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, Christine R. Hamiel, Alden H. Harken

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


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)-κB. The purposes of this study were to examine the effects of IL-11 on human vascular smooth muscle cell (VSMC) proliferation and NF-κB 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-κB p65. Similarly, IL-11 attenuated VSMC expression of two NF-κB-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-κB.

Original languageEnglish (US)
Pages (from-to)H175-H180
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1 52-1
StatePublished - 2002


  • IL-11
  • Nuclear factor-κB

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)
  • Physiology


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