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Characterization of the roles of connexin 32 in zebrafish vascular development
Author(s) -
Chen YiTing
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.518.6
Subject(s) - angiogenesis , gene knockdown , connexin , biology , morpholino , zebrafish , microbiology and biotechnology , vasculogenesis , gap junction , vascular endothelial growth factor , pathology , cancer research , medicine , genetics , cell culture , gene , progenitor cell , stem cell , vegf receptors , intracellular
The process of vascular development in vertebrates are mainly divided into vasculogenesis and angiogenesis. We previously identified the transcription factors Islet2 ( isl2 ) and Nr2f1b required for the growth of intersegmental vessels (ISV) and caudal vein plexus (CVP) in zebrafish. Microarray analysis showed Connexin 32 is regulated by Isl2/Nr2f1b . Gap junction protein Connexins32 (Cx32) has been shown functions on the blood vessels in injury mice and enhances angiogenesis in cell‐based study, however, there is no reference on the vascular development in animal study. In addition, signal pathways related to cx32 and angiogenesis have not yet been clarified. In this study, we first showed cx32 mRNA is expressed is expressed in developing vessels from 18S to 30 hpf stages, suggesting its roles in vasculature. Knockdown of cx32 by morpholino injection causes vascular defects in ISV and CVP, suggesting the role of cx32 in vascular growth. TUNEL assay showed that vascular defects do not caused by cell death, but likely due to the impairment of endothelial cell proliferation and migration. Consistent with vascular growth defects, loss of cx32 affects the expression of the vascular markers flt4 , mrc1 , flk , stabilin , and ephrinb2 . Furthermore, the overexpression of cx32 does not impair the vascular growth, but rescue the cx32 morphant, suggesting the specificity of morpholino knockdown. Finally, we examine the interaction between cx32 and multiple signals and observed that cx32 is regulated by VEGF signals for ISV growth and BMP signals for CVP patterning. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .