Increased tenascin expression is an early feature of the development of transplant renal arteriopathy in humans.

Abstract

Transplant renal arteriopathy (TRA) is a major obstacle to the long-term survival of human renal allografts. Tenascin (TN) is an extracellular matrix glycoprotein associated with cell growth and differentiation. We investigated TN expression in intrarenal arteries with TRA, in association with cellular components, with phenotypic expression of smooth muscle cells (SMC) and with fibronectin expression. Ten renal allografts that had been removed due to rejection were available. Monoclonal antibodies against SMC, macrophages, T cells, B cells, fibronectin, and TN were used. In the early stages, medial SMC showed a de-differentiated phenotype and the neointima consisted largely of T cells and macrophages. At these stages, increased expression of TN was observed in the media. In later stages, the neointima consisted almost entirely of SMC of a differentiated phenotype and no TN expression was found. Up-regulation of TN may play a role in the migration and phenotypic modulation of SMC at an early stage of TRA in humans.