|  Help  |  About  |  Contact Us

Publication : Impaired expression of myogenic regulatory molecules in the pelvic floor muscles of murine embryos with anorectal malformations.

First Author  Aoi S Year  2005
Journal  J Pediatr Surg Volume  40
Issue  5 Pages  805-9
PubMed ID  15937819 Mgi Jnum  J:101477
Mgi Id  MGI:3604088 Doi  10.1016/j.jpedsurg.2005.01.047
Citation  Aoi S, et al. (2005) Impaired expression of myogenic regulatory molecules in the pelvic floor muscles of murine embryos with anorectal malformations. J Pediatr Surg 40(5):805-9
abstractText  BACKGROUND/PURPOSE: Recent biological studies have elucidated the molecular mechanism of muscle development, in which various regulatory factors (myogenic regulatory factors [MRFs]) play key roles during embryogenesis. To investigate the development of anorectal malformations (ARMs), we studied MRF expressions in myogenic cells in the pelvic floor using murine embryos affected with ARM. METHODS: Anorectal malformation embryos were obtained from the 10.5th embryonal day (E10.5) to the 7.0th postnatal day (D7.0) in a natural mutant strain (Sd/+, RSV/Le). Serial frozen sections were prepared for immunohistochemistry using specific antibodies to M-cadherin, myoD, Myogenin, myosin heavy chain, and alfa-actin molecule. RESULTS: In normal mice, embryonal caudal somites differentiated into myogenic stem cells and migrated to the pelvic floor between E11.0 and E14.0. In the ARM mice, however, caudal somites were irregularly arranged and MRF expressions in myogenic cells were markedly decreased in the dorsocaudal region at E11.5 to E13.0, leading to hypoplastic pelvic floor muscles. CONCLUSIONS: The maldevelopment of pelvic floor muscles in ARM is derived from a deficient supply of myogenic stem cells, with impaired MRF expression. These results suggest that myogenic stem cells, available from bone marrow contents, may be used for postnatal muscle regeneration to reinforce the pelvic floor muscle function in children with ARM.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

4 Bio Entities

Trail: Publication

0 Expression