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Verfasst von:Bonaterra, Gabriel [VerfasserIn]   i
 Hildebrandt, Wulf [VerfasserIn]   i
 Bodens, Anne [VerfasserIn]   i
 Sauer, Roland [VerfasserIn]   i
 Dugi, Klaus A. [VerfasserIn]   i
 Deigner, Hans-Peter [VerfasserIn]   i
 Dröge, Wulf [VerfasserIn]   i
 Metz, Jürgen [VerfasserIn]   i
 Kinscherf, Ralf [VerfasserIn]   i
Titel:Increased cyclooxygenase-2 expression in peripheral blood mononuclear cells of smokers and hyperlipidemic subjects
Verf.angabe:Gabriel A. Bonaterra, Wulf Hildebrandt, Anne Bodens, Roland Sauer, Klaus A. Dugi, Hans-Peter Deigner, Wulf Dröge, Jürgen Metz, Ralf Kinscherf
Jahr des Originals:2004
Umfang:8 S.
Fussnoten:Available online: 11 November 2004 ; Gesehen am 23.10.2017
Titel Quelle:Enthalten in: Free radical biology and medicine
Jahr Quelle:2005
Band/Heft Quelle:38(2005), 2, S. 235-242
ISSN Quelle:1873-4596
Abstract:Cyclooxygenase (COX)-2 is expressed in macrophages of arteriosclerotic lesions and promotes inflammation. We investigated whether COX-2 is already expressed in peripheral blood mononuclear cells (PBMCs) of subjects possessing risk-related factors, such as in smokers and hyperlipidemics. PBMCs were isolated from the venous blood of normolipidemic nonsmokers (NL-NSM; n = 15), normolipidemic smokers (NL-SM; n = 12), hyperlipidemic nonsmokers (HL-NSM; n = 10), and hyperlipidemic smokers (HL-SM; n = 10). RNA from PBMCs was used for RT-PCR. Plasma concentrations of oxidized low-density lipoproteins (oxLDL) were measured by ELISA, those of glutamate and cystine by HPLC. The results show that COX-2 expression in PBMCs was significantly increased in the groups with cardiovascular risk factors (NL-SM, HL-SM, HL-NSM) compared with NL-NSM. COX-2 expression in PBMCs was positively correlated with concentrations of total serum cholesterol, oxLDL, glutamate, or cystine. We suggest that the elevated COX-2 expression indicates a priming of PBMCs as a response to a systemic pro-oxidative and proinflammatory shift in subjects with cardiovascular risk factors, which might also contribute to growth and instability of arteriosclerotic lesions.
DOI:doi:10.1016/j.freeradbiomed.2004.10.021
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Verlag: http://dx.doi.org/10.1016/j.freeradbiomed.2004.10.021
 Verlag: http://www.sciencedirect.com/science/article/pii/S0891584904008433
 DOI: https://doi.org/10.1016/j.freeradbiomed.2004.10.021
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1564642593
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