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Research Article Free access | 10.1172/JCI118658

Chymase in exocytosed rat mast cell granules effectively proteolyzes apolipoprotein AI-containing lipoproteins, so reducing the cholesterol efflux-inducing ability of serum and aortic intimal fluid.

L Lindstedt, M Lee, G R Castro, J C Fruchart, and P T Kovanen

Wihuri Research Institute, Helsinki, Finland.

Find articles by Lindstedt, L. in: JCI | PubMed | Google Scholar

Wihuri Research Institute, Helsinki, Finland.

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Wihuri Research Institute, Helsinki, Finland.

Find articles by Castro, G. in: JCI | PubMed | Google Scholar

Wihuri Research Institute, Helsinki, Finland.

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Wihuri Research Institute, Helsinki, Finland.

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Published May 15, 1996 - More info

Published in Volume 97, Issue 10 on May 15, 1996
J Clin Invest. 1996;97(10):2174–2182. https://doi.org/10.1172/JCI118658.
© 1996 The American Society for Clinical Investigation
Published May 15, 1996 - Version history
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Abstract

Degranulated mast cells are present in human fatty streaks. Chymase in granules released from degranulated rat serosal mast cells, i.e., in granule remnants, proteolyzes human high density lipoprotein3 (HDL3), and so reduces its ability to induce cholesterol efflux from macrophage foam cells in vitro. In this study we found that remnant chymase, by proteolyzing human serum and human aortic intimal fluid, prevents these two physiologic fluids from effectively inducing cholesterol efflux from cultured macrophage foam cells. Inhibition was strongest when remnants were added to apolipoprotein AI (apoAI)-containing lipoproteins; the remnants had no effect on the weaker efflux produced by apoAI-deficient serum. Western blot analysis showed that granule remnants degrade apoAI in serum and in internal fluid. When released from remnants, chymase lost its ability to proteolyze HDL3 in the presence of serum. Thus, remnant chymase (but not isolated chymase) was able to resist the natural protease inhibitors present in serum and in intimal fluid. The results imply participation of exocytosed mast cell granules in foam cell formation in atherogenesis.

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