Masahiro Takeda1, Katsumi Miyahara1, Manabu Okawada2, Chihiro Akazawa3, Geoffrey J Lane1, Atsuyuki Yamataka1. 1. Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. 2. 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. 3. Department of Biochemistry and Biophysics, Graduate School of Health Care Sciences Tokyo Medical and Dental University, Tokyo, Japan.
Abstract
PURPOSE: 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. CONCLUSION: We are the first to demonstrate a correlation between Sema3A expression and ENS damage following intestinal I/R in Sox10-Venus mice.
PURPOSE: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. CONCLUSION: We are the first to demonstrate a correlation between Sema3A expression and ENS damage following intestinal I/R in Sox10-Venus mice.