Vol. 283, Issue 1, H175-H180, July 2002
Interleukin-11 attenuates human vascular smooth muscle cell
proliferation
Michael A.
Zimmerman,
Craig
H.
Selzman,
Leonid L.
Reznikov,
Christopher D.
Raeburn,
Katherine
Barsness,
Robert C.
McIntyre Jr.,
Christine R.
Hamiel, and
Alden H.
Harken
Division of Cardiothoracic Surgery, University of
Colorado Health Sciences Center, Denver, Colorado 80262
Interleukin (IL)-11 is a growth factor
for megakaryocytes, osteoclasts, and intestinal mucosa. IL-11 is also
an anti-inflammatory agent, mediating many of its effects by inhibition
of the transcriptional activator nuclear factor (NF)-
B. The purposes
of this study were to examine the effects of IL-11 on human vascular
smooth muscle cell (VSMC) proliferation and NF-B activity. VSMC were
cultured from human transplant donor aortas, stimulated with basic
fibroblastic growth factor (bFGF), and treated with IL-11. VSMC
stimulated with bFGF demonstrated an increase in cell number by direct
cell counting and mitochondrial activity. IL-11 caused a
concentration-dependent decrease in bFGF-induced VSMC proliferation.
Furthermore, IL-11 attenuated bFGF-induced increases in cytoplasmic and
intranuclear unbound NF-B p65. Similarly, IL-11 attenuated VSMC
expression of two NF-B-dependent cytokines, IL-8 and IL-6.
Stimulated VSMC did not secrete IL-11, suggesting that endogenous IL-11
did not account for our observations. In conclusion, IL-11 inhibits
human VSMC proliferation in vitro and is associated with suppression of
NF-B.
IL-11; nuclear factor-B
