TY - JOUR
T1 - Foxl1-deficient mice exhibit aberrant epithelial cell positioning resulting from dysregulated EphB/EphrinB expression in the small intestine
AU - Takano-Maruyama, Masumi
AU - Hase, Koji
AU - Fukamachi, Hiroshi
AU - Kato, Yasutaka
AU - Koseki, Haruhiko
AU - Ohno, Hiroshi
PY - 2006/7/14
Y1 - 2006/7/14
N2 - The winged helix transcription factor Foxl1, expressed in the gut mesenchyme, regulates epithelial cell proliferation and differentiation through the Wnt/β-catenin pathway. To better understand the role of Foxl1 in epithelial morphogenesis, we examined the tissue structure and positioning of epithelial cells in the small intestine of Foxl1-deficient mice. The small intestine of Foxl1-deficient mice manifested aberrant crypt structure, including widely distributed Paneth cells, which coincided with the ectopic and increased expression of EphB2 and EphB3, which are key regulators of epithelial cell positioning. Furthermore, real-time quantitative PCR indicated that a subset of Wnt family genes was highly expressed in the gut mesenchyme of Foxl1-deficient mice compared with that of wild-type mice. Such an increase in Wnt expression was remarkable in the mesenchyme, where the aberrant Paneth cell positioning was observed by in situ hybridization. Foxl1 plays an important role in the maintenance of crypt architecture and epithelial cell positioning through the mesenchymal-epithelial interaction in the small intestine. This interaction is essential for the normal regulation of the Wnt/β-catenin pathway and the subsequent EphB/EphrinB expression.
AB - The winged helix transcription factor Foxl1, expressed in the gut mesenchyme, regulates epithelial cell proliferation and differentiation through the Wnt/β-catenin pathway. To better understand the role of Foxl1 in epithelial morphogenesis, we examined the tissue structure and positioning of epithelial cells in the small intestine of Foxl1-deficient mice. The small intestine of Foxl1-deficient mice manifested aberrant crypt structure, including widely distributed Paneth cells, which coincided with the ectopic and increased expression of EphB2 and EphB3, which are key regulators of epithelial cell positioning. Furthermore, real-time quantitative PCR indicated that a subset of Wnt family genes was highly expressed in the gut mesenchyme of Foxl1-deficient mice compared with that of wild-type mice. Such an increase in Wnt expression was remarkable in the mesenchyme, where the aberrant Paneth cell positioning was observed by in situ hybridization. Foxl1 plays an important role in the maintenance of crypt architecture and epithelial cell positioning through the mesenchymal-epithelial interaction in the small intestine. This interaction is essential for the normal regulation of the Wnt/β-catenin pathway and the subsequent EphB/EphrinB expression.
KW - EphB/EphrinB
KW - Foxl1
KW - Gut
KW - Mesenchymal-epithelial interaction
KW - Wnt
UR - http://www.scopus.com/inward/record.url?scp=33745798204&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33745798204&partnerID=8YFLogxK
U2 - 10.1152/ajpgi.00019.2006
DO - 10.1152/ajpgi.00019.2006
M3 - Article
C2 - 16469829
AN - SCOPUS:33745798204
VL - 291
SP - G163-G170
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
SN - 0363-6135
IS - 1
ER -