An essential role for gp130 in neointima formation following arterial injury

Dong Wang, Zhimin Liu, Quanyi Li, Manjula Karpurapu, Venkatesh Kundumani-Sridharan, Huiqing Cao, Nagadhara Dronadula, Farhan Rizvi, Arun K. Bajpai, Chunxiang Zhang, Gerhard Müller-Newen, Kevin W. Harris, Rao Gadiparthi

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Interleukin (IL)-6 induced vascular smooth muscle cell (VSMC) motility in a dose-dependent manner. In addition, IL-6 stimulated tyrosine phosphorylation of gp130, resulting in the recruitment and activation of STAT-3. IL-6-induced VSMC motility was found to be dependent on activation of gp130/STAT-3 signaling. IL-6 also induced cyclin D1 expression in a time- and gp130/STAT-3-dependent manner in VSMCs. Suppression of cyclin D1 levels via the use of its small interfering RNA molecules inhibited IL-6-induced VSMC motility. Furthermore, balloon injury induced IL-6 expression both at mRNA and protein levels in rat carotid artery. Balloon injury also caused increased STAT-3 phosphorylation and cyclin D1 expression, leading to smooth muscle cell migration from the media to the intimal region. Blockade of gp130/STAT-3 signaling via adenovirus-mediated expression of dngp130 or dnSTAT-3 attenuated balloon injury-induced STAT-3 phosphorylation and cyclin D1 induction, resulting in reduced smooth muscle cell migration from media to intima and decreased neointima formation. Together, these observations for the first time suggest that IL-6/gp130/STAT-3 signaling plays an important role in vascular wall remodeling particularly in the settings of postangioplasty and thereby in neointima formation.

Original languageEnglish (US)
Pages (from-to)807-816
Number of pages10
JournalCirculation research
Volume100
Issue number6
DOIs
StatePublished - Mar 1 2007

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Neointima
Interleukin-6
Smooth Muscle Myocytes
Cyclin D1
Cell Movement
Wounds and Injuries
Vascular Smooth Muscle
Phosphorylation
Tunica Intima
Carotid Arteries
Adenoviridae
Small Interfering RNA
Tyrosine
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

An essential role for gp130 in neointima formation following arterial injury. / Wang, Dong; Liu, Zhimin; Li, Quanyi; Karpurapu, Manjula; Kundumani-Sridharan, Venkatesh; Cao, Huiqing; Dronadula, Nagadhara; Rizvi, Farhan; Bajpai, Arun K.; Zhang, Chunxiang; Müller-Newen, Gerhard; Harris, Kevin W.; Gadiparthi, Rao.

In: Circulation research, Vol. 100, No. 6, 01.03.2007, p. 807-816.

Research output: Contribution to journalArticle

Wang, D, Liu, Z, Li, Q, Karpurapu, M, Kundumani-Sridharan, V, Cao, H, Dronadula, N, Rizvi, F, Bajpai, AK, Zhang, C, Müller-Newen, G, Harris, KW & Gadiparthi, R 2007, 'An essential role for gp130 in neointima formation following arterial injury', Circulation research, vol. 100, no. 6, pp. 807-816. https://doi.org/10.1161/01.RES.0000261350.61711.9e
Wang D, Liu Z, Li Q, Karpurapu M, Kundumani-Sridharan V, Cao H et al. An essential role for gp130 in neointima formation following arterial injury. Circulation research. 2007 Mar 1;100(6):807-816. https://doi.org/10.1161/01.RES.0000261350.61711.9e
Wang, Dong ; Liu, Zhimin ; Li, Quanyi ; Karpurapu, Manjula ; Kundumani-Sridharan, Venkatesh ; Cao, Huiqing ; Dronadula, Nagadhara ; Rizvi, Farhan ; Bajpai, Arun K. ; Zhang, Chunxiang ; Müller-Newen, Gerhard ; Harris, Kevin W. ; Gadiparthi, Rao. / An essential role for gp130 in neointima formation following arterial injury. In: Circulation research. 2007 ; Vol. 100, No. 6. pp. 807-816.
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