spastic segments as experimental group. Neuroligin2 expression was detected with immunohistochemical staining, Western blotting, and qRT-PCR. Results Western blotting revealed that Neuroligin2 protein in spastic segments (0.012±0.001) was lower than that in transitional segments and normal segments (0.039±0.001 and 0.057±0.002, respectively; P<0.05). qRT-PCR revealed that Neuroligin2 mRNA level was consistent with the protein expression. A large number of Neuroligin2 positive gangliocytes were observed in the control group, while none was observed in spastic segments. Significantly fewer Neuroligin2 positive gangliocytes were found in the transitional segments. Conclusion Neuroligin2 is significantly down-regulated in spastic colon segments, which may be associated with the pathogenesis of HD.

Key words: Neuroligin2 gene, Quantitative real-time polymerase chain reactions, Hirschsprung’s disease

CLC Number: 

  • R726
[1] Bergeron K F, Silversides D W, Pilon N. The developmental genetics of Hirschsprung's disease[J]. Clin Genet, 2013, 83(1): 15-22.
[2] Yamamoto T, Ono K, Hitomi S, et al. Endothelin receptor-mediated responses in trigeminal ganglion neurons[J]. J Dent Res, 2013, 92(4): 335-339.
[3] Fritschy J M, Panzanelli P, Tyagarajan S K. Molecular and functional heterogeneity of GABAergic synapses[J]. Cell Mol Life Sci, 2012, 69(15): 2485-2499.
[4] Comletti D, De Jaco A, Jennings L L. The Arg451 Cys-neuroligin-3 mutation associated with autism reveals a defect in protein processing[J]. J Neurosci, 2004, 24(43): 4889-4893.
[5] Hampton T. Scientists scan genome for autism clues[J]. JAMA, 2007, 297(12): 1303-1304.
[6] Holschneider A M, Meier-Ruge W, Ure B M. Hirschsprung's disease and allied disorders- a review[J]. Eur J Pediatr Surg, 1994, 4(5): 260-266.
[7] Dang R, Torigoe D, Sasaki N, et al. QTL Analysis identifies a modifier locus of aganglionosis in the rat model of hirschsprung disease carrying Ednrb(sl) mutations[J]. PLOS ONE, 2011, 6(11): e27902 doi: 10.1371/journal.pone.0027902.
[8] Sudhof T C. Neuroligins and neurexins link synaptic function to cognitive disease[J]. Nature, 2008, 455(7215): 903-911.
[9] Chih B, Afridi S K, Clark L, et al. Disorder-associated mutations lead to functional inactivation of neuroligins[J]. Hum Mol Genet, 2004, 13(14): 1471-1477.
[10] Poulopoulos A, Aramuni G, Meyer G, et al. Neuroligin 2 drives postsynaptic assembly at perisomatic inhibitory synapses through gephyrin and collybistin[J]. Neuron, 2009, 63(5): 628-642.
[11] Chi B, Engelman H, Scheiffele P. Control of excitatory and inhibitory synapse formation by neuroligins[J]. Science, 2005, 307(5713): 1471-1477.
[12] Graf E R, Kang Y, Hauner A M, et al. Structure function and splice site analysis of the synaptogenic activity of the neurexin-1b LNS domain[J]. Neuro Sci, 2006, 26(16): 4256-4265.
[13] Moore S W. Hirschsprung's disease and the brain[J]. Pediatr Surg In, 2011, 27(4): 347-352.
[14] Krueger D D, Tuffy L P, Papadopoulos T, et al. The role of neurexins and neuroligins in the formation, maturation, and function of vertebrate synapses[J]. Curr Opin Neurobiol, 2012, 22(3): 412-422.
[1] LIU Chao, YAN Dong, LI Xiang, ZHANG Lei, LI Yan. Clinical analysis of laparoscopy assisted small incision of umbilicus in the treatment of Meckels diverticulum in children [J]. Journal of Shandong University (Health Sciences), 2020, 1(9): 40-44.
[2] XU Jialong, SUN Xiaogang, WANG Junfeng, LIU Qian, MA Nan, LI Dianguo, CHEN Weixiu, LI Jinliang, WANG Ruoyi. Comparision of the therapeutic effects of laparoscopic surgery and open surgery on primary bladder diverticula [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2017, 55(7): 95-99.
[3] WANG Junfeng, LIU Qian, SUN Xiaogang, LI Jinliang, XU Jialong, LÜ Qigang, MA Nan, WANG Ruoyi. Evaluation of the therapeutic effect of Rex shunt in the treatment of cavernous transformation of the portal vein in children [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2016, 54(7): 28-32.
[4] WANG Xue, LI Qian, WANG Li, SUN Shuzhen, MA Aihua. CXCL16 gene silencing alleviates injury of mouse podocytes treated with the oxidized low-density lipoprotein [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2016, 54(6): 16-21.
[5] CHEN Shuai, HU Yuanjun, WU Yurui, ZHANG Shisong, WANG Hefeng. Treatment of transumbilical double-port laparoscopic high ligation of hernia sac on pediatric indirect inguinal hernia [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2016, 54(4): 74-77.
[6] WANG Cong, SUN Shuzhen, ZHEN Junhui, LI Qian, XU Yihuai. Role of CXCL16 in mice with adriamycin induced nephropathy and the protective effects of simvastatin [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2015, 53(9): 24-29.
[7] CHEN Shuai1， WANG Kelai1， ZHUANG Yan1， QU Hongyi2. Acetabular morphology in children with developmental dysplasia of the hip by MRI  [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2011, 49(8): 144-.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
Copyright 2018 © Editorial office of Journal of Shandong University (Health Sciences)
Supported by Beijing Magtech Co.Ltd