Quantification of beta-adrenoceptors and beta-adrenoceptor kinase
on protein and mRNA levels in heart failure
M. Bohm, and M. Lohse. Eur Heart J, (December 1994)Bohm, M Lohse, M J Research Support, Non-U.S. Gov't Review England
European heart journal Eur Heart J. 1994 Dec;15 Suppl D:30-4..
Abstract
The alterations of the beta-adrenoceptor adenylyl cyclase are reviewed.
In failing myocardium, the down-regulation of beta 1-adrenoceptors
is accompanied by a decrease in steady state mRNA levels, as studied
with quantitative polymerase chain reactions in dilated and ischaemic
cardiomyopathy. The density of beta 2-adrenoceptors and beta 2-adrenoceptor
mRNA was unchanged in both pathological conditions compared to non-failing
myocardium. In addition to down-regulation of beta 1-receptor protein
and mRNA, an increased activity of the beta-adrenoceptor kinase (beta-ARK)
was observed. Correspondingly, quantification of beta-ARK mRNA by
a 5' and a middle portion PCR-product suggests that increased enzyme
activity could be due to increased transcription. In summary, decreased
steady state levels of beta 1-adrenoceptor mRNA could contribute
to reduced beta-adrenoceptor density in failing myocardium. The known
uncoupling of beta-adrenoceptors could be due to an increased mRNA
expression and activity of beta-ARK.
%0 Journal Article
%1 Bohm1994
%A Bohm, M.
%A Lohse, M. J.
%D 1994
%J Eur Heart J
%K AMP-Dependent Animals Chain Cyclic Down-Regulation/genetics Enzymologic/physiology Expression Failure/*genetics Gene Genetic Heart Humans Kinases Kinases/*genetics Messenger/genetics Myocardium/enzymology Norepinephrine/physiology Polymerase Protein RNA, Reaction/methods Receptor Regulation, Transcription, beta-Adrenergic beta/*genetics Adrenergic
%P 30-4
%T Quantification of beta-adrenoceptors and beta-adrenoceptor kinase
on protein and mRNA levels in heart failure
%U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7713110
%V 15 Suppl D
%X The alterations of the beta-adrenoceptor adenylyl cyclase are reviewed.
In failing myocardium, the down-regulation of beta 1-adrenoceptors
is accompanied by a decrease in steady state mRNA levels, as studied
with quantitative polymerase chain reactions in dilated and ischaemic
cardiomyopathy. The density of beta 2-adrenoceptors and beta 2-adrenoceptor
mRNA was unchanged in both pathological conditions compared to non-failing
myocardium. In addition to down-regulation of beta 1-receptor protein
and mRNA, an increased activity of the beta-adrenoceptor kinase (beta-ARK)
was observed. Correspondingly, quantification of beta-ARK mRNA by
a 5' and a middle portion PCR-product suggests that increased enzyme
activity could be due to increased transcription. In summary, decreased
steady state levels of beta 1-adrenoceptor mRNA could contribute
to reduced beta-adrenoceptor density in failing myocardium. The known
uncoupling of beta-adrenoceptors could be due to an increased mRNA
expression and activity of beta-ARK.
@article{Bohm1994,
abstract = {The alterations of the beta-adrenoceptor adenylyl cyclase are reviewed.
In failing myocardium, the down-regulation of beta 1-adrenoceptors
is accompanied by a decrease in steady state mRNA levels, as studied
with quantitative polymerase chain reactions in dilated and ischaemic
cardiomyopathy. The density of beta 2-adrenoceptors and beta 2-adrenoceptor
mRNA was unchanged in both pathological conditions compared to non-failing
myocardium. In addition to down-regulation of beta 1-receptor protein
and mRNA, an increased activity of the beta-adrenoceptor kinase (beta-ARK)
was observed. Correspondingly, quantification of beta-ARK mRNA by
a 5' and a middle portion PCR-product suggests that increased enzyme
activity could be due to increased transcription. In summary, decreased
steady state levels of beta 1-adrenoceptor mRNA could contribute
to reduced beta-adrenoceptor density in failing myocardium. The known
uncoupling of beta-adrenoceptors could be due to an increased mRNA
expression and activity of beta-ARK.},
added-at = {2010-12-14T18:12:02.000+0100},
author = {Bohm, M. and Lohse, M. J.},
biburl = {https://www.bibsonomy.org/bibtex/2d2229055d7ebe756219f4c9224da6588/pharmawuerz},
endnotereftype = {Journal Article},
interhash = {abf1fe3f809b4919bb317535f3dad0e1},
intrahash = {d2229055d7ebe756219f4c9224da6588},
issn = {0195-668X (Print) 0195-668X (Linking)},
journal = {Eur Heart J},
keywords = {AMP-Dependent Animals Chain Cyclic Down-Regulation/genetics Enzymologic/physiology Expression Failure/*genetics Gene Genetic Heart Humans Kinases Kinases/*genetics Messenger/genetics Myocardium/enzymology Norepinephrine/physiology Polymerase Protein RNA, Reaction/methods Receptor Regulation, Transcription, beta-Adrenergic beta/*genetics Adrenergic},
month = Dec,
note = {Bohm, M Lohse, M J Research Support, Non-U.S. Gov't Review England
European heart journal Eur Heart J. 1994 Dec;15 Suppl D:30-4.},
pages = {30-4},
shorttitle = {Quantification of beta-adrenoceptors and beta-adrenoceptor kinase
on protein and mRNA levels in heart failure},
timestamp = {2010-12-14T18:22:38.000+0100},
title = {Quantification of beta-adrenoceptors and beta-adrenoceptor kinase
on protein and mRNA levels in heart failure},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7713110},
volume = {15 Suppl D},
year = 1994
}