スエヨシ　リヨウ   SUEYOSHI Riyou   末吉　亮    所属   医学部 医学科（東京女子医科大学病院）    職種   講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Decreased expression of β1 integrin in enteric neural crest cells of the endothelin receptor B null mouse model.
掲載誌名	正式名：Pediatric surgery international 略　 称：Pediatr Surg Int ISSNコード：14379813/01790358
掲載区分	国外
巻・号・頁	36(1),pp.43-48
著者・共著者	Nakazawa-Tanaka Nana, Miyahara Katsumi, Fujiwara Naho, Ochi Takanori, Sueyoshi Ryo, Nojiri Shuko, Akazawa Chihiro, Urao Masahiko, Yamataka Atsuyuki
発行年月	2020/01
概要	BACKGROUND:Interactions between enteric neural crest-derived cells (ENCC) and the surrounding intestinal microenvironment, such as the extracellular matrix (ECM), are critical for regulating enteric nervous system (ENS) development. Integrins are the major receptors for ECM molecules, such as laminin, which have been reported to be involved in the pathogenesis of Hirschsprung's disease. In this study, we examined the expression of β1 integrin in the endothelin receptor B (Ednrb) knock out (KO) mouse gut, which presents with an aganglionic colon.METHODS:A Sox10-Venus-positive Ednrb KO mouse, where ENCC is labeled with fluorescent protein, 'Venus', was created. Sox10-Venus-positive Ednrb wild type (WT) were used as controls. Small intestine, proximal colon and distal colon were dissected on E13.5 and E15.5 and β1 integrin expression of the gut tissue was examined by immunohistochemistry and real time RT-PCR. The cells of the gut dissected on E11.5 were isolated and cultured for 2 days. Venus-positive ENCC were immunostained with β1 integrin and Tuj-1, which is a marker for neurons.RESULTS:The expression of β1 integrin was not significantly different between KO and WT in all parts of the gut examined. However, the β1 integrin expression in the isolated ENCC was significantly decreased in KO compared to WT. The average threshold area was 42.98 ± 17.47% in KO and 73.53 ± 13.77 in WT (p < 0.001).CONCLUSIONS:We demonstrated that β1 integrin expression was specifically decreased in ENCC in Ednrb KO mice. Our results suggest that impaired interaction between integrin and its ligands may disturb normal ENS development, resulting in an aganglionic colon.
DOI	10.1007/s00383-019-04578-y
PMID	31576467