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KMID : 0357019960120020148
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Journal of the Korean Vascular Surgery Society
1996 Volume.12 No. 2 p.148 ~ p.158
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Effects of Density-Dependent Conditioned Medium of Endothelial Cells on Smooth Muscle Cell Proliferation
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박호철
배영만/오수명/주홍재/박재경
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Abstract
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Vascular wall biology is under intense study by researchers interested in the cause of intimal hyperplasia and atherosclerosis. In vivo studies of vascular wall disease are limited by difficulty controlling numerous variables in a complex
environment.
This has led to study of cellular process in vitro, where these variables can be more precisely controlled. A role for interactions between endothelial cells(EC) and smooth muscle cells(SMC) in vascular growth control has been suggested by
developmental
studies. Although it is well documented that EC produce a vairety of diffusible factors known to influence SMC behavior, the signals that regulate the expression of these factors in EC and the precise role that EC-SMC interactions play in
vascular
growth control remain elusive.
During vessel deyelopment, both EC and SMC grow and proliferate, but once the blood vessel matures, these cells rarely divide. The Author hypothesize that EC are ivolved in the control of SMC proliferation. In this study the author provide
evidence
for
the density-dependent production of a novel SMC growth inhibitor by EC.
And to better stimualte the vascular wall in an invitro environment, EC and SMC are grown on opposite side of a thin semipermeable collagen membrane with a molecular weight cutoff 2,000 da. This technique maintains the normal luminal/abluminal
orientatio of the EC and SMC and allows the cells to grow within close proximity, limiting the diffusion barrier for potential biologic mediators.
@ES The results were as follows;
@EN 1) Preconfluent conditioned medium(CM) of HUVEC stimulated SMC proliferation and postconfluent CM of HUVEC inhibited SMC proliferation. And also SMC DNA content and 3H-thymidine incorporation was increased by preconfluent CM and decreased by
postconfluent CM.
2) Preconfluent CM of BAEC also stimulated SMC proliferation(13%) and postcofluent CM of BAEC inhibited SMC proliferation(5.95%).
3) Preconfluent HUVEC/SMC coculture stimulated SMC proliferation(7.0%) and postconfluent HUVEC/SMC coculture inhibited SMC proliferation(13.67%). And 3H-thymidine incorporation of SMC was increased 24.0% by preconfluent HUVEC/SMC coculture but
decreased 10.48% by postconfluent HUVEC/SMC coculture.
4) Preconfluent CM of BAEC/SMC coculture stimulated SMC proliferation(18.0%) and postconfleunt CM of BAEC/SMC coculture inhibited(14.11%).
As a conclusion, this study suggest the inhibitor of SMC secreted from EC is smaller than 2,000 dalton and is not well known biologic mediator.
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KEYWORD
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