scholarly journals Oxidative stress induces heme oxygenase 1 in rat lung microvascular endothelial cells (RLMVECs)

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Mairead A Carroll ◽  
Ben Eng ◽  
Michael I Pucci
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Heme Oxygenase ◽  
Microvascular Endothelial Cells ◽  
Heme Oxygenase 1 ◽  
Rat Lung ◽  
Microvascular Endothelial

Galantamine and carbon monoxide protect brain microvascular endothelial cells by heme oxygenase-1 induction

2008 ◽  
Vol 367 (3) ◽  
pp. 674-679 ◽  
Author(s):  
Atsunori Nakao ◽  
David J. Kaczorowski ◽  
Brian S. Zuckerbraun ◽  
Jing Lei ◽  
Gaetano Faleo ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Endothelial Cells ◽  
Heme Oxygenase ◽  
Microvascular Endothelial Cells ◽  
Heme Oxygenase 1 ◽  
Brain Microvascular Endothelial Cells ◽  
Microvascular Endothelial

Abstract 235: Hypoxia Enhanced Delivery of Mitochondria-Targeted Catalase Protects Choroid Retinal Microvascular Endothelial Cells from Oxidative Stress

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Christopher J Dougherty ◽  
Howard Prentice ◽  
Kathleen Dorey ◽  
Keith A Webster ◽  
Janet C Blanks
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
High Glucose ◽  
Endothelial Permeability ◽  
Luciferase Assay ◽  
Expression Vectors ◽  
Microvascular Endothelial Cells ◽  
Tissue Specific ◽  
Microvascular Endothelial

Loss of pericytes is a critical event early in the progression of microvascular dysfunction in diabetic retinopathy. Pericyte loss may be linked to high glucose mediated reactive oxygen species generation, blocking N-cadherin trafficking to the endothelial cell surface preventing pericyte recruitment and vessel stabilization. Hydrogen peroxide has been identified as a major free radical produced during high glucose exposure in endothelial cells. The goal of this research is to determine if tissue-specific hypoxia-regulated expression of a mitochondria-targeted catalase can prevent or limit RF/6A microvascular endothelial cell apoptosis and decrease vascular permeability by limiting cellular oxidative stress. For the development of tissue-specific and hypoxia-enhanced expression vectors, promoters were constructed with nine tandem combinations of HREs. This 9x HRE oligomer enhancer was inserted together into a pGL3 firefly luciferase plasmid with the Tie2( short ) promoter for endothelial-specific expression. The 9xHRE-Tie2( sh ) promoter construct was highly selective for RF/6A cells producing a basal amount of mitochondria-targeted catalase equivalent to the Tie2( short ) promoter alone. In response to hypoxia ( pO 2 = 1% ), the 9xHRE-Tie2( short ) promoter showed a 21-fold hypoxia-inducible activation similar in strength to the CMV promoter , measured by dual luciferase assay. The hybrid promoters were incorporated into a replication deficient AAV delivery system for apoptosis and cell culture based endothelial permeability assays. In preliminary assays using RF/6A microvascular endothelial cells, apoptosis was reduced by 58% and permeability was reduced by 46%. The results suggest that mitochondria-targeted catalase protects RF/6A microvascular endothelial cells from apoptosis and reduces endothelial permeability in a high-glucose, low-oxygen environment.

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