PUBLICATION

Functional inhibition of UQCRB suppresses angiogenesis in zebrafish

Authors
Cho, Y.S., Jung, H.J., Seok, S.H., Payumo, A.Y., Chen, J.K., and Kwon, H.J.
ID
ZDB-PUB-130313-13
Date
2013
Source
Biochemical and Biophysical Research Communications   433(4): 396-400 (Journal)
Registered Authors
Chen, James K., Jung, Hye
Keywords
none
MeSH Terms
  • Amino Acid Sequence
  • Animals
  • Bridged Bicyclo Compounds/pharmacology
  • Carrier Proteins/genetics
  • Carrier Proteins/metabolism*
  • Dose-Response Relationship, Drug
  • Embryo, Nonmammalian/drug effects
  • Embryo, Nonmammalian/physiology
  • Embryonic Development
  • Gene Expression Regulation, Developmental*
  • Gene Knockdown Techniques
  • Mitochondria/genetics
  • Mitochondria/metabolism
  • Molecular Sequence Data
  • Morpholinos/pharmacology
  • Neovascularization, Physiologic/genetics*
  • Prognosis
  • Vascular Endothelial Growth Factor A/genetics
  • Vascular Endothelial Growth Factor A/metabolism
  • Zebrafish/genetics
  • Zebrafish/physiology*
PubMed
23454382 Full text @ Biochem. Biophys. Res. Commun.
Abstract

As a subunit of mitochondrial complex III, UQCRB plays an important role in complex III stability, electron transport, and cellular oxygen sensing. Herein, we report UQCRB function regarding angiogenesis in vivo with the zebrafish (Danio rerio). UQCRB knockdown inhibited angiogenesis in zebrafish leading to the suppression of VEGF expression. Moreover, the UQCRB-targeting small molecule terpestacin also inhibited angiogenesis and VEGF levels in zebrafish, supporting the role of UQCRB in angiogenesis. Collectively, UQCRB loss of function by either genetic and pharmacological means inhibited angiogenesis, indicating that UQCRB plays a key role in this process and can be a prognostic marker of angiogenesis- and mitochondria-related diseases.

Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping