Ecule(VCAM)-1, interleukin(IL)-33, interleukin 1 receptor-like 1 (ST2), interleukin(IL

Ecule(VCAM)-1, interleukin(IL)-33, interleukin 1 receptor-like 1 (ST2), interleukin(IL)-19 and signal transducer and activator of transcription(STAT)-3 in 6-month sham (white bars) and 6-month shunt (black bars) piglets. Panel B: Relative lung tissue protein content for the heme-oxygenase(HO)-1 in 6-month sham (white bars) and 6-month shunt (black bars) piglets. Panel C: Correlation between slope of mPpa/Q relationships and lung protein content for hemeoxygenase(HO)-1, lung mRNA content for intercellular adhesion molecule(ICAM)-1, interleukin(IL)-33 and interleukin(IL)-19. Values expressed as mean6SEM. doi:10.1371/journal.pone.0069470.gresponsible for the non-aggravation of the pulmonary vascular remodeling in the 6-month compared to the 3-month shunted pigs [5,8].In the present study, we found a trend to the decreased expression of HO-1 in the lungs after 6-month systemic-topulmonary shunting. Overexpression of HO-1 16574785 has been shown toInflammation and HO-1 in Right Ventricular FailureFigure 4. Panel A: Relative right ventricular (RV) tissue mRNA content for the heme-oxygenase(HO)-1 and -2, tumor necrosis factor(TNF)-a, intercellular adhesion molecule(ICAM)-1 and -2, vascular cell adhesion molecule(VCAM)-1, interleukin(IL)-33, interleukin 1 receptor-like 1 (ST2), interleukin(IL)-19 and signal transducer and activator of transcription(STAT)-3 in 6-month sham (white bars) and 6-month shunt (black bars) piglets. Relative right ventricular (RV) tissue protein content for the heme-oxygenase(HO)-1 in 6month sham (white bars) and 6-month shunt (black bars) piglets. Correlation between Ees/Ea ratio and right ventricular (RV) protein content for heme-oxygenase (HO)-1 and right ventricular (RV) mRNA content for intercellular adhesion molecule (ICAM)-2. Values expressed as mean6SEM. doi:10.1371/journal.pone.0069470.gprevent the development of hypoxia-induced PH, associated with reduced pulmonary inflammation (characterized by increased macrophage activity and IL-10 expression [40])and vascularremodeling [41?2]. HO-1 mediates in vivo the protective effects in monocrotaline-induced PH and in vitro the anti-proliferative effects in smooth muscle cells of rapamycin [43]. In contrast,Inflammation and HO-1 in Right Ventricular Failurepulmonary HO-1 expression has been shown to be increased in monocrotaline- and monocrotaline/pneumectomy-induced PH [44]. Here, we also showed decreased gene expression of HO-1 in the failing RV. These results suggest a similar tendency to changes in HO-1 in the lungs and the failing RV in the present experimental model of advanced PAH, probably through divergent HO-1 enzymatic PS-1145 web products [45]. Indeed, biliverdin has been shown to prevent RV BTZ043 dysfunction, but did not reduce the pulmonary artery remodeling, while inhaled CO reduced the pulmonary vascular remodeling, but did not have any effect on the RV (45). In mice exposed to chronic hypoxia, administration of mesenchymal cells overexpressing HO-1 has been shown to reduce the RV hypertrophy, to stabilize the infarction zones and to decrease the RV systolic pressure to normal values [46]. The RV HO-1 expression has been shown to be increased and decreased 23977191 respectively in experimental models of RV pressure overload [47] and RV failure [48]. In patients with end-stage congenital heart disease, RV levels of HO-1 were increased with variable magnitude [49]. This suggests that HO-1 expression seems to depend on the stress-induced cardiomyocyte damage and the evolution of RV failure.Ecule(VCAM)-1, interleukin(IL)-33, interleukin 1 receptor-like 1 (ST2), interleukin(IL)-19 and signal transducer and activator of transcription(STAT)-3 in 6-month sham (white bars) and 6-month shunt (black bars) piglets. Panel B: Relative lung tissue protein content for the heme-oxygenase(HO)-1 in 6-month sham (white bars) and 6-month shunt (black bars) piglets. Panel C: Correlation between slope of mPpa/Q relationships and lung protein content for hemeoxygenase(HO)-1, lung mRNA content for intercellular adhesion molecule(ICAM)-1, interleukin(IL)-33 and interleukin(IL)-19. Values expressed as mean6SEM. doi:10.1371/journal.pone.0069470.gresponsible for the non-aggravation of the pulmonary vascular remodeling in the 6-month compared to the 3-month shunted pigs [5,8].In the present study, we found a trend to the decreased expression of HO-1 in the lungs after 6-month systemic-topulmonary shunting. Overexpression of HO-1 16574785 has been shown toInflammation and HO-1 in Right Ventricular FailureFigure 4. Panel A: Relative right ventricular (RV) tissue mRNA content for the heme-oxygenase(HO)-1 and -2, tumor necrosis factor(TNF)-a, intercellular adhesion molecule(ICAM)-1 and -2, vascular cell adhesion molecule(VCAM)-1, interleukin(IL)-33, interleukin 1 receptor-like 1 (ST2), interleukin(IL)-19 and signal transducer and activator of transcription(STAT)-3 in 6-month sham (white bars) and 6-month shunt (black bars) piglets. Relative right ventricular (RV) tissue protein content for the heme-oxygenase(HO)-1 in 6month sham (white bars) and 6-month shunt (black bars) piglets. Correlation between Ees/Ea ratio and right ventricular (RV) protein content for heme-oxygenase (HO)-1 and right ventricular (RV) mRNA content for intercellular adhesion molecule (ICAM)-2. Values expressed as mean6SEM. doi:10.1371/journal.pone.0069470.gprevent the development of hypoxia-induced PH, associated with reduced pulmonary inflammation (characterized by increased macrophage activity and IL-10 expression [40])and vascularremodeling [41?2]. HO-1 mediates in vivo the protective effects in monocrotaline-induced PH and in vitro the anti-proliferative effects in smooth muscle cells of rapamycin [43]. In contrast,Inflammation and HO-1 in Right Ventricular Failurepulmonary HO-1 expression has been shown to be increased in monocrotaline- and monocrotaline/pneumectomy-induced PH [44]. Here, we also showed decreased gene expression of HO-1 in the failing RV. These results suggest a similar tendency to changes in HO-1 in the lungs and the failing RV in the present experimental model of advanced PAH, probably through divergent HO-1 enzymatic products [45]. Indeed, biliverdin has been shown to prevent RV dysfunction, but did not reduce the pulmonary artery remodeling, while inhaled CO reduced the pulmonary vascular remodeling, but did not have any effect on the RV (45). In mice exposed to chronic hypoxia, administration of mesenchymal cells overexpressing HO-1 has been shown to reduce the RV hypertrophy, to stabilize the infarction zones and to decrease the RV systolic pressure to normal values [46]. The RV HO-1 expression has been shown to be increased and decreased 23977191 respectively in experimental models of RV pressure overload [47] and RV failure [48]. In patients with end-stage congenital heart disease, RV levels of HO-1 were increased with variable magnitude [49]. This suggests that HO-1 expression seems to depend on the stress-induced cardiomyocyte damage and the evolution of RV failure.

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