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Blood-Borne Origin of Neointimal Smooth Muscle Cells in Transplant Arteriosclerosis

Flip A. Klatter

Paul Nieuwenhuis

Jan Rozing

Transplant arteriosclerosis (TA) is a major complication after solid organ transplantation. TA is characterized by persistent perivascular inflammation and concentric intimal thickening consisting of -actin-positive vascular smooth muscle (VSM) cells. The current view on TA is that donor-derived medial VSM cells of affected arteries migrate and proliferate into the subendothelial space, resulting in luminal narrowing. Following this concept, the VSM cells present in the arteriosclerotic lesions are of donor origin. In this study, the authors analyzed the origin (donor vs recipient) of endothelium (EC) and neointimal -actin-positive VSM cells in 2 different experimental transplant models. Aortic and cardiac allografting was performed in the PVG (RT-1^c) to AO (RT-1^u) rat strain combination. Aorta recipients were not immunosuppressed, whereas cardiac allograft recipients were intrathymically immune modulated to prevent acute rejection. Transplants were performed from female donor to male recipient rats. The -actin-positive VSM cells present in arteriosclerotic lesions, in aortic as well as cardiac allografts, were of recipient, rather than donor, origin. Following aortic allografts, the ECs are completely replaced by host-derived ECs, whereas in cardiac allografts the ECs are still of donor origin.

Key Words: transplantation • chronic rejection • transplant arteriosclerosis • smooth muscle cells

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