Title of article :
Immunohistochemical phenotypic alterations of rabbit autologous vein grafts implanted under arterial circulation with or without poor distal runoff-implications of vein graft remodeling
Author/Authors :
Masaru Ishida، نويسنده , , Kimihiro Komori، نويسنده , , Yoshikazu Yonemitsu، نويسنده , , Kenichi Taguchi، نويسنده , , Toshihiro Onohara، نويسنده , , Keizo Sugimachi، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2001
Pages :
10
From page :
345
To page :
354
Abstract :
Although intimal hyperplasia is a major cause limiting the long-term patency of the vein grafts, its precise mechanisms, including the effect of poor runoff, has not yet been well characterized. We thus designed the present study to try to determine the effect of poor runoff arterial flow to the phenotypic alterations of the graft wall by immnohistochemistry using anti-intermediate filaments (α-SM actin, desmin, and vimentin) and anti-myosin heavy chain (SM1, SM2, and SMemb) specific antibodies. Vein grafts implanted under the poor runoff hind limb of rabbits showed enhanced intimal hyperplasia, however, no apparent difference in the cytoskeleton expression, including intermediate filaments and MHC, between two groups until 4 weeks. Interestingly, six of eight vein grafts at 2 weeks after implantation in both groups showed the accumulations of perivascular fibroblast-like phenotype (negative for SM1, α-SM actin, and desmin) in some parts of the outer neointima, whereas the inner neointima at 2 weeks and the whole neointima at 4 weeks were mainly occupied by a smooth muscle phenotype (positive for these three). Although the cellular origin of these cells is still unknown, these results suggest that the migration of non-muscle mesenchymal cells is involved in the neointima and thus may provide a clue for better understanding vein graft remodeling.
Keywords :
myosin heavy chain , Poor runoff , intimal hyperplasia
Journal title :
Atherosclerosis
Serial Year :
2001
Journal title :
Atherosclerosis
Record number :
630221
Link To Document :
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