Literature DB >> 21656899

Semaphorin 3A expression in the colon of Hirschsprung disease.

Li-Li Wang1, Yang Fan, Feng-Hua Zhou, Hui Li, Yi Zhang, Jia-Ning Miao, Hui Gu, Tian-Chu Huang, Zheng-Wei Yuan.   

Abstract

BACKGROUND: Hirschsprung disease (HSCR) is a congenital disorder characterized by an absence of intrinsic ganglion cells in the nerve plexuses of the lower colon. The Semaphorin 3A (SEMA3A) gene is involved in the migration of enteric neural precursors (ENPs). To analyze the function of SEMA3A in HSCR, the SEMA3A expression in different colon segments in HSCR was examined.
METHODS: The expression levels of SEMA3A in both ganglionic and aganglionic colon tissues of 32 patients with HSCR and in colon tissue of 5 newborn unaffected individuals were examined by real-time RT-PCR, Western-blot, and immunohistology.
RESULTS: Comparison of SEMA3A expression levels between ganglionic and aganglionic tissues in HSCR revealed upregulation of SEMA3A expression in 43.75% (14/32) of the aganglionic colons. SEMA3A was expressed in the ganglion cells of the myenteric plexus, submucosa, as well as in the longitudinal and circular muscle layer of the normal colon of both unaffected newborns and patients with HSCR. In the aganglionic segment of patients with HSCR, SEMA3A was highly expressed in the circular muscle layer and was also detected in the submucosa and in the longitudinal muscles layer. The fluorescence intensity of SEMA3A in the circular muscle layer in the aganglionic segment was much higher than that in ganglionic segment (p < .001).
CONCLUSION: SEMA3A expression was upregulated in the aganglionic smooth muscle layer of the colon in some patients with HSCR and our data suggest that increased SEMA3A expression may be a risk factor for HSCR pathology in a subset of patients.
Copyright © 2011 Wiley-Liss, Inc.

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Year:  2011        PMID: 21656899     DOI: 10.1002/bdra.20837

Source DB:  PubMed          Journal:  Birth Defects Res A Clin Mol Teratol        ISSN: 1542-0752


  6 in total

1.  Population variation in total genetic risk of Hirschsprung disease from common RET, SEMA3 and NRG1 susceptibility polymorphisms.

Authors:  Ashish Kapoor; Qian Jiang; Sumantra Chatterjee; Prakash Chakraborty; Maria X Sosa; Courtney Berrios; Aravinda Chakravarti
Journal:  Hum Mol Genet       Date:  2015-02-09       Impact factor: 6.150

2.  Testing the Ret and Sema3d genetic interaction in mouse enteric nervous system development.

Authors:  Ashish Kapoor; Dallas R Auer; Dongwon Lee; Sumantra Chatterjee; Aravinda Chakravarti
Journal:  Hum Mol Genet       Date:  2017-05-15       Impact factor: 6.150

Review 3.  Hirschsprung's disease: clinical dysmorphology, genes, micro-RNAs, and future perspectives.

Authors:  Consolato Maria Sergi; Oana Caluseriu; Hunter McColl; David D Eisenstat
Journal:  Pediatr Res       Date:  2016-09-28       Impact factor: 3.756

4.  Mutational spectrum of semaphorin 3A and semaphorin 3D genes in Spanish Hirschsprung patients.

Authors:  Berta Luzón-Toro; Raquel M Fernández; Ana Torroglosa; Juan Carlos de Agustín; Cristina Méndez-Vidal; Dolores Isabel Segura; Guillermo Antiñolo; Salud Borrego
Journal:  PLoS One       Date:  2013-01-23       Impact factor: 3.240

5.  Up-regulated FHL1 expression maybe involved in the prognosis of Hirschsprung's disease.

Authors:  Li-Li Wang; Hui Gu; Yang Fan; Yi Zhang; Di Wu; Jia-Ning Miao; Tian-Chu Huang; Hui Li; Zheng-Wei Yuan
Journal:  Int J Med Sci       Date:  2014-01-20       Impact factor: 3.738

6.  Semaphorin 3A controls enteric neuron connectivity and is inversely associated with synapsin 1 expression in Hirschsprung disease.

Authors:  Jacques Gonzales; Catherine Le Berre-Scoul; Anne Dariel; Paul Bréhéret; Michel Neunlist; Hélène Boudin
Journal:  Sci Rep       Date:  2020-09-15       Impact factor: 4.379

  6 in total

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