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Cholesterol depleti...
Cholesterol depletion disrupts caveolae and differentially impairs agonist-induced arterial contraction.
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- Dreja, Karl (författare)
- Lund University,Lunds universitet,Kärlfysiologi,Forskargrupper vid Lunds universitet,Institutionen för kliniska vetenskaper, Malmö,Medicinska fakulteten,Vascular Physiology,Lund University Research Groups,Department of Clinical Sciences, Malmö,Faculty of Medicine
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Voldstedlund, Marianne (författare)
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Vinten, Jørgen (författare)
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Tranum-Jensen, Jørgen (författare)
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- Hellstrand, Per (författare)
- Lund University,Lunds universitet,Kärlfysiologi,Forskargrupper vid Lunds universitet,Vascular Physiology,Lund University Research Groups
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- Swärd, Karl (författare)
- Lund University,Lunds universitet,Kärlfysiologi,Forskargrupper vid Lunds universitet,Vascular Physiology,Lund University Research Groups
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(creator_code:org_t)
- 2002
- 2002
- Engelska.
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Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - 1524-4636. ; 22:8, s. 1267-1272
- Relaterad länk:
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http://dx.doi.org/10...
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https://lup.lub.lu.s...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- OBJECTIVE: This study assessed the role of cholesterol-rich membrane regions, including caveolae, in the regulation of arterial contractility. Methods and Results- Rat tail artery devoid of endothelium was treated with the cholesterol acceptor methyl-beta-cyclodextrin, and the effects on force and Ca2+ handling were evaluated. In cholesterol-depleted preparations, the force responses to alpha1-adrenergic receptors, membrane depolarization, inhibition of myosin light chain phosphatase, and activation of G proteins with a mixture of 20 mmol/L NaF and 60 micro mol/L AlCl3 were unaffected. In contrast, responses to 5-hydroxytryptamine (5-HT), vasopressin, and endothelin were reduced by >50%. The rise in global intracellular free Ca2+ concentration in response to 5-HT was attenuated, as was the generation of Ca2+ waves at the cellular level. By electron microscopy, cholesterol depletion was found to disrupt caveolae. The 5-HT response could be restored by exogenous cholesterol, which also restored caveolae. Western blots showed that the levels of 5-HT2A receptor and of caveolin-1 were unaffected by cholesterol extraction. Sucrose gradient centrifugation showed enrichment of 5-HT2A receptors, but not alpha1-adrenergic receptors, in the caveolin-1-containing fractions, suggesting localization of the former to caveolae. CONCLUSIONS: These results show that a subset of signaling pathways that regulate smooth muscle contraction depends specifically on cholesterol. Furthermore, the cholesterol-dependent step in serotonergic signaling occurs early in the pathway and depends on the integrity of caveolae.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Kardiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)
Nyckelord
- 5-hydroxytryptamine
- intracellular calcium
- endothelin
- smooth muscle
- caveolae
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
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