Roles for Redox Signaling by NADPH Oxidase in Hyperglycemia-Induced Heme Oxygenase-1 Expression in the Diabetic Retina

2013 ◽  
Vol 54 (6) ◽  
pp. 4092 ◽  
Author(s):  
Meihua He ◽  
Hong Pan ◽  
Chunxia Xiao ◽  
Mingliang Pu
Cancer ◽  
2011 ◽  
Vol 118 (13) ◽  
pp. 3433-3445 ◽  
Author(s):  
Melissa M. Singh ◽  
Mary E. Irwin ◽  
Yin Gao ◽  
Kechen Ban ◽  
Ping Shi ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Philip Wenzel ◽  
Heidi Rossmann ◽  
Christian Müller ◽  
Sabine Kossmann ◽  
Canan Simsek ◽  
...  

Background: Heme oxygenase-1 (HO-1) confers protection to the vasculature and suppresses inflammatory properties of monocytes and macrophages. It is unclear how HO-1 activity and expression determine the extent of vascular dysfunction in mice and humans. Methods and results: Decreasing HO activity was parallelled by decreasing aortic HO-1, eNOS and phospho-eNOS (ser1177) protein expression in HO-1 deficient mice, whereas aortic expression of nox2 showed a stepwise increase in HO-1+/- and HO-1-/- mice as compared to HO-1+/+ controls. Aortic superoxide formation increased depending on the extent of HO-1 deficiency and was blunted by the PKC inhibitor chelerythrine, indicating activation of the NADPH oxidase. When subjected to disease models of vascular dysfunction - angiotensin II-infusion (ATII, 0.1mg/kg/d for 7d), streptozotocin-induced diabetes mellitus and aging - HO-1 deficient mice showed an increased vascular dysfunction (shown by isometric tension studies) that was inversely correlated with HO activity. In a primary prevention population based cohort (the Gutenberg Health Study, GHS), we assessed length polymorphisms of the HO-1 promoter region, established a bipolar frequency pattern of allele length (long vs short repeats) in 4937 individuals and found a moderately significant association with flow mediated dilation of the brachial artery (FMD) in individuals with arterial hypertension. Monocytic HO-1 mRNA expression was positively correlated with CD14 expression indicating proinflammatory monocytes (p<0.001) and inversely with FMD in 733 hypertensive individuals of the GHS. ATII-infused HO-1+/+ mice had a significant infiltration of proinflammatory CD11b+Ly6Chi monocytes into the aortic wall, which was sharpely increased in HO-1+/- and HO-1-/- mice, providing a mechanistic link of the monocyte phenotype determined by HO-1 and vascular dysfunction in arterial hypertension. Conclusions: We here present evidence that HO activity and expression and inversely correlates with vascular dysfunction and NADPH oxidase mediated oxidative stress in mice and humans. We conclude, that HO-1 is a regulator of vascular function in hypertension via determining the phenotype of inflammatory circulating and infiltrating monocytes.


Hypertension ◽  
2006 ◽  
Vol 48 (5) ◽  
pp. 950-957 ◽  
Author(s):  
Fan Jiang ◽  
Sarah J. Roberts ◽  
Srinivasa raju Datla ◽  
Gregory J. Dusting

2006 ◽  
Vol 45 (3) ◽  
pp. e78
Author(s):  
Fan Jiang ◽  
Sarah J. Roberts ◽  
Srinivasa Raju Datla ◽  
Gregory J. Dusting

2019 ◽  
Vol 671 ◽  
pp. 69-76 ◽  
Author(s):  
Mengjuan Luo ◽  
Rong Tian ◽  
Ziyi Yang ◽  
Yi-Yuan Peng ◽  
Naihao Lu

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