NF-kappaB signaling mediates vascular smooth muscle endothelin type B receptor expression in resistance arteries.
(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:
https://lup.lub.lu.se/record/1595130
- author
- Zheng, Jian-Pu ; Zhang, Yaping LU ; Edvinsson, Lars LU ; Hjalt, Tord LU and Xu, Cang-Bao LU
- organization
- publishing date
- 2010
- 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
- 2024-10-12 15:11:26
@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}}, }