Effect of lgals3a on embryo development of zebrafish.


Journal

Transgenic research
ISSN: 1573-9368
Titre abrégé: Transgenic Res
Pays: Netherlands
ID NLM: 9209120

Informations de publication

Date de publication:
12 2021
Historique:
received: 02 03 2021
accepted: 27 07 2021
pubmed: 5 8 2021
medline: 3 5 2022
entrez: 4 8 2021
Statut: ppublish

Résumé

Our study was aimed to investigate the effects of lgals3a (Gal-3 encoding gene) on the development of zebrafish embryo and its underlying mechanisms. Morpholino (MO) technology was used to inhibit the expression of zebrafish lgals3a, and the effect of lgals3a gene knockdown on zebrafish embryo development and the number of monocyte macrophages was observed. Effect of lgals3a-e3i3-MO on apoptosis of zebrafish was detected by acridine orange staining. In addition, the mRNA expression levels of Wnt/β-catenin signaling pathway-related genes were detected by RT-qPCR. Compared with control-MO group, the zebrafish embryos injected with lgals3a-e3i3-MO had obvious defects in the head, eyes, and tail, and pericardial edema. Lgals3a-e3i3-MO significantly reduced the number of mononuclear macrophages in zebrafish embryos compared with the control-MO group. The results of acridine orange staining showed that compared with the control-MO group, lgals3a-e3i3-MO promoted cardiomyocyte apoptosis in zebrafish. Furthermore, lgals3a-e3i3-MO significantly up-regulated the expression of dkk1b, wnt9a, lrp5, fzd7a, β-catenin, Gsk-3β, mycn, myca in the Wnt/β-catenin pathway, and decreased the expression of lef1. These results indicate that lgals3a-e3i3-MO inhibits zebrafish embryo development, reduces the number of mononuclear macrophages, activates Wnt/β-catenin signaling pathway and promotes cardiomyocyte apoptosis.

Identifiants

pubmed: 34347236
doi: 10.1007/s11248-021-00276-5
pii: 10.1007/s11248-021-00276-5
doi:

Substances chimiques

Receptors, Cell Surface 0
Wnt Proteins 0
Wnt9a protein, zebrafish 0
Zebrafish Proteins 0
beta Catenin 0
fzd7a protein, zebrafish 0
Glycogen Synthase Kinase 3 beta EC 2.7.11.1
Acridine Orange F30N4O6XVV

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

739-750

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

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Auteurs

Kan Chen (K)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China.

Yuqi Fan (Y)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China.

Jun Gu (J)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China.

Zhihua Han (Z)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China.

Yue Wang (Y)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China.

Lin Gao (L)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China.

Huasu Zeng (H)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China.

Chengyu Mao (C)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China.

Changqian Wang (C)

Department of Cardiology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiaotong University School of Medicine, No. 639 Zhizaoju Road, Shanghai, 200011, China. wang_changqian452@21cn.com.

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