Abstract：
:The present study examines the signal transduction mechanism that is involved in the growth of vascular smooth muscle cells exposed to 4-hydroxynonenal (HNE) in vitro. This aldehyde component of oxidized low-density lipoprotein has been identified in atherosclerotic lesion. Exposure to HNE caused ERK, JNK, and p38 MAP kinase activation as well as the induction of c-fos and c-jun gene expression. AP-1 activity was also significantly induced by HNE treatment. These intracellular activities appear to be the mechanism of HNE-caused mitogenesis. Indeed, HNE induced vascular smooth muscle cell proliferation as determened by Alamar-Blue assay and stimulated DNA synthesis as determined by bromodeoxyuridine incorporation. These observations are consistent with a role of lipid peroxidation products in vascular smooth muscle cell growth in atherogenesis.
journal_name
Life Scijournal_title
Life sciencesauthors
Kakishita H,Hattori Ydoi
10.1016/s0024-3205(01)01166-3subject
Has Abstractpub_date
2001-06-29 00:00:00pages
689-97issue
6eissn
0024-3205issn
1879-0631pii
S0024320501011663journal_volume
69pub_type
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