Secondhand cigarette smoke induces increased expression of contractile endothelin receptors in rat coronary arteries via a MEK1/2 sensitive mechanism
(2021) In Scandinavian Cardiovascular Journal 55(1). p.50-55- Abstract
Objectives: Cigarette smoke, a strong risk factor for cardiovascular diseases, upregulates contractile endothelin (ET) receptors in coronary arteries. The present study examined the effects of second hand cigarette smoke exposure on the contractile endothelin receptors and the role of the MEK1/2 pathway in rat coronary arteries. Design: Rats were exposed to secondhand smoke (SHS) for 8 weeks followed by intraperitoneal injection of a MEK1/2 inhibitor, U0126 daily for another 4 weeks. Contractile responses of isolated coronary arteries were recorded by a sensitive wire myograph. The receptor protein expression levels were examined by Western blotting. Results: The results showed that SHS in vivo caused increased expression of ET... (More)
Objectives: Cigarette smoke, a strong risk factor for cardiovascular diseases, upregulates contractile endothelin (ET) receptors in coronary arteries. The present study examined the effects of second hand cigarette smoke exposure on the contractile endothelin receptors and the role of the MEK1/2 pathway in rat coronary arteries. Design: Rats were exposed to secondhand smoke (SHS) for 8 weeks followed by intraperitoneal injection of a MEK1/2 inhibitor, U0126 daily for another 4 weeks. Contractile responses of isolated coronary arteries were recorded by a sensitive wire myograph. The receptor protein expression levels were examined by Western blotting. Results: The results showed that SHS in vivo caused increased expression of ET receptors ETA and ETB, and that the MEK1/2 blocker U0126 significantly reversed SHS exposure-increased ETA-mediated contractile responses and protein levels. Similar alterations were observed in ETB receptors. U0126 showed dose-dependent effects on SHS-induced response on contractile property and protein levels of the ETB receptor. However, only the higher dose U0126 (15 mg/kg) had inhibitory effects on the ETA receptor. Conclusions: Taken together, our data show that SHS increases contractile ET receptors and MEK1/2 pathway inhibitor offsets SHS exposure-induced ETA and ETB receptor upregulation in rat coronary arteries.
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- author
- Cao, Lei LU ; Lindstedt, Isak LU ; Edvinsson, Marie Louise LU ; Ping, Na Na ; Cao, Yong Xiao and Edvinsson, Lars LU
- organization
- publishing date
- 2021
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- coronary artery, endothelin, ET receptor, MEK1/2 inhibition, rat, Second hand smoke
- in
- Scandinavian Cardiovascular Journal
- volume
- 55
- issue
- 1
- pages
- 50 - 55
- publisher
- Taylor & Francis
- external identifiers
-
- pmid:32400208
- scopus:85084805517
- ISSN
- 1401-7431
- DOI
- 10.1080/14017431.2020.1762916
- language
- English
- LU publication?
- yes
- id
- 47cbf927-69f5-41ef-8782-a2fb86f194d0
- date added to LUP
- 2020-06-26 10:52:19
- date last changed
- 2024-10-31 06:42:37
@article{47cbf927-69f5-41ef-8782-a2fb86f194d0,
abstract = {{<p>Objectives: Cigarette smoke, a strong risk factor for cardiovascular diseases, upregulates contractile endothelin (ET) receptors in coronary arteries. The present study examined the effects of second hand cigarette smoke exposure on the contractile endothelin receptors and the role of the MEK1/2 pathway in rat coronary arteries. Design: Rats were exposed to secondhand smoke (SHS) for 8 weeks followed by intraperitoneal injection of a MEK1/2 inhibitor, U0126 daily for another 4 weeks. Contractile responses of isolated coronary arteries were recorded by a sensitive wire myograph. The receptor protein expression levels were examined by Western blotting. Results: The results showed that SHS in vivo caused increased expression of ET receptors ET<sub>A</sub> and ET<sub>B</sub>, and that the MEK1/2 blocker U0126 significantly reversed SHS exposure-increased ET<sub>A</sub>-mediated contractile responses and protein levels. Similar alterations were observed in ET<sub>B</sub> receptors. U0126 showed dose-dependent effects on SHS-induced response on contractile property and protein levels of the ET<sub>B</sub> receptor. However, only the higher dose U0126 (15 mg/kg) had inhibitory effects on the ET<sub>A</sub> receptor. Conclusions: Taken together, our data show that SHS increases contractile ET receptors and MEK1/2 pathway inhibitor offsets SHS exposure-induced ET<sub>A</sub> and ET<sub>B</sub> receptor upregulation in rat coronary arteries.</p>}},
author = {{Cao, Lei and Lindstedt, Isak and Edvinsson, Marie Louise and Ping, Na Na and Cao, Yong Xiao and Edvinsson, Lars}},
issn = {{1401-7431}},
keywords = {{coronary artery; endothelin; ET receptor; MEK1/2 inhibition; rat; Second hand smoke}},
language = {{eng}},
number = {{1}},
pages = {{50--55}},
publisher = {{Taylor & Francis}},
series = {{Scandinavian Cardiovascular Journal}},
title = {{Secondhand cigarette smoke induces increased expression of contractile endothelin receptors in rat coronary arteries via a MEK1/2 sensitive mechanism}},
url = {{http://dx.doi.org/10.1080/14017431.2020.1762916}},
doi = {{10.1080/14017431.2020.1762916}},
volume = {{55}},
year = {{2021}},
}