Smooth Muscle Cells Healing Atherosclerotic Plaque Disruptions Are of Local, Not Blood, Origin in Apolipoprotein E Knockout Mice
Author(s) -
Jacob Fog Bentzon,
Claus S. Søndergaard,
Moustapha Kassem,
Erling Falk
Publication year - 2007
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.107.722355
Subject(s) - apolipoprotein e , medicine , bone marrow , pathology , fibrous cap , wound healing , knockout mouse , genetically modified mouse , progenitor cell , bone healing , apolipoprotein b , transgene , stem cell , anatomy , microbiology and biotechnology , biology , immunology , endocrinology , receptor , cholesterol , biochemistry , disease , gene
Signs of preceding episodes of plaque rupture and smooth muscle cell (SMC)-mediated healing are common in atherosclerotic plaques, but the source of the healing SMCs is unknown. Recent studies suggest that activated platelets adhering to sites of injury recruit neointimal SMCs from circulating bone marrow-derived progenitor cells. Here, we analyzed the contribution of this mechanism to plaque healing after spontaneous and mechanical plaque disruption in apolipoprotein E knockout (apoE-/-) mice.
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