Intimal Lesion (intimal + lesion)

Distribution by Scientific Domains


Selected Abstracts


Arteriopathy in chronic allograft rejection in liver transplantation

LIVER TRANSPLANTATION, Issue 4 2004
Aya Miyagawa-Hayashino
Chronic rejection is an important cause of liver allograft failures. The allograft undergoing chronic rejection shows affected large- and medium-sized muscular arteries with homing of foamy macrophages and enlargement of the intimal area. The objective of this study was to elucidate the pathogenesis of the intimal lesion that causes obliterative arteriopathy by identifying the origin of the foamy macrophages and mesenchymal cells present in the intimal area. Nine allografted livers (6 male and 3 female patients) from sex-mismatched donors undergoing chronic rejection were studied by combined staining of the macrophages or the mesenchymal cells in the intimal area with immunohistochemistry and in situ hybridization using a probe for the human Y chromosome. By using the specimens from female donor allografts transplanted to male recipients, it was found that 62 11% of CD68+ foamy macrophages and 71 4% of smooth muscle actin-positive mesenchymal cells in the intimal lesions and a few interstitial myofibroblasts were positive for the Y chromosome probe. This indicated that they were derived from the recipients. In conclusion, the thickening intimal lesion seen in obliterative vasculopathy in liver allografts consists of the foamy macrophages and mesenchymal cells of recipient origin. These circulating recipient cells migrated to the areas in advance of remodeling arteries. (Liver Transpl 2004;10:513,519.) [source]


The extracellular matrix can regulate vascular cell migration, proliferation, and survival: relationships to vascular disease

INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 3 2000
Elaine W. Raines
The extra cellular matrix (ECM) of the normal artery wall is a collection of fibrous proteins and associated glycoproteins embedded in a hydrated ground substance of glycosaminoglycans and proteoglycans. These distinct molecules are organized into a highly ordered network that are closely associated with the vascular cells that produce them. In addition to providing the architectural framework for the artery wall that imparts mechanical support and viscoelasticity, the ECM can regulate the behaviour of vascular cells, including their ability to migrate, proliferate and survive injury. The composition of the ECM is different within intimal lesions of atherosclerosis, which are composed of monocytes and lymphocytes from the circulation and smooth muscle cells (SMC) that migrate from the media to the intima ( Ross 1993, 1999), and these differences may contribute to the altered phenotype of vascular cells within lesions. This review will briefly outline the ECM changes observed in atherosclerosis and restenosis and the potential relationship of these changes to altered vascular cell functions. [source]


Arteriopathy in chronic allograft rejection in liver transplantation

LIVER TRANSPLANTATION, Issue 4 2004
Aya Miyagawa-Hayashino
Chronic rejection is an important cause of liver allograft failures. The allograft undergoing chronic rejection shows affected large- and medium-sized muscular arteries with homing of foamy macrophages and enlargement of the intimal area. The objective of this study was to elucidate the pathogenesis of the intimal lesion that causes obliterative arteriopathy by identifying the origin of the foamy macrophages and mesenchymal cells present in the intimal area. Nine allografted livers (6 male and 3 female patients) from sex-mismatched donors undergoing chronic rejection were studied by combined staining of the macrophages or the mesenchymal cells in the intimal area with immunohistochemistry and in situ hybridization using a probe for the human Y chromosome. By using the specimens from female donor allografts transplanted to male recipients, it was found that 62 11% of CD68+ foamy macrophages and 71 4% of smooth muscle actin-positive mesenchymal cells in the intimal lesions and a few interstitial myofibroblasts were positive for the Y chromosome probe. This indicated that they were derived from the recipients. In conclusion, the thickening intimal lesion seen in obliterative vasculopathy in liver allografts consists of the foamy macrophages and mesenchymal cells of recipient origin. These circulating recipient cells migrated to the areas in advance of remodeling arteries. (Liver Transpl 2004;10:513,519.) [source]