Document Detail


Disruption of growth hormone secretion alters Ca2+ current density and expression of Ca2+ channel and insulin-like growth factor genes in rat atria.
MedLine Citation:
PMID:  15486038     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The influence of the growth hormone (GH)-insulin-like growth factor I (IGF-I) axis on expression of low-voltage-activated (LVA) Ca2+ current in atrial tissue was investigated using spontaneous dwarf (SpDwf) rats, a mutant strain that lacks GH. Atrial myocytes from SpDwf rats express LVA and high-voltage-activated (HVA) Ca2+ currents and the Ca2+ channel alpha1-subunit genes CaV1.2, CaV2.3, CaV3.1, and CaV3.2. LVA current density decreases significantly beginning at, or shortly after, birth in normal animals; however, its density is maintained in SpDwf rats at 1 pA/pF for > or =12 wk after birth. The abundance of mRNAs encoding CaV2.3 and CaV3.2 declines with advancing age in normal atrial development, yet expression of CaV2.3 mRNA remains significantly elevated in older SpDwf animals. Quantitation of local transcript levels for mRNAs encoding IGF-I and IGF-I receptor (IGF-IR) also reveals significant differences in expression of these transcripts in atrial tissue of SpDwf animals compared with controls. In SpDwf rats, the abundance of IGF-IR mRNA remains elevated at many postnatal ages, whereas mRNA encoding IGF-I is maintained only in older animals. Physiological concentrations of IGF-I cause two- to threefold increases in LVA current density in primary cultures of atrial myocytes, and this effect is blocked by an antisense oligonucleotide targeting the IGF-IR. Thus disruption of GH production in SpDwf animals alters expression of atrial LVA Ca2+ channel and IGF genes as well as postnatal regulation of LVA Ca2+ current density, most likely acting through compensatory mechanisms via the local IGF-IR.
Authors:
Janice K Larsen; Chien-Chang Chen; Philip M Best
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-10-14
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  288     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-01-14     Completed Date:  2005-02-23     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H829-38     Citation Subset:  IM    
Affiliation:
Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. jlarsen@life.uiuc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Weight
Calcium Channels / genetics*,  metabolism
Dwarfism / metabolism,  pathology,  physiopathology*
Growth Hormone / deficiency*,  secretion
Heart / physiology*
Heart Atria / metabolism,  pathology
Insulin-Like Growth Factor I / genetics,  metabolism
Membrane Potentials / physiology
Myocardium / metabolism,  pathology
Organ Size
RNA, Messenger / metabolism
Rats
Rats, Mutant Strains
Rats, Sprague-Dawley
Receptor, IGF Type 1 / genetics*,  metabolism
Grant Support
ID/Acronym/Agency:
R01 AR-44352/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/RNA, Messenger; 67763-96-6/Insulin-Like Growth Factor I; 9002-72-6/Growth Hormone; EC 2.7.10.1/Receptor, IGF Type 1

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


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