Abstract:
:To test directly whether fibrin(ogen) is a key binding site for apolipoprotein(a) [apo(a)] in vessel walls, apo(a) transgenic mice and fibrinogen knockout mice were crossed to generate fibrin(ogen)-deficient apo(a) transgenic mice and control mice. In the vessel wall of apo(a) transgenic mice, fibrin(ogen) deposition was found to be essentially colocalized with focal apo(a) deposition and fatty-streak type atherosclerotic lesions. Fibrinogen deficiency in apo(a) transgenic mice decreased the average accumulation of apo(a) in vessel walls by 78% and the average lesion (fatty streak type) development by 81%. Fibrinogen deficiency in wild-type mice did not significantly reduce lesion development. Our results suggest that fibrin(ogen) provides one of the major sites to which apo(a) binds to the vessel wall and participates in the generation of atherosclerosis.
journal_name
Proc Natl Acad Sci U S Aauthors
Lou XJ,Boonmark NW,Horrigan FT,Degen JL,Lawn RMdoi
10.1073/pnas.95.21.12591subject
Has Abstractpub_date
1998-10-13 00:00:00pages
12591-5issue
21eissn
0027-8424issn
1091-6490journal_volume
95pub_type
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