Display Settings:


Send to:

Choose Destination
Ann Thorac Surg. 1999 May;67(5):1227-31; discussion 1231-2.

The NFkappaB inhibitory peptide, IkappaBalpha, prevents human vascular smooth muscle proliferation.

Author information

  • 1Department of Surgery, University of Colorado Health Sciences Center, Denver 80262, USA. craig.selzman@UCHSC.edu



Vessel injury results in an inflammatory response characterized by the elaboration of cytokines and growth factors, which ultimately influence vascular smooth muscle cell (VSMC) growth and contribute to atherogenesis. Nuclear factor-kappa B (NFkappaB) is a central transcription factor important in mediating stress and inflammatory-induced signals. We hypothesized that strategies aimed at inhibiting NFkappaB would abrogate mitogen-induced human VSMC proliferation.


Human aortic VSMC were stimulated with basic fibroblast growth factor (FGF) and tumor necrosis factor-alpha (TNF), and proliferation was quantified by a colormetric assay. The influence of NFkappaB on VSMC proliferation was examined by both nonspecific NFkappaB blockade with calpain inhibitor-1 (CI-1) and dexamethasone (Dex) and specific NFkappaB blockade with liposomal delivery of the NFkappaB inhibitory peptide, IkappaBalpha.


FGF and TNF induced concentration-dependent VSMC proliferation (p < 0.002). Neither CI-1, Dex, nor liposomal IkappaBalpha influenced proliferation of unstimulated VSMC. However, both FGF- and TNF-stimulated VSMC proliferation was inhibited to the level of control with CI-1, Dex, and liposomal IkappaBalpha (p < 0.001).


The mitogenic effect of FGF and TNF on human arterial VSMC may be prevented by inhibiting NFkappaB. Furthermore, liposomal delivery of endogenous inhibitory proteins such as IkappaBalpha may represent a novel, therapeutically accessible method for selective transcriptional suppression in the response to vascular injury.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk