TY - JOUR
T1 - Interleukin-11 attenuates human vascular smooth muscle cell proliferation
AU - Zimmerman, Michael A.
AU - Selzman, Craig H.
AU - Reznikov, Leonid L.
AU - Raeburn, Christopher D.
AU - Barsness, Katherine
AU - McIntyre, Robert C.
AU - Hamiel, Christine R.
AU - Harken, Alden H.
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
KW - IL-11
KW - Nuclear factor-κB
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UR - http://www.scopus.com/inward/citedby.url?scp=0036302623&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.00987.2001
DO - 10.1152/ajpheart.00987.2001
M3 - Article
C2 - 12063288
AN - SCOPUS:0036302623
SN - 0363-6135
VL - 283
SP - H175-H180
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 1 52-1
ER -