Objective: To study the kinetics and distribution of smooth muscle cell (SMC) proliferation, phe-notypic modulation, and various extracellular matrix (ECM) components accumulation during vein graft remodeling. Methods...Objective: To study the kinetics and distribution of smooth muscle cell (SMC) proliferation, phe-notypic modulation, and various extracellular matrix (ECM) components accumulation during vein graft remodeling. Methods: Normal vein and vein graft in carotid arteries were examined on d 4, d 7, d 14, d 60 and d180 after bypass grafting with immunohistochemical markers of cellular proliferation (proliferating cell nuclear antigen, PCNA), cytoskeletal protein production (a-actin SMC), myosin heavy chain (MHO iso-forms, ECM proteins, and histochemistry (hematoxylin eosin and Elastica-van Gieson stain). Results: Normal veins demonstrated an extremely low level of cellular proliferation and expressed as adult phenotype SM-Cs in media. After bypass grafting, medial SMCs in the graft appeared to be damaged and began to proliferate on d 4, and subsequently migrated and formed the neointima on d 7. Thereafter, the neointima thickened throughout the 180-day period of the experiment, although the neointimal SMC proliferation decreased after d 14. Meanwhile SMCs underwent a distinct phenotypic change from normal adult type to embryonic type. On d 60, embryonic phenotype SMCs began to return to the adult phenotype, but remain to be present in the neointima for as long as 180 d. ECM components including type I collagen, heparin sulfate proteoglucan (HSPG), and dermatan sulfate proteoglcan (decorin) were detected within the neointima on d 7. Thereafter, the accumulation of ECM increased progressively with time. On d 180, a large amount of ECM components were found in the neointima. HSPG mainly accumulated in the superficial and cellular region of the neointima , decorin, on other hand, located in hypocellular area deep in neointima. Type I collagen scatted in both regions. The elastic fibers became rich and arranged continuously in the neointima. Conclusion: The neointima of vein graft was initially formed by proliferation of the embryonic-type SMCs and then thickened infinitely due to ECM accumulation. Prolonged existence of the embryonic-type SMCs in the neointima may contribute to ECM accumulation and increase in the neointima thickness infinitely, which may predispose accelerated stenosis in the vein graft.展开更多
文摘Objective: To study the kinetics and distribution of smooth muscle cell (SMC) proliferation, phe-notypic modulation, and various extracellular matrix (ECM) components accumulation during vein graft remodeling. Methods: Normal vein and vein graft in carotid arteries were examined on d 4, d 7, d 14, d 60 and d180 after bypass grafting with immunohistochemical markers of cellular proliferation (proliferating cell nuclear antigen, PCNA), cytoskeletal protein production (a-actin SMC), myosin heavy chain (MHO iso-forms, ECM proteins, and histochemistry (hematoxylin eosin and Elastica-van Gieson stain). Results: Normal veins demonstrated an extremely low level of cellular proliferation and expressed as adult phenotype SM-Cs in media. After bypass grafting, medial SMCs in the graft appeared to be damaged and began to proliferate on d 4, and subsequently migrated and formed the neointima on d 7. Thereafter, the neointima thickened throughout the 180-day period of the experiment, although the neointimal SMC proliferation decreased after d 14. Meanwhile SMCs underwent a distinct phenotypic change from normal adult type to embryonic type. On d 60, embryonic phenotype SMCs began to return to the adult phenotype, but remain to be present in the neointima for as long as 180 d. ECM components including type I collagen, heparin sulfate proteoglucan (HSPG), and dermatan sulfate proteoglcan (decorin) were detected within the neointima on d 7. Thereafter, the accumulation of ECM increased progressively with time. On d 180, a large amount of ECM components were found in the neointima. HSPG mainly accumulated in the superficial and cellular region of the neointima , decorin, on other hand, located in hypocellular area deep in neointima. Type I collagen scatted in both regions. The elastic fibers became rich and arranged continuously in the neointima. Conclusion: The neointima of vein graft was initially formed by proliferation of the embryonic-type SMCs and then thickened infinitely due to ECM accumulation. Prolonged existence of the embryonic-type SMCs in the neointima may contribute to ECM accumulation and increase in the neointima thickness infinitely, which may predispose accelerated stenosis in the vein graft.
