These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Blockade of smooth muscle cell migration and proliferation in baboon aortic explants by interleukin-1beta and tumor necrosis factor-alpha is nitric oxide-dependent and nitric oxide-independent.
    Author: Kenagy RD, Clowes AW.
    Journal: J Vasc Res; 2000; 37(5):381-9. PubMed ID: 11025401.
    Abstract:
    Interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNFalpha) are found in injured and atherosclerotic vessels and have been shown to influence smooth muscle cell (SMC) function in vitro. We have investigated the effects of IL-1beta and TNFalpha on SMC migration and proliferation in baboon aortic explants, an in vitro model of arterial injury. Because platelet-derived growth factor (PDGF) is also present in the vessel wall, we have studied the interaction of PDGF with the cytokines. IL-1beta and TNFalpha inhibited migration of SMCs and synthesis of DNA by SMCs. Cell death (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive cells and total DNA) was not altered by the cytokines. The cytokines increased levels of nitrite in the medium and L-nitroarginine partly reversed the inhibitory effects of the cytokines indicating a role for nitric oxide in these inhibitory effects. Treatment with indomethacin partially reversed the inhibition of migration, but not DNA synthesis by IL-1beta suggesting cyclooxygenase products play an inhibitory role in migration. PDGF-BB reversed the inhibitory effect of the cytokines on SMC migration, but not mitogenesis, without changing levels of nitrite in the medium. These data show that IL-1beta and TNFalpha decrease primate SMC migration and proliferation in arterial tissue partly through production of NO, and that PDGF antagonizes the effect of the cytokines. IL-1beta and TNFalpha may act directly to limit injury-induced intimal hyperplasia by decreasing SMC migration and proliferation.
    [Abstract] [Full Text] [Related] [New Search]