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Surfactant protein D is proatherogenic in mice
Grith L Sorensen1, Jens Madsen, Karin Kejling
1Medical Biotechnology Center, University of Southern Denmark, Winsloewparken 25,3, 5000 Odense C, Denmark.
American Journal of Physiology. Heart and Circulatory Physiology
|January 3, 2006
Summary
Surfactant protein D (SP-D) deficiency reduces atherosclerosis development in mice by improving lipid metabolism and reducing inflammation. SP-D appears to be proatherogenic, impacting cholesterol levels and inflammatory markers.
Area of Science:
- Cardiovascular Biology
- Immunology
- Lipid Metabolism
Background:
- Surfactant protein D (SP-D) is an innate immune molecule involved in pathogen clearance and inflammation.
- SP-D influences lipid homeostasis, with pulmonary phospholipid accumulation noted in SP-D-deficient mice.
- Atherosclerosis involves inflammation and lipid deposition, suggesting a potential role for SP-D.
Purpose of the Study:
- To investigate the role of SP-D in the development of atherosclerosis.
- To determine if SP-D influences lipid metabolism and inflammatory processes relevant to atherogenesis.
Main Methods:
- Comparison of atherosclerotic lesion areas in SP-D-deficient (Spd-/-) mice and wild-type mice on an atherogenic diet.
- Analysis of plasma lipid profiles (HDL-C, total cholesterol, LDL-C) and TNF-alpha levels.
- Treatment of Spd-/- mice with a recombinant human SP-D fragment.
Main Results:
- Spd-/- mice exhibited significantly smaller atherosclerotic lesion areas (5.6-fold reduction) in aortic roots.
- Spd-/- mice showed elevated HDL cholesterol and reduced plasma TNF-alpha.
- Recombinant SP-D treatment decreased HDL-C, total cholesterol, and LDL-C in Spd-/- mice.
Conclusions:
- SP-D is proatherogenic in this mouse model.
- SP-D deficiency confers protection against atherosclerosis, likely due to improved lipid metabolism and altered inflammatory responses.
- SP-D's role in lipid homeostasis and inflammation impacts its contribution to atherosclerosis.
