末吉　亮    Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine    Position   Assistant Professor
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	Distraction-induced intestinal growth: the role of mechanotransduction mechanisms in a mouse model of short bowel syndrome.
Journal	Formal name：Tissue engineering. Part A Abbreviation：Tissue Eng Part A ISSN code：1937335X/19373341
Domestic / Foregin	Foregin
Volume, Issue, Page	20(3-4),pp.830-841
Author and coauthor	Sueyoshi Ryo†, Woods Ignatoski Kathleen M, Okawada Manabu, Teitelbaum Daniel H
Authorship	Lead author
Publication date	2014/02
Summary	Novel strategies are needed to address the problem of patients with short bowel syndrome. We previously demonstrated a three-fold lengthening of pig bowel after 2 weeks of applied distractive forces, but we have not elucidated the mechanisms facilitating this growth. We used a mouse model of distraction-induced enterogenesis. High molecular weight polyethylene glycol (PEG) osmotically stretched an isolated small bowel segment (PEG-stretch). Significant increases in villus height and crypt depth and in intestinal epithelial cell length and numbers suggested epithelial remodeling in addition to proliferation during enterogenesis. LC-MS/MS analysis showed a two-fold upregulation of α-actinin-1 and -4. We also demonstrated that p-focal adhesion kinase (FAK), FAK, α-actinin, and Rac1 were significantly upregulated and that F-actin was relocalized in PEG-stretch versus controls. Blockade of the phosphotidyl inositol 3' kinase pathway failed to influence the increase in proliferation or decline in apoptosis after stretch, suggesting alternative signaling pathways are used, including MEK and P38MAPK, which were both upregulated during enterogenesis. Our data suggests that several known mechanotransduction pathways drive distraction-induced enterogenesis.
DOI	10.1089/ten.TEA.2013.0383
PMID	24070252