Inhibition of smooth muscle cell proliferation and DNA synthesis by Vasoprin — a biologic response modifier

Vlasic, Niksa; Ramos, Lillian; Mittelman, Abraham; Stemerman, Michael B.

doi:10.1016/0021-9150(93)90178-w

Cited by 2 publications

(2 citation statements)

References 23 publications

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“…This result indicates that balloon injury-induced and gp130/STAT-3-mediated cyclin D1 expression occurs in SMCs rather than in inflammatory cells. Peak aortic SMC proliferation occurs in the medium between the second and third days after balloon injury 33,34 and is followed by the migration of SMCs to intima. Intimal SMC proliferation takes place between the fourth and seventh days after balloon injury.…”

Section: Gp130/stat-3 Signaling Mediates Balloon Injury-induced Cyclimentioning

confidence: 99%

“…Intimal SMC proliferation takes place between the fourth and seventh days after balloon injury. 33,34 Because SMC migration from media to intima is an important factor in the formation of neointima, we next studied the effect of adenovirus-mediated expression of green fluorescent protein (GFP), dngp130, and dnSTAT-3 on balloon injury-induced SMC migration. Compared with the effect of GFP, adenovirus-mediated expression of either dngp130 or dnSTAT-3 inhibited balloon injury-induced SMC migration ( Figure 8A).…”

Section: Gp130/stat-3 Signaling Mediates Balloon Injury-induced Cyclimentioning

confidence: 99%

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An Essential Role for gp130 in Neointima Formation Following Arterial Injury

Wang

Liu

et al. 2007

Circulation Research

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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. (Circ Res. 2007;100:807-816.)

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Section: Gp130/stat-3 Signaling Mediates Balloon Injury-induced Cyclimentioning

confidence: 99%

Section: Gp130/stat-3 Signaling Mediates Balloon Injury-induced Cyclimentioning

confidence: 99%

An Essential Role for gp130 in Neointima Formation Following Arterial Injury

Wang

Liu

et al. 2007

Circulation Research

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Suppression of Activation of Signal Transducer and Activator of Transcription-5B Signaling in the Vessel Wall Reduces Balloon Injury-Induced Neointima Formation

Kundumani‐Sridharan

Wang

Karpurapu

et al. 2007

The American Journal of Pathology

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Previously, we have demonstrated that STAT-5B plays a role in thrombin-induced vascular smooth muscle cell (VSMC) growth and motility. To learn more about the role of STAT-5B in vessel wall remodeling, we examined its involvement in platelet-derived growth factor-BB (PDGF-BB)-stimulated VSMC growth and motility and balloon injury-induced neointima formation. PDGF-BB activated STAT-5B as measured by its tyrosine phosphorylation, DNA binding, and reporter gene activity. PDGF-BB induced cyclin D1 expression, CDK4 activity, and Rb protein phosphorylation, leading to VSMC growth and motility, and these responses were suppressed by the blockade of STAT-5B. Increased cyclin D1 levels, CDK4 activity, and Rb protein phosphorylation were observed in 1-week balloon-injured arteries compared with uninjured arteries, and these responses were also suppressed by adenovirus-mediated expression of dnSTAT-5B. In addition, adenovirus-mediated expression of dnSTAT-5B attenuated balloon injury-induced smooth muscle cell migration from media to intima and their proliferation in intima, resulting in reduced neointima formation. These observations indicate that STAT-5B plays an important role in PDGF-BB-induced VSMC growth and motility in vitro and balloon injury-induced neointima formation in vivo. (Am J

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Inhibition of smooth muscle cell proliferation and DNA synthesis by Vasoprin — a biologic response modifier

Cited by 2 publications

References 23 publications

An Essential Role for gp130 in Neointima Formation Following Arterial Injury

An Essential Role for gp130 in Neointima Formation Following Arterial Injury

Suppression of Activation of Signal Transducer and Activator of Transcription-5B Signaling in the Vessel Wall Reduces Balloon Injury-Induced Neointima Formation

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