Advanced

Down-regulation of alpha-adrenoceptor expression by lipid-soluble smoke particles through transcriptional factor nuclear factor-kappaB pathway.

Zhang, W; Cao, YX; He, JY and Xu, Cang-Bao LU (2007) In Basic & Clinical Pharmacology & Toxicology 101(6). p.401-406
Abstract
Smoking is a strong risk factor for cardiovascular disease that is a leading cause of death and disability in Western countries. The present study was designed to investigate the effect of lipid-soluble smoke particles (DSP) on alpha-adrenoceptor expression in organ culture of rat mesenteric arteries and human epiploon arteries. Myograph and real-time reverse transcription-polymerase chain reaction were employed to assess vascular smooth muscle contractibility and the receptor mRNA expression in the smooth muscle cells. Organ culture of the arterial segments in the presence of DSP (0.2 microl/ml) resulted in a significantly decreased contractile response to norepinephrine, compared to control (i.e. in the presence of dimethyl sulfoxide) (P... (More)
Smoking is a strong risk factor for cardiovascular disease that is a leading cause of death and disability in Western countries. The present study was designed to investigate the effect of lipid-soluble smoke particles (DSP) on alpha-adrenoceptor expression in organ culture of rat mesenteric arteries and human epiploon arteries. Myograph and real-time reverse transcription-polymerase chain reaction were employed to assess vascular smooth muscle contractibility and the receptor mRNA expression in the smooth muscle cells. Organ culture of the arterial segments in the presence of DSP (0.2 microl/ml) resulted in a significantly decreased contractile response to norepinephrine, compared to control (i.e. in the presence of dimethyl sulfoxide) (P < 0.05). This was in parallel with a down-regulation of alpha(1A)-adrenoceptor mRNA expression in the smooth muscle, while alpha(2)-adrenoceptor mRNA expression remained unchanged. General transcription inhibitor actinomycin D (10(-5.4 )M), but not the translational inhibitor cycloheximide (10(-5 )M), significantly abolished the DSP-induced depressed contraction to norepinephrine. IMD-0354 (10(-7.5 )M), a specific nuclear factor-kappaB (NF-kappaB) pathway inhibitor, markedly reversed the DSP-induced down-regulation of alpha(1A)-adrenoceptor expression in the smooth muscle at both functional and mRNA levels. Thus, we have demonstrated that smoking-induced down-regulation of alpha(1A)-adrenoceptor expression was via the transcriptional factor NF-kappaB pathway. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Basic & Clinical Pharmacology & Toxicology
volume
101
issue
6
pages
401 - 406
publisher
Wiley-Blackwell
external identifiers
  • wos:000251028900003
  • scopus:36248939613
ISSN
1742-7843
DOI
10.1111/j.1742-7843.2007.00163.x
language
English
LU publication?
yes
id
969fffe3-b311-4011-9829-478329a31545 (old id 1142845)
date added to LUP
2008-07-31 14:34:50
date last changed
2017-01-01 04:31:23
@article{969fffe3-b311-4011-9829-478329a31545,
  abstract     = {Smoking is a strong risk factor for cardiovascular disease that is a leading cause of death and disability in Western countries. The present study was designed to investigate the effect of lipid-soluble smoke particles (DSP) on alpha-adrenoceptor expression in organ culture of rat mesenteric arteries and human epiploon arteries. Myograph and real-time reverse transcription-polymerase chain reaction were employed to assess vascular smooth muscle contractibility and the receptor mRNA expression in the smooth muscle cells. Organ culture of the arterial segments in the presence of DSP (0.2 microl/ml) resulted in a significantly decreased contractile response to norepinephrine, compared to control (i.e. in the presence of dimethyl sulfoxide) (P &lt; 0.05). This was in parallel with a down-regulation of alpha(1A)-adrenoceptor mRNA expression in the smooth muscle, while alpha(2)-adrenoceptor mRNA expression remained unchanged. General transcription inhibitor actinomycin D (10(-5.4 )M), but not the translational inhibitor cycloheximide (10(-5 )M), significantly abolished the DSP-induced depressed contraction to norepinephrine. IMD-0354 (10(-7.5 )M), a specific nuclear factor-kappaB (NF-kappaB) pathway inhibitor, markedly reversed the DSP-induced down-regulation of alpha(1A)-adrenoceptor expression in the smooth muscle at both functional and mRNA levels. Thus, we have demonstrated that smoking-induced down-regulation of alpha(1A)-adrenoceptor expression was via the transcriptional factor NF-kappaB pathway.},
  author       = {Zhang, W and Cao, YX and He, JY and Xu, Cang-Bao},
  issn         = {1742-7843},
  language     = {eng},
  number       = {6},
  pages        = {401--406},
  publisher    = {Wiley-Blackwell},
  series       = {Basic & Clinical Pharmacology & Toxicology},
  title        = {Down-regulation of alpha-adrenoceptor expression by lipid-soluble smoke particles through transcriptional factor nuclear factor-kappaB pathway.},
  url          = {http://dx.doi.org/10.1111/j.1742-7843.2007.00163.x},
  volume       = {101},
  year         = {2007},
}