Catalase activity prevents exercise-induced up-regulation of vasoprotective proteins in venous tissue.
Physical activity induces favourable changes of arterial gene expression and protein activity, although little is known about its effect in venous tissue. Although our understanding of the initiating molecular signals is still incomplete, increased expression of endothelial nitric oxide synthase (eNOS) is considered a key event. This study sought to investigate the effects of two different training protocols on the expression of eNOS and extracellular superoxide dismutase (ecSOD) in venous and lung tissue and to evaluate the underlying molecular mechanisms. C57Bl/6 mice underwent voluntary exercise or forced physical activity. Changes of vascular mRNA and protein levels and activity of eNOS, ecSOD and catalase were determined in aorta, heart, lung and vena cava. Both training protocols similarly increased relative heart weight and resulted in up-regulation of aortic and myocardial eNOS. In striking contrast, eNOS expression in vena cava and lung remained unchanged. Likewise, exercise up-regulated ecSOD in the aorta and in left ventricular tissue but remained unchanged in lung tissue. Catalase expression in lung tissue and vena cava of exercised mice exceeded that in aorta by 6.9- and 10-fold, respectively, suggesting a lack of stimulatory effects of hydrogen peroxide. In accordance, treatment of mice with the catalase inhibitor aminotriazole for 6 weeks resulted in significant up-regulation of eNOS and ecSOD in vena cava. These data suggest that physiological venous catalase activity prevents exercise-induced up-regulation of eNOS and ecSOD. Furthermore, therapeutic inhibition of vascular catalase might improve pulmonary rehabilitation.
Institute for Pharmacology and Clinical Pharmacology, University Hospital, Heinrich-Heine-University, Duesseldorf, Germany.
Vu Thao-Vi
VT
Dao
Melanie
M
Floeren
Stephanie
S
Kumpf
Charlotte
C
Both
Bärbel
B
Peter
Vera
V
Balz
Tatsiana
T
Suvorava
Georg
G
Kojda
D000640:Amitrole / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000378:metabolism; D002374:Catalase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009043:Motor Activity; D009206:Myocardium / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D010805:Physical Conditioning, Animal; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D013482:Superoxide Dismutase / Q000096:biosynthesis*; D014684:Venae Cavae / Q000378:metabolism*
D012333:RNA, Messenger; D002374:Catalase; D052250:Nitric Oxide Synthase Type III; D013482:Superoxide Dismutase; D000640:Amitrole