Intimai hyperplasia (IH) is a major cause of autologous vein graft failure. The (actors involved in this process are not clearly understood. Testin is a functional protein that promotes the migration of germ cells in the testes and ovaries as well as in the epididymis, kidney and intestine. These observations led us to investigate the role of testin In the development of experimental vein gran IH. Epigastric vein to femoral artery Interposition grafts were performed bilaterally on 32 Sprague-Oawley rats. Grafts were harvested at 6 hours, 2 days, 1 week, 2 weeks and 4 weeks after grafting. Longitudinal sections were studied using a standard histologie, electron microscopic and Immunohistologlc technique. A polyclonal antibody raised in rabbits against rat testin was used to identify testin protein expression. Ungrafted epigastric vein was used as a baseline control. The percentage of cells expressing testin was assessed at each time Interval using a semiquantitative scale: + = 0-20%; ++ = 20-50%; +++ - 50-80%; ++++ = 80-100%. Inflammatory cell Infiltration was observed as early as 6 hours after grafting. Vascular smooth muscle cells were noted to have increased in number by 2 days and to have reached a maximum by 2 weeks. Testin expression at baseline was low (++) and was limited to the immediate subendothelial region. However, by 6 hours, expression had increased dramatically (++++) and was present throughout the graft. Testin expression remained significantly elevated at 2 days (+++) and returned to baseline by 1 week (++) where It remained through the second (++) and fourth weeks (++). The early rise In testin expression corresponded to the migration of inflammatory cells and vascular smooth muscle cells into the graft. These observations suggest a possible role for testin In Initiating the cellular migration that results In vein graft IH.
|State||Published - 1996|