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Attenuation of Neointima Formation Following Arterial Injury in PAI‐1 Deficient Mice
Author(s) -
PLOPLIS VICTORIA A.,
CASTELLINO FRANCIS J.
Publication year - 2001
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2001.tb03533.x
Subject(s) - neointima , fibrin , medicine , lesion , pathology , vascular disease , anatomy , restenosis , immunology , stent
A bstract : Atherosclerosis is a chronic inflammatory disease in which the fibrinolytic system has been implicated as playing a major role. In order to directly assess the physiological impact an imbalanced fibrinolytic system has on both early and late stages of this disease, mice deficient for PAI‐1 ( PAI‐1 −/− ) were used in a model of vascular injury/repair and compared to wildtype mice ( WT ). Copper‐containing cuffs were placed around the carotid arteries of these mice and the injured arteries were removed at either 7 or 21 days for histological analyses. At both times after injury, fibrin was prevalent in WT arteries, whereas only diffuse in PAI‐1 −/− arteries. At 21 days after injury, a prominent, multilayered neointima was evident in WT arteries, with no evidence of a neointima in PAI‐1 −/− arteries. Results from this study directly confirm the involvement of the fibrinolytic system in vascular repair processes following injury and indicate that fibrin could potentially play a role in lesion formation by stimulating smooth muscle cell proliferation, collagen synthesis, and intracellular cholesterol accumulation.