PUBLICATION
Cyclooxygenase-1 signaling is required for vascular tube formation during development
- Authors
- Cha, Y.I., Kim, S.H., Solnica-Krezel, L., and Dubois, R.N.
- ID
- ZDB-PUB-050607-18
- Date
- 2005
- Source
- Developmental Biology 282(1): 274-283 (Journal)
- Registered Authors
- Kim, Seok-Hyung, Solnica-Krezel, Lilianna
- Keywords
- Cyclooxygenase; Prostaglandin; Prostaglandin E2 (PGE2); Zebrafish; Tubulogenesis; Vascular tube; Angiogenesis; Kidney; Nephric duct; Posterior mesoderm
- MeSH Terms
-
- Animals
- Blood Vessels/drug effects
- Blood Vessels/embryology*
- Cyclooxygenase 1
- Cyclooxygenase Inhibitors/pharmacology*
- Dinoprostone/pharmacology
- Gastrula/drug effects
- Gastrula/physiology*
- In Situ Hybridization
- Mesoderm/metabolism
- Microinjections
- Oligonucleotides, Antisense/genetics
- Prostaglandin-Endoperoxide Synthases/metabolism*
- Signal Transduction/drug effects
- Signal Transduction/physiology*
- Zebrafish/embryology*
- PubMed
- 15936346 Full text @ Dev. Biol.
Citation
Cha, Y.I., Kim, S.H., Solnica-Krezel, L., and Dubois, R.N. (2005) Cyclooxygenase-1 signaling is required for vascular tube formation during development. Developmental Biology. 282(1):274-283.
Abstract
Prostaglandin endoperoxide synthases (PTGS), commonly referred to as cyclooxygenases (COX-1 and COX-2), catalyze the key step in the synthesis of biologically active prostaglandins (PGs), the conversion of arachidonic acid (AA) into prostaglandin H2 (PGH2). Although COX and prostaglandins have been implicated in a wide variety of physiologic processes, an evaluation of the role of prostaglandins in early mammalian development has been difficult due to the maternal contribution of prostaglandins from the uterus: COX null mouse embryos develop normally during embryogenesis. Here, we verify that inhibition of COX-1 results in zebrafish gastrulation arrest and shows that COX-1 expression becomes restricted to the posterior mesoderm during somitogenesis and to posterior mesoderm organs at pharyngula stage. Inhibition of COX-1 signaling after gastrulation results in defective vascular tube formation and shortened intersomitic vessels in the posterior body region. These defects are rescued completely by PGE(2) treatment or, to a lesser extent, by PGF(2alpha), but not by other prostaglandins, such as PGI(2), TxB(2), or PGD(2). Functional knockdown of COX-1 using antisense morpholino oligonucleotide translation interference also results in posterior vessel defect in addition to enlarged posterior nephric duct, phenocopying the defects caused by inhibition of COX-1 activity. Together, we provide the first evidence that COX-1 signaling is required for development of posterior mesoderm organs, specifically in the vascular tube formation and posterior nephric duct development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping