| Summary: | 碩士 === 國立成功大學 === 生物化學研究所 === 82 === Over the past years, numerous studies have indicated that
oxidatively modified low density lipoprotein (LDL) plays a
critical role in the pathogenesis of atherosclerosis. On the
other hand, arterial smooth muscle cell migration and
proliferation contribute to the development of atherosclerotic
lesions. In the present studies we investigated the effects of
oxidized LDL on the proliferation of smooth muscle cells. The
effect of oxidized LDL on the growth of smooth muscle cells was
assayed by the [3H]-thymidine incorporation into DNA. Results
showed that smooth muscle cells were incubated with oxidized
LDL that was oxidized by incubating with endothelial cells,
copper ion or with combination of both, the incorporation of [3
H]- thymidine into DNA was decreased and the release of lactate
dehydrogenase (LDH) into the medium was increased. But smooth
muscle cells that were incubated with 10% FBS-DMEM released
more LDH, suggested that the inhibitory effect on smooth muscle
cells proliferation was not related to cell damage. On the
other hand, incubation of cells with oxidized LDL and PDGF (10
ng/ml) resulted in a marked dose-dependent inhibition of the
PDGF- induced cell proliferation. Fucoidin, the acetyl-LDL
receptor inhibitor, counld not reverse the smooth muscle cells
proliferation that was inhibited by oxidized LDL. Oxidized LDL
counldn't block PDGF-induced signals, such as DAG formation.
The results suggested that receptor-mediated signal of oxidized
LDL was not a prerequisite for the inhibitory effect on smooth
muscle cells proliferation. The growth signals in smooth muscle
cells could not be reduced by oxidized LDL, suggested that the
inhibitory effect was not related to signal transduction. Ox-
LDL inhibited cell proliferation in cultured smooth muscle by
undefined mechanism.
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