title: Semaphorin 3A expression following intestinal ischemia/reperfusion injury in Sox10-Venus mice.
abstract: OBJECTIVE
  Semaphorin 3A (Sema3A) is a protein secreted during development of the nervous system that plays an important role in neuronal pathophysiology. However, there is no known correlation between Sema3A and intestinal ischemia/reperfusion (I/R) injury. We assessed Sema3A expression and distribution in relation to enteric nervous system (ENS) damage seen after intestinal I/R injury in Sox10-Venus mice.
  
  
  METHODS
  Intestinal I/R injury was induced by vascular occlusion for 3 h. Ileal specimens were harvested 0, 3, 12, 24, 48, and 96 h after reperfusion. Stereoscopic microscopy and fluorescence microscopy were used to assess sox10-Venus+cells and PGP9.5+cells.
  
  
  RESULTS
  By 3 h after reperfusion, Sema3A expression had increased to a maximum and Sox10-Venus+cells had faded to a minimum in harvested ileal segments. Both differences were statistically significant. By 96 h after reperfusion, both Sema3A and Sox10-Venus+cell fluorescence had reverted to original levels. Hematoxylin and eosin staining identified histologic damage mimicking Sema3A expression, while PGP9.5+cell response was minimal.
  
  
  CONCLUSIONS
  We are the first to demonstrate a correlation between Sema3A expression and ENS damage following intestinal I/R in Sox10-Venus mice.
authors.affiliation: Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Takeda
authors.affiliation: Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
authors.forename: Katsumi
authors.initials: K
authors.lastname: Miyahara
authors.affiliation: Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. manabu-o@juntendo.ac.jp.
authors.forename: Manabu
authors.initials: M
authors.lastname: Okawada
authors.affiliation: Department of Biochemistry and Biophysics, Graduate School of Health Care Sciences Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Chihiro
authors.initials: C
authors.lastname: Akazawa
authors.affiliation: Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
authors.forename: Geoffrey J
authors.initials: GJ
authors.lastname: Lane
authors.affiliation: Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
authors.forename: Atsuyuki
authors.initials: A
authors.lastname: Yamataka
mesh_terms: D000818:Animals; D017615:Enteric Nervous System / Q000378:metabolism / Q000503:physiopathology; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008856:Microscopy, Fluorescence; D015427:Reperfusion Injury / Q000235:genetics* / Q000378:metabolism*; D055757:SOXE Transcription Factors; D040121:Semaphorin-3A / Q000235:genetics* / Q000378:metabolism*
chemical_list: D055757:SOXE Transcription Factors; D040121:Semaphorin-3A; C527924:Sox10 protein, mouse
keywords: Ischemia/reperfusion injury; Semaphorin 3A; Sox10-Venus/C57BL GFP; Transgenic mice