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001-es BibID:BIBFORM041943
Első szerző:Bak István (vegyész, analitikus, farmakológus)
Cím:Heme oxygenase-1 related carbon monoxide production and ventricular fibrillation in isolated ischemic/reperfused mouse myocardium / Istvan Bak, Levente Szendrei, Tibor Turoczi, Gabor Papp, Ferenc Joo, Dipak K. Das, Joel de Leiris, Peter Der, Bela Juhasz, Edit Varga, Ildiko Bacskay, Jozsef Balla, Peter Kovacs, Arpad Tosaki
Dátum:2003
ISSN:0892-6638
Megjegyzések:Heme oxygenase-1 (HO-1)-dependent carbon monoxide (CO) production related to reperfusion-induced ventricular fibrillation (VF) was studied in HO-1 wild-type (+/+), heterozygous (+/-), and homozygous (-/-) isolated ischemic/reperfused mouse heart. In HO-1 homozygous myocardium, under aerobic conditions, HO-1 enzyme activity, HO-1 mRNA, and protein expression were not detected in comparison with aerobically perfused wild-type and heterozygous myocardium. In wild-type, HO-1 hetero- and homozygous hearts subjected to 20 min ischemia followed by 2 h of reperfusion, the expression of HO-1 mRNA, protein, and HO-1 enzyme activity was detected in various degrees. A reduction in the expression of HO-1 mRNA, protein, and enzyme activity in fibrillated wild-type and heterozygous myocardium was observed. In reperfused/nonfibrillated wild-type and heterozygous hearts, a reduction in HO-1 mRNA, protein expression, and HO-1 enzyme activity was not observed, indicating that changes in HO-1 mRNA, protein, and enzyme activity could be related to the development of VF. These changes were reflected in the HO-1-related endogenous CO production measured by gas chromatography. In HO-1 knockout ischemic/reperfused myocardium, all hearts showed VF, and no detection in HO-1 mRNA, protein, and enzyme activity was observed. Thus, interventions that are able to increase endogenous CO may prevent the development of VF.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Faseb Journal 17 : 14 (2003), p. 2133-2135. -
További szerzők:Szendrei Levente Turóczi Tibor (1976-) (molekuláris biológus) Papp Gábor (farmakológus) Joó Ferenc (1949-) (vegyész) Das, Dipak Kumar de Leiris, Joel Dér Péter Juhász Béla (1978-) (kísérletes farmakológus) Varga Edit (gyógyszerész) Bácskay Ildikó (1969-) (gyógyszerész, gyógyszertechnológus) Balla József (1959-) (belgyógyász, nephrológus) Kovács Péter (1939-) (farmakológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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001-es BibID:BIBFORM023027
Első szerző:Qin, Zhenyu
Cím:Essential role for the Menkes ATPase in activation of extracellular superoxide dismutase : implication for vascular oxidative stress / Qin Z., Itoh S., Jeney V., Ushio-Fukai M., Fukai T.
Dátum:2006
ISSN:0892-6638
Megjegyzések:Extracellular superoxide dismutase (SOD3), a secretory copper enzyme, plays an important role in atherosclerosis and hypertension by modulating the levels of extracellular superoxide anion (O2*-) in the vasculature. Little is known about the mechanisms by which SOD3 obtains its catalytic copper cofactor. Menkes ATPase (MNK) has been shown to transport cytosolic copper to the secretory pathway in nonvascular cells. We performed the present study to determine whether MNK is required for the activation of SOD3 in the vasculature. Here we show that MNK was highly expressed in the various vascular tissues and cells. Aortas and cultured fibroblasts from MNK mutant (MNK(mut)) mice showed a marked decrease in specific activity of SOD3, but not SOD1 (cytosolic form), which was partially restored by copper addition. Copper treatment in wild-type cells promoted the direct interaction and colocalization of SOD3 with MNK in the trans-Golgi network (TGN), suggesting that MNK transports copper to SOD3 in the TGN. Aortas of MNK(mut) mice revealed a decrease in activity of SOD3, but not SOD1, in association with a robust increase in O2*- levels. Finally, both MNK and SOD3 proteins were highly expressed in the intimal lesions of atherosclerotic vessels. In conclusion, vascular MNK plays an essential role in full activity of SOD3 through transporting copper to SOD3 in the TGN, thereby regulating O2*- levels in the vasculature. These studies provide a novel insight into vascular MNK as a critical modulator of "superoxide" stress, which may contribute to cardiovascular disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Faseb Journal. - 20 : 2 (2006), p. 334-336. -
További szerzők:Itoh, Shinichi Jeney Viktória (1971-) (vegyész, kémia tanár) Ushio-Fukai, Masuko Fukai, Tohru
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