scholarly journals Heme oxygenase-1 suppresses a pro-inflammatory phenotype in monocytes and determines endothelial function and arterial hypertension in mice and humans

2015 ◽  
Vol 36 (48) ◽  
pp. 3437-3446 ◽  
Author(s):  
Philip Wenzel ◽  
Heidi Rossmann ◽  
Christian Müller ◽  
Sabine Kossmann ◽  
Matthias Oelze ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Arterial Hypertension ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Inflammatory Phenotype

Heme oxygenase-1 induction restores high-blood-flow-dependent remodeling and endothelial function in mesenteric arteries of old rats

2011 ◽  
Vol 29 (1) ◽  
pp. 102-112 ◽  
Author(s):  
Mohamed Lamine Freidja ◽  
Emilie Vessieres ◽  
Nicolas Clere ◽  
Valerie Desquiret ◽  
Anne-Laure Guihot ◽  
...  
Keyword(s):  
Blood Flow ◽  
Endothelial Function ◽  
Heme Oxygenase ◽  
Mesenteric Arteries ◽  
Heme Oxygenase 1 ◽  
Old Rats

Abstract 18540: Heme Oxygenase 1 Activity and Expression Suppresses a Proinflammatory Phenotype in Monocytes and Correlates With Endothelial Function in Mice and Humans

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Philip Wenzel ◽  
Heidi Rossmann ◽  
Christian Müller ◽  
Sabine Kossmann ◽  
Canan Simsek ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Arterial Hypertension ◽  
Heme Oxygenase ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Isometric Tension ◽  
Health Study ◽  
Heme Oxygenase 1 ◽  
Frequency Pattern ◽  
Deficient Mice

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.

scholarly journals 1082: EICOSAPENTAENOIC ACID INCREASES ENDOTHELIAL FUNCTION AND HEME OXYGENASE-1 IN PULMONARY INFLAMMATION

2021 ◽  
Vol 50 (1) ◽  
pp. 539-539
Author(s):  
Samuel Sherratt ◽  
Peter Libby ◽  
Hazem Dawoud ◽  
Deepak Bhatt ◽  
Tadeusz Malinski ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Eicosapentaenoic Acid ◽  
Heme Oxygenase ◽  
Pulmonary Inflammation ◽  
Heme Oxygenase 1

scholarly journals Irisin Regulates Heme Oxygenase-1/Adiponectin Axis in Perivascular Adipose Tissue and Improves Endothelial Dysfunction in Diet-Induced Obese Mice

2017 ◽  
Vol 42 (2) ◽  
pp. 603-614 ◽  
Author(s):  
Ningning Hou ◽  
Gang Du ◽  
Fang Han ◽  
Jin Zhang ◽  
Xiaotong Jiao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Heme Oxygenase ◽  
Ex Vivo ◽  
Heme Oxygenase 1 ◽  
No Production ◽  
Obese Mice ◽  
Perivascular Adipose Tissue ◽  
Tnf Α

Aims: To determine whether irisin could improve endothelial dysfunction by regulating heme oxygenase-1(HO-1)/adiponectin axis in perivascular adipose tissue (PVAT) in obesity. Methods: Male C57BL/6 mice were fed with a high-fat diet (HFD) with or without irisin treatment. Endothelium-dependent vasorelaxation of the thoracic aorta with or without PVAT (PVAT+ or PVAT–) was determined. Western blot was employed to determine the levels of HO-1 and adiponectin in PVAT. UCP-1, Cidea, and TNF-α gene expression in PVAT were tested by real-time PCR. Results: The presence of PVAT significantly impaired endothelial function in the HFD mice. Treatment of HFD mice with irisin significantly restored this impairment and improved endothelial function in vivo or ex vivo. Incubated aortic rings (PVAT-) with PVAT-derived conditioned medium (CM) from HFD mice impaired endothelial function in control mice. This impairment was prevented by incubating the aortic rings (PVAT-) from HFD mice with PVAT-derived CM from irisin. However, the beneficial effects were partly attenuated in the presence of HO-1 inhibitor and adiponectin receptor blocking peptide. Treatment of HFD mice with irisin significantly increased NO production, protein levels of HO-1 and adiponectin, mRNA expressions of UCP-1 and Cidea, and decreased superoxide production and TNF-α expression in PVAT. Conclusion: Irisin improved endothelial function by modulating HO-1/ adiponectin axis in PVAT in HFD-induced obese mice. These findings suggest that regulating PVAT function may be a potential mechanism by which irisin improves endothelial function in obesity.

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