onr:"swepub:oai:lup.lub.lu.se:8ad4fe2e-6e8b-49d7-ada7-58b32a4f0841"
Sökning: onr:"swepub:oai:lup.lub.lu.se:8ad4fe2e-6e8b-49d7-ada7-58b32a4f0841" > The effects of MEK1...
- 1 av 1
- Föregående post
- Nästa post
- Till träfflistan
The effects of MEK1/2 inhibition on cigarette smoke exposure-induced ET receptor upregulation in rat cerebral arteries
-
- Cao, Lei (författare)
- Lund University,Lunds universitet,Experimentell kärlforskning,Forskargrupper vid Lunds universitet,Experimental Vascular Research,Lund University Research Groups,Xi'an Jiaotong University
-
- Ping, Na Na (författare)
- Xi'an Jiaotong University
-
- Cao, Yong Xiao (författare)
- Xi'an Jiaotong University
- visa fler...
- visa färre...
- (creator_code:org_t)
- Elsevier BV, 2016
- 2016
- Engelska 9 s.
- Ingår i: Toxicology and Applied Pharmacology. - : Elsevier BV. - 0041-008X. ; 304, s. 70-78
- Tidskriftsartikel (refereegranskat)
Abstract
Ämnesord
Stäng
- Cigarette smoking, a major stroke risk factor, upregulates endothelin receptors in cerebral arteries. The present study examined the effects of MEK1/2 pathway inhibition on cigarette smoke exposure-induced ET receptor upregulation. Rats were exposed to the secondhand smoke (SHS) for 8 weeks followed by intraperitoneal injection of MEK1/2 inhibitor, U0126 for another 4 weeks. The urine cotinine levels were assessed with high-performance liquid chromatography. Contractile responses of isolated cerebral arteries were recorded by a sensitive wire myograph. The mRNA and protein expression levels of receptor and MEK/ERK1/2 pathway molecules were examined by real-time PCR and Western blotting, respectively. Cerebral artery receptor localization was determined with immunohistochemistry. The results showed the urine cotinine levels from SHS exposure group were significantly higher than those from the fresh group. In addition, the MEK1/2 inhibitor, U0126 significantly reduced SHS exposure-increased ETA receptor mRNA and protein levels as well as contractile responses mediated by ETA receptors. The immunoreactivity of increased ETA receptor expression was primarily cytoplasmic in smooth muscle cells. In contrast, ETB receptor was noted in endothelial cells. However, the SHS-induced decrease in endothelium-dependent relaxation was unchanged after U0126 treatment. Furthermore, SHS increased the phosphorylation of MEK1/2 and ERK1/2 protein in cerebral arteries. By using U0126 could inhibit the phosphorylated ERK1/2 protein but not MEK1/2. Taken together, our data show that treatment with MEK1/2 pathway inhibitor offsets SHS exposure-induced ETA receptor upregulation in rat cerebral arteries.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Farmakologi och toxikologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Pharmacology and Toxicology (hsv//eng)
Nyckelord
- Cerebral artery
- Cigarette smoke
- Endothelin receptor
- MEK1/2
- Rat
- Receptor upregulation
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
Hitta via bibliotek
- Toxicology and Applied Pharmacology (Sök värdpublikationen i LIBRIS)
Till lärosätets databas
- 1 av 1
- Föregående post
- Nästa post
- Till träfflistan
Hitta mer i SwePub
- Av författaren/redakt...
- Cao, Lei
- Ping, Na Na
- Cao, Yong Xiao
- Li, Wei
- Cai, Yan
- Warfvinge, Karin
- visa fler...
- Edvinsson, Lars
- visa färre...
- Om ämnet
-
- MEDICIN OCH HÄLSOVETENSKAP
- MEDICIN OCH HÄLS ...
- och Medicinska och f ...
- och Farmakologi och ...
- Artiklar i publikationen
- Toxicology and A ...
- Av lärosätet
- Lunds universitet
Sök utanför SwePub
- Sök vidare i:
- Google Book Search
- Google Scholar
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.
- Copyright © LIBRIS - Nationella bibliotekssystem
- LIBRIS.kb.se
