Document Detail


Chronic reduction in cardiac output induces hypoxic signaling in larval zebrafish even at a time when convective oxygen transport is not required.
MedLine Citation:
PMID:  20571107     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the present study, the zebrafish breakdance mutant (bre) was used to assess the role of blood flow in development because it has been previously shown that bre larvae have a chronically reduced cardiac output as a result of ventricular contraction following only every second atrial contraction in addition to an atrial bradycardia. We confirmed a 50% reduction compared with control fish and further showed that blood flow in the caudal part of the dorsal aorta decreased by 80%. Associated with these reductions in blood flow were indications of developmental retardation in bre mutants, specifically delayed hatching, reduced cell proliferation, and a transiently decreased growth rate. Surprisingly, an increased red blood cell concentration and an earlier appearance of trunk vessels in bre larvae indicated some compensation to convective oxygen transport, although in previous studies it has been shown that zebrafish larvae at this stage obtain oxygen by bulk diffusion. In bre animals immunohistochemical analyses showed a significant increase in hypoxia inducible factor 1 (HIF)-α protein expression, comparable with wild-type larvae that were raised under hypoxic conditions. Accordingly, the expression of some hif downstream genes was affected. Furthermore, Affymetrix microarray analyses revealed a large number of genes that were differently expressed comparing control and bre larvae, and the number even increased with proceeding development. The results showed that a chronic reduction in blood flow generated hypoxic molecular signals despite partial compensation by increased oxygen carrying capacity and transiently slowed the overall development of zebrafish bre larvae.
Authors:
Renate Kopp; Thorsten Schwerte; Margit Egg; Adolf Michael Sandbichler; Bernhard Egger; Bernd Pelster
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-22
Journal Detail:
Title:  Physiological genomics     Volume:  42A     ISSN:  1531-2267     ISO Abbreviation:  Physiol. Genomics     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-20     Completed Date:  2010-12-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9815683     Medline TA:  Physiol Genomics     Country:  United States    
Other Details:
Languages:  eng     Pagination:  8-23     Citation Subset:  IM    
Affiliation:
Institute of Zoology and Center for Molecular Biosciences, University of Innsbruck, Innsbruck, Austria. Renate.Kopp@uibk.ac.at
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / genetics,  metabolism*
Biological Transport / genetics,  physiology
CLOCK Proteins / genetics
Cardiac Output / genetics,  physiology*
Cell Cycle Proteins / genetics
Cyclin B1 / genetics
Erythropoietin / genetics
Hypoxia-Inducible Factor 1, alpha Subunit / genetics,  metabolism
Immunohistochemistry
Larva / genetics,  metabolism,  physiology*
Oligonucleotide Array Sequence Analysis
Oxygen / metabolism*
Polymerase Chain Reaction
Vascular Endothelial Growth Factor A / genetics,  metabolism
Zebrafish / genetics,  metabolism,  physiology*
Zebrafish Proteins / genetics
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Cyclin B1; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/Vascular Endothelial Growth Factor A; 0/Zebrafish Proteins; 0/epo protein, zebrafish; 11096-26-7/Erythropoietin; 7782-44-7/Oxygen; EC 2.3.1.48/CLOCK Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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