Endoderm and mesoderm reciprocal signaling mediated by CXCL12 and CXCR4 regulates the migration of angioblasts and establishes the pancreatic fate

Material type: 文書・図像類

Author: Katsumoto, Keiichiほか

Publisher: The Company of Biologists

Publication date: 2011-05-15

Material Format: Digital

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Note (General)：: type:プレプリントWe have discovered that angioblasts trigger an early inductive event in pancreatic differentiation. This event occurs soon after gastrulati...

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Material Type: 文書・図像類
Title: Endoderm and mesoderm reciprocal signaling mediated by CXCL12 and CXCR4 regulates the migration of angioblasts and establishes the pancreatic fate
Author/Editor: Katsumoto, Keiichi
Kume, Shoen
勝本, 恵一
粂, 昭苑
Author Heading: Katsumoto, Keiichi
Kume, Shoen
勝本, 恵一
粂, 昭苑
Publication, Distribution, etc.: The Company of Biologists
Publication Date: 2011-05-15
Publication Date (W3CDTF): 2011-05-15
Periodical title: Development
No. or year of volume/issue: 138
Volume: 138
Pages: 1947-1955
ISSN (Periodical Title): ISSN : 0950-1991
Text Language Code: eng
Subject Heading: angioblasts
pancreatic differentiation
CXCL12
CXCR4
endoderm
493.47
Target Audience: 一般
Note (General): type:プレプリント
We have discovered that angioblasts trigger an early inductive event in pancreatic differentiation. This event occurs soon after gastrulation, before the formation of blood vessels. Morphological studies revealed that Lmo2-expressing angioblasts reside in proximity to the somitic mesoderm and the gut endoderm from which pancreatic progenitors arise. The chemokine ligand CXCL12 expressed in the gut endoderm functions to attract the angioblasts that express its receptor CXCR4. Angioblasts then signal back to the gut endoderm to induce Pdx1 expression. Gain-of-function and loss-of-function experiments for CXCL12 and CXCR4 were performed to test their function in blood vessel formation and pancreatic differentiation. The ectopic expression of Cxcl12 in the endoderm attracted the angioblasts and induced ectopic Pdx1 expression, resulting in an expanded pancreatic bud and an increased area of insulin-expressing cells. By contrast, in chick embryos treated with beads soaked in AMD3100, an inhibitor of CXCR4, the migration of angioblasts towards the Cxcl12-expressing gut endoderm was arrested, causing a malformation of blood vessels. This led to the generation of a smaller pancreatic bud and a reduced area of insulin-expressing cells. Taken together, these results indicate that the gut endoderm and angioblasts attract each other through reciprocal CXCL12 and CXCR4 signaling. This has a pivotal role in the fate establishment of the pancreatic progenitor cells and in the potentiation of further differentiation into endocrine β-cells.
identifier:http://dev.biologists.org/content/138/10/1947
Format (IMT): application/pdf
Source: https://kumadai.repo.nii.ac.jp/?action=repository_action_common_download&item_id=25524&item_no=1&attribute_id=21&file_no=1
https://kumadai.repo.nii.ac.jp/?action=repository_action_common_download&item_id=25524&item_no=1&attribute_id=21&file_no=1
Access Restrictions: 限定公開
Related Material (DOI): 10.1242/dev.058719
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 熊本大学 : 熊本大学学術リポジトリ