The loss of Foxc2 expression in the outflow tract links the interrupted arch in the conditional Foxc2 knockout mouse

Mohammad Khaja Mafij Uddin, Wataru Kimura, Mohammed Badrul Amin, Kasumi Nakamura, Mohammod Johirul Islam, Hiroyuki Yamagishi, Naoyuki Miura

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Congenital heart disease is the most common birth defects, affecting 1 % live births [1]. The cardiovascular system undergoes a series of morphogenetic events to form a heart and an aorta in fetuses. Formation of the heart and aorta requires migration, differentiation, and precise interactions among multiple cells from several embryonic origins [2]. Forkhead box2 (Foxc2) encodes a transcription factor and is expressed in mesodermal tissues, such as the pharyngeal artery, outflow tract endothelial/surrounding mesenchyme, bone, and kidney [3]. Simple knockout of Foxc2 in mouse causes an interrupted aortic arch, ventricular septal defect, cleft palate, and skeletal malformation [4]. The heart is made from primary and secondary heart field progenitors. The primary heart field gives rise to the left ventricle and atria, while the secondary heart field contributes mainly to the right ventricle and outflow tract [5] (Fig. 27.1).

Original languageEnglish
Title of host publicationEtiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology
PublisherSpringer Japan
Pages211-213
Number of pages3
ISBN (Electronic)9784431546283
ISBN (Print)9784431546276
DOIs
Publication statusPublished - 2016 Jan 1

Fingerprint

Arches
Knockout Mice
Heart Ventricles
Aorta
Ventricular Heart Septal Defects
Cardiovascular system
Live Birth
Cleft Palate
Mesoderm
Defects
Cardiovascular System
Heart Atria
Thoracic Aorta
Heart Diseases
Fetus
Transcription Factors
Arteries
Bone
Kidney
Bone and Bones

Keywords

  • Conditional knockout
  • Foxc2
  • Interruption of aortic arch

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Uddin, M. K. M., Kimura, W., Amin, M. B., Nakamura, K., Islam, M. J., Yamagishi, H., & Miura, N. (2016). The loss of Foxc2 expression in the outflow tract links the interrupted arch in the conditional Foxc2 knockout mouse. In Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology (pp. 211-213). Springer Japan. https://doi.org/10.1007/978-4-431-54628-3_27

The loss of Foxc2 expression in the outflow tract links the interrupted arch in the conditional Foxc2 knockout mouse. / Uddin, Mohammad Khaja Mafij; Kimura, Wataru; Amin, Mohammed Badrul; Nakamura, Kasumi; Islam, Mohammod Johirul; Yamagishi, Hiroyuki; Miura, Naoyuki.

Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology. Springer Japan, 2016. p. 211-213.

Research output: Chapter in Book/Report/Conference proceedingChapter

Uddin, MKM, Kimura, W, Amin, MB, Nakamura, K, Islam, MJ, Yamagishi, H & Miura, N 2016, The loss of Foxc2 expression in the outflow tract links the interrupted arch in the conditional Foxc2 knockout mouse. in Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology. Springer Japan, pp. 211-213. https://doi.org/10.1007/978-4-431-54628-3_27
Uddin MKM, Kimura W, Amin MB, Nakamura K, Islam MJ, Yamagishi H et al. The loss of Foxc2 expression in the outflow tract links the interrupted arch in the conditional Foxc2 knockout mouse. In Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology. Springer Japan. 2016. p. 211-213 https://doi.org/10.1007/978-4-431-54628-3_27
Uddin, Mohammad Khaja Mafij ; Kimura, Wataru ; Amin, Mohammed Badrul ; Nakamura, Kasumi ; Islam, Mohammod Johirul ; Yamagishi, Hiroyuki ; Miura, Naoyuki. / The loss of Foxc2 expression in the outflow tract links the interrupted arch in the conditional Foxc2 knockout mouse. Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology. Springer Japan, 2016. pp. 211-213
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