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Short Communication |
From the Vascular Biology*
and Transplant
Immunobiology
Groups, the John P.
Robarts Research Institute, and The University of Western
Ontario,
London, Canada; and the Department
of Surgery,
The Johns Hopkins University
School of Medicine, Baltimore, Maryland
Intimal expansion by vascular smooth muscle cells (SMCs) is a
characteristic feature of graft vascular disease. Whether graft intimal
SMCs arise from donor or recipient tissue is not well established but
has important pathogenetic implications. We examined for the presence
of male cells in the expanded intima of sex-mismatched mouse aortic
allografts (C57BL/6-to-BALB/c) at 30 or 60 days after transplant by
in situ hybridization using a Y-chromosome probe. Study
groups included male-to-female allografts, female-to-male
allografts, and female-to-female allografts in recipients
previously engrafted with male bone marrow. Although intimal expansion
developed in all allografts, male-to-female allografts lacked
Y-chromosome-positive intimal cells. In contrast, such cells
were abundant in female-to-male allografts and most of these cells
co-labeled for smooth muscle 
-actin by immunostain. Female-to-female
allografts in recipients with male bone marrow showed a limited number
of intimal Y-chromosome-positive cells. However, none of these
clearly co-labeled for smooth muscle -actin and their numbers
declined throughout time, consistent with graft-infiltrating
inflammatory cells. We conclude that intimal expansion of mouse aortic
allografts is mediated by SMCs that originated from the recipient.
There was little evidence of their derivation from the bone
marrow, suggesting instead the adjacent host aorta as the
primary source of intimal SMCs.
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