Downregulation of Micall2a Gene Expression Inhibited Vascular Development in Zebrafish
10.12300/j.issn.1674-5817.2022.166
- VernacularTitle:Micall2a基因表达下调抑制斑马鱼血管发育
- Author:
Jinxian YANG
1
;
Shujuan WANG
1
;
Jinyun ZHAI
1
;
Shunxing ZHU
1
Author Information
1. Xinglin College of Nantong University, Nantong 226001, China
- Publication Type:Journal Article
- Keywords:
Micall2a gene;
In situ hybridization;
Vascular development;
Embryonic development;
Zebrafish;
Vascular dependent diseases
- From:
Laboratory Animal and Comparative Medicine
2023;43(3):282-287
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the expression pattern of Micall2a gene during the early development of zebrafish embryos and the effect of this gene on zebrafish vascular development.MethodsWhole embryo in situ hybridization was used to detect Micall2a expression levels at different stages of early embryo development of Tg (fli:GFP) transgenic (labeled with green fluorescent protein) and wild type zebrafish (AB). Micall2a gene expression was downregulated by microinjection of a morpholine antisense oligonucleotide, and real-time fluorescent quantitative PCR was used to detect mRNA expression of the gene at different developmental stages of zebrafish embryos. Laser confocal microscopy was used to observe and analyze vascular phenotypic changes in zebrafish after the downregulation of Micall2a. ResultsMicall2a was expressed in the brain, heart, and vascular system of zebrafish embryos at the 24th, 36th, and 48th hours post fertilization. The mRNA level of Micall2a increased after microinjection of morpholine antisense oligonucleotides, inhibiting vascular development in zebrafish embryos, resulting in internode angiogenesis defects in zebrafish. ConclusionDownregulation of Micall2a expression inhibits the development of blood vessels in zebrafish.
