[JLR] Good Cholesterol, Good Lungs

JLR

ApoA1-KO lung sections (bottom) show increased level and colocalization of pulmonary 4-hydroxynonenal adducts and transforming growth factor β-1.

High-density lipoprotein is predominantly composed of the apolipoproteins apoAI and apoAII. These apolipoproteins are responsible for collecting lipids from arteries and transporting them back to the liver for reutilization, which provides protection against cardiovascular diseases. While many studies examine the cardiovascular effects of HDL and its apolipoproteins, few have looked at whether these molecules maintain the health of other bodily systems and organs. In this study, the authors show that apoA1 maintains pulmonary function in mice. Along with inhibiting stressors such as proinflammatory HDL formation and the activity of paranoxonase 1 (PON1) and 3-nitrotyrosine (3NT) in the plasma, apoA1 was shown to limit pulmonary inflammation and oxidative stress markers, such as 3NT, 4-hydroxynonenal adducts (4-HNE), transforming growth factor-β (TGFβ), xanthineoxidase, myeloperoxidase and endothelial nitric oxide synthase in the lung milieu. Additionally, apoA1 was shown to enhance arterial relaxation responses, as well as decrease airway hyper-responsiveness and the presence of pulmonary collagen deposition. Thus, apolipoproteins appear to sustain the function of both the pulmonary and cardiovascular systems. Together, these data suggest that apoA1 limits pulmonary inflammation and maintains airway physiology, findings that may clarify observations linking abnormal cholesterol and/or apolipoprotein levels with pulmonary irregularities.

Genetic Deletion of Apolipoprotein A-I Increases Airway Hyperresponsiveness, Inflammation and Collagen Deposition in the Lung

Weiling Wang, Hao Xu, Yang Shi, Sandhya Nandedkar, Hao Zhang, Haiqing Gao, Thom Feroah, Dorothee Weihrauch, Marie L. Schulte, Deron W. Jones, Jason Jarzembowski, Mary Sorci-Thomas and Kirkwood A. Pritchard, Jr.

J. Lipid Res. published online May 24, 2010 

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