PUBLICATION
Tissue factor pathway inhibitor-2 is critical in zebrafish cardiogenesis
- Authors
- Zhang, Y., Wang, H., Zhang, J., Zheng, F., Jiang, N., Ma, D.
- ID
- ZDB-PUB-141217-21
- Date
- 2015
- Source
- Biochemical and Biophysical Research Communications 456(3): 827-33 (Journal)
- Registered Authors
- Keywords
- Cardiac development, Notch pathway, Tfpi-2, Zebrafish
- MeSH Terms
-
- Animals
- Gene Knockdown Techniques
- Glycoproteins/genetics
- Glycoproteins/physiology*
- Heart/embryology*
- Hematopoiesis/genetics
- Hematopoiesis/physiology
- Metabolic Networks and Pathways
- Organogenesis/genetics
- Organogenesis/physiology*
- Proteinase Inhibitory Proteins, Secretory/genetics
- Proteinase Inhibitory Proteins, Secretory/physiology*
- Sarcomeres/physiology
- Sarcomeres/ultrastructure
- Zebrafish/blood
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish Proteins/genetics
- Zebrafish Proteins/physiology*
- PubMed
- 25498503 Full text @ Biochem. Biophys. Res. Commun.
Citation
Zhang, Y., Wang, H., Zhang, J., Zheng, F., Jiang, N., Ma, D. (2015) Tissue factor pathway inhibitor-2 is critical in zebrafish cardiogenesis. Biochemical and Biophysical Research Communications. 456(3):827-33.
Abstract
Human tissue factor pathway inhibitor-2 (Tfpi-2) is an extracellular matrix-associated Kunitz-type serine proteinase inhibitor and plays an important role in various cellular processes. We have previously shown that zebrafish Tfpi-2 (zTfpi-2) mainly expressed in the brain and heart of zebrafish, and it is involved in the development of central nervous system. Here, we identified zTfpi-2 as an evolutionarily conserved protein essential for zebrafish heart development, as embryos depleted of zTfpi-2 failed to undergo cardiogenesis. Changes of cardiogenic markers, vmhc, amhc and bmp4, confirmed zTfpi-2 knockdown caused cardiac defects, including retrenched ventricle, enlarged atrium and malformation of atrioventricular boundary. The sarcomeric organization was also disrupted by embryonic depletion of zTfpi-2, thus establishing the functional role of zTfpi-2 in cardiac contractility. In addition, hematopoietic defects were detected in the zTfpi-2-deficiency embryos. Importantly, injection of ztfpi-2 mRNA attenuated those cardiac and hematopoietic defects. Taken together, this study demonstrated a critical role of zTfpi-2 during embryonic cardiac development, as well as an important regulator of hematopoiesis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping