Secondhand cigarette smoke exposure causes upregulation of cerebrovascular 5-HT(1B) receptors via the Raf/ERK/MAPK pathway in rats.
(2013) In Acta Physiologica 207(1). p.183-193- Abstract
- AIM:
Cigarette smoke exposure increases the risk of stroke. Upregulation of 5-hydroxytryptamine 1B (5-HT(1B) ) receptors is associated with the pathogenesis of cerebral ischemia. The present study examined the hypothesis that the expression of 5-HT(1B) receptors is altered in brain vessels after secondhand smoke (SHS) exposure.
METHODS:
Rats were exposed to SHS in vivo for 200 min daily for 8 weeks. The contractile responses of isolated cerebral arteries were studies by a sensitive myograph. The mRNA and protein expression for 5-HT(1B) receptors were examined by real-time PCR, Western blot and immunofluorescence, respectively. In addition, the phosphorylation of Raf/extracellular signal-regulated... (More) - AIM:
Cigarette smoke exposure increases the risk of stroke. Upregulation of 5-hydroxytryptamine 1B (5-HT(1B) ) receptors is associated with the pathogenesis of cerebral ischemia. The present study examined the hypothesis that the expression of 5-HT(1B) receptors is altered in brain vessels after secondhand smoke (SHS) exposure.
METHODS:
Rats were exposed to SHS in vivo for 200 min daily for 8 weeks. The contractile responses of isolated cerebral arteries were studies by a sensitive myograph. The mRNA and protein expression for 5-HT(1B) receptors were examined by real-time PCR, Western blot and immunofluorescence, respectively. In addition, the phosphorylation of Raf/extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinases (MAPK) pathway was evaluated.
RESULTS:
The results showed that SHS exposure shifted the 5-HT(1B) receptor-mediated concentration-contraction curve toward the left with a markedly increased maximum contraction. Furthermore, there were significant elevations in mRNA level and protein expression of 5-HT(1B) receptors in SHS-exposed rats. Immunostaining revealed that the 5-HT(1B) receptors were localized to the smooth muscle cells of cerebral arteries. SHS was also found to induce the phosphorylation of Raf-1 and ERK1/2 proteins. The administration of a Raf-1 inhibitor GW5074 attenuated the 5-HT(1B) receptor upregulation.
CONCLUSION:
SHS exposure upregulates cerebrovascular 5-HT(1B) receptors in rats. The receptor upregulation is associated with Raf/ERK/MAPK activation. © 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/3047583
- author
- Cao, Lei LU ; Xu, Cang-Bao LU ; Zhang, Yao LU ; Cao, Y X and Edvinsson, Lars LU
- organization
- publishing date
- 2013
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- cerebral artery, 5-HT1B receptors, Raf, ERK, MAPK pathway, secondhand, smoke exposure
- in
- Acta Physiologica
- volume
- 207
- issue
- 1
- pages
- 183 - 193
- publisher
- Wiley-Blackwell
- external identifiers
-
- wos:000312340900018
- pmid:22883081
- scopus:84870848024
- pmid:22883081
- ISSN
- 1748-1716
- DOI
- 10.1111/j.1748-1716.2012.02478.x
- language
- English
- LU publication?
- yes
- id
- 44695bf9-0125-4a6b-9b3a-9807e2be69fd (old id 3047583)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/22883081?dopt=Abstract
- date added to LUP
- 2016-04-01 10:24:55
- date last changed
- 2024-01-06 16:03:30
@article{44695bf9-0125-4a6b-9b3a-9807e2be69fd,
abstract = {{AIM: <br/><br>
Cigarette smoke exposure increases the risk of stroke. Upregulation of 5-hydroxytryptamine 1B (5-HT(1B) ) receptors is associated with the pathogenesis of cerebral ischemia. The present study examined the hypothesis that the expression of 5-HT(1B) receptors is altered in brain vessels after secondhand smoke (SHS) exposure. <br/><br>
<br/><br>
METHODS: <br/><br>
Rats were exposed to SHS in vivo for 200 min daily for 8 weeks. The contractile responses of isolated cerebral arteries were studies by a sensitive myograph. The mRNA and protein expression for 5-HT(1B) receptors were examined by real-time PCR, Western blot and immunofluorescence, respectively. In addition, the phosphorylation of Raf/extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinases (MAPK) pathway was evaluated. <br/><br>
<br/><br>
RESULTS: <br/><br>
The results showed that SHS exposure shifted the 5-HT(1B) receptor-mediated concentration-contraction curve toward the left with a markedly increased maximum contraction. Furthermore, there were significant elevations in mRNA level and protein expression of 5-HT(1B) receptors in SHS-exposed rats. Immunostaining revealed that the 5-HT(1B) receptors were localized to the smooth muscle cells of cerebral arteries. SHS was also found to induce the phosphorylation of Raf-1 and ERK1/2 proteins. The administration of a Raf-1 inhibitor GW5074 attenuated the 5-HT(1B) receptor upregulation. <br/><br>
<br/><br>
CONCLUSION: <br/><br>
SHS exposure upregulates cerebrovascular 5-HT(1B) receptors in rats. The receptor upregulation is associated with Raf/ERK/MAPK activation. © 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society.}},
author = {{Cao, Lei and Xu, Cang-Bao and Zhang, Yao and Cao, Y X and Edvinsson, Lars}},
issn = {{1748-1716}},
keywords = {{cerebral artery; 5-HT1B receptors; Raf; ERK; MAPK pathway; secondhand; smoke exposure}},
language = {{eng}},
number = {{1}},
pages = {{183--193}},
publisher = {{Wiley-Blackwell}},
series = {{Acta Physiologica}},
title = {{Secondhand cigarette smoke exposure causes upregulation of cerebrovascular 5-HT(1B) receptors via the Raf/ERK/MAPK pathway in rats.}},
url = {{http://dx.doi.org/10.1111/j.1748-1716.2012.02478.x}},
doi = {{10.1111/j.1748-1716.2012.02478.x}},
volume = {{207}},
year = {{2013}},
}