Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

NF-kappaB signaling mediates vascular smooth muscle endothelin type B receptor expression in resistance arteries.

Zheng, Jian-Pu ; Zhang, Yaping LU ; Edvinsson, Lars LU ; Hjalt, Tord LU and Xu, Cang-Bao LU (2010) In European Journal of Pharmacology Mar 4. p.148-154
Abstract
Vascular smooth muscle cells (SMC) endothelin type B (ET(B)) receptor upregulation results in strong vasoconstriction and reduction of local blood flow. We hypothesizes that the underlying molecular mechanisms involve transcriptional factor nuclear factor-kappaB (NF-kappaB) pathway. ET(B) receptor upregulation and activation of NF-kappaB were studied at functional contraction (in vitro myograph), mRNA (real-time PCR), and protein (Western blot and immunocytochemistry) levels during organ culture of rat mesenteric arteries. Organ culture the artery segments induced a time-dependent strong contractile response to sarafotoxin 6c in parallel with enhanced expression of ET(B) receptor mRNA and protein in the SMC. Western blot experiments... (More)
Vascular smooth muscle cells (SMC) endothelin type B (ET(B)) receptor upregulation results in strong vasoconstriction and reduction of local blood flow. We hypothesizes that the underlying molecular mechanisms involve transcriptional factor nuclear factor-kappaB (NF-kappaB) pathway. ET(B) receptor upregulation and activation of NF-kappaB were studied at functional contraction (in vitro myograph), mRNA (real-time PCR), and protein (Western blot and immunocytochemistry) levels during organ culture of rat mesenteric arteries. Organ culture the artery segments induced a time-dependent strong contractile response to sarafotoxin 6c in parallel with enhanced expression of ET(B) receptor mRNA and protein in the SMC. Western blot experiments demonstrated that phosphorylation of NF-kappaB p65 was time-dependently induced during organ culture starting at 1h. In addition, cytoplasmic IkB degradation occurred in parallel with nuclear NF-kappaB accumulation following organ culture. The enhanced expression of ET(B) receptor protein was apparent at 3h in the SMC and while enhanced ET(B) receptor-mediated contractions occurred first at 12h. The specific IkappaB inhibitors, IMD-0354 (N-(3,5-Bis-trifluoromethylphenyl)-5-chloro-2-hydroxybenzamide) and Wedelolactone (7-Methoxy-5,11,12-trihydroxycoumestan), abolished the organ culture induced ET(B) receptor upregulation. The intracellular NF-kappaB pathway is involved in the process of induced expression of vascular SMC ET(B) receptors. (Less)
Please use this url to cite or link to this publication:
author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
European Journal of Pharmacology
volume
Mar 4
pages
148 - 154
publisher
Elsevier
external identifiers
  • wos:000278878900020
  • pmid:20399772
  • scopus:77953290712
  • pmid:20399772
ISSN
1879-0712
DOI
10.1016/j.ejphar.2010.04.006
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuronal Survival (013212041), Medicine (Lund) (013230025), Clinical and Experimental Allergy Research (013243510)
id
fff0059a-4bb4-4d7f-8261-428688b57131 (old id 1595130)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20399772?dopt=Abstract
date added to LUP
2016-04-04 07:42:50
date last changed
2024-01-12 02:22:53
@article{fff0059a-4bb4-4d7f-8261-428688b57131,
  abstract     = {{Vascular smooth muscle cells (SMC) endothelin type B (ET(B)) receptor upregulation results in strong vasoconstriction and reduction of local blood flow. We hypothesizes that the underlying molecular mechanisms involve transcriptional factor nuclear factor-kappaB (NF-kappaB) pathway. ET(B) receptor upregulation and activation of NF-kappaB were studied at functional contraction (in vitro myograph), mRNA (real-time PCR), and protein (Western blot and immunocytochemistry) levels during organ culture of rat mesenteric arteries. Organ culture the artery segments induced a time-dependent strong contractile response to sarafotoxin 6c in parallel with enhanced expression of ET(B) receptor mRNA and protein in the SMC. Western blot experiments demonstrated that phosphorylation of NF-kappaB p65 was time-dependently induced during organ culture starting at 1h. In addition, cytoplasmic IkB degradation occurred in parallel with nuclear NF-kappaB accumulation following organ culture. The enhanced expression of ET(B) receptor protein was apparent at 3h in the SMC and while enhanced ET(B) receptor-mediated contractions occurred first at 12h. The specific IkappaB inhibitors, IMD-0354 (N-(3,5-Bis-trifluoromethylphenyl)-5-chloro-2-hydroxybenzamide) and Wedelolactone (7-Methoxy-5,11,12-trihydroxycoumestan), abolished the organ culture induced ET(B) receptor upregulation. The intracellular NF-kappaB pathway is involved in the process of induced expression of vascular SMC ET(B) receptors.}},
  author       = {{Zheng, Jian-Pu and Zhang, Yaping and Edvinsson, Lars and Hjalt, Tord and Xu, Cang-Bao}},
  issn         = {{1879-0712}},
  language     = {{eng}},
  pages        = {{148--154}},
  publisher    = {{Elsevier}},
  series       = {{European Journal of Pharmacology}},
  title        = {{NF-kappaB signaling mediates vascular smooth muscle endothelin type B receptor expression in resistance arteries.}},
  url          = {{http://dx.doi.org/10.1016/j.ejphar.2010.04.006}},
  doi          = {{10.1016/j.ejphar.2010.04.006}},
  volume       = {{Mar 4}},
  year         = {{2010}},
}