Ankrd17, an ubiquitously expressed ankyrin factor, is essential for the vascular integrity during embryogenesis

Hou, Shin-Chen; Chan, Li-Wei; Chou, Yu-Chi; Su, Ching-Yuan; Chen, Xin; Shih, Yen-Ling; Tsai, Pei-Chun; Shen, C.-K. James; Yan, Yu-Ting

doi:10.1016/j.febslet.2009.07.025

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Volume 583, Issue 17 , Pages 2765-2771, 3 September 2009

Ankrd17, an ubiquitously expressed ankyrin factor, is essential for the vascular integrity during embryogenesis

Edited by Ned Mantei

Shin-Chen Hou
- Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, ROC
- Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, ROC
Li-Wei Chan
- Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, ROC
Yu-Chi Chou
- Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, ROC
Ching-Yuan Su
- Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, ROC
Xin Chen
- Division of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhu Nan Town, Miaoli, Taiwan, ROC
Yen-Ling Shih
- Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC
Pei-Chun Tsai
- Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC
C.-K. James Shen
- Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, ROC
- Corresponding authors. Fax: +886 2 26518055 (C.-K.J. Shen).
Yu-Ting Yan
- Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC
- Corresponding authors. Fax: +886 2 26518055 (C.-K.J. Shen).

Received 5 January 2009; received in revised form 30 June 2009; accepted 9 July 2009. published online 20 July 2009.

Abstract

Ankyrin repeat domain 17 (Ankrd17) encodes an ubiquitously expressed protein with two clusters of ankyrin repeats. We have used gene targeting strategy to ablate the Ankrd17 gene in mouse. The Ankrd17-deficient mice died between embryonic day (E) 10.5 and E11.5 due to cardiovascular defects. Serious hemorrhages were detected and the vascular smooth muscle cells (vSMCs) surrounding the vessels were drastically reduced in the Ankrd17-deficient embryos, suggesting that the vascular maturation was not completed. Interestingly, vSMC differentiation marker genes were up-regulated in the mutant embryos. Our data have demonstrated the indispensability of Ankrd17 functioning for vascular maturation during early development. The Ankrd17-deficient mice also provide a new animal model for the analysis of the regulatory pathways of the differentiation of vSMC precursor cells.

Keywords: Ankyrin factor, Mouse gene targeting, Vascular integrity, SM α-actin gene, Smooth muscle cell