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S-phase kinase-associated protein-2 (Skp2) promotes vascular smooth muscle cell proliferation and neointima formation in vivo  Yih-Jer Wu, MD, PhD, Graciela.

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Presentation on theme: "S-phase kinase-associated protein-2 (Skp2) promotes vascular smooth muscle cell proliferation and neointima formation in vivo  Yih-Jer Wu, MD, PhD, Graciela."— Presentation transcript:

1 S-phase kinase-associated protein-2 (Skp2) promotes vascular smooth muscle cell proliferation and neointima formation in vivo  Yih-Jer Wu, MD, PhD, Graciela B. Sala-Newby, PhD, Kuo-Tung Shu, PhD, Hung-I. Yeh, PhD, Keiichi I. Nakayama, MD, PhD, Keiko Nakayama, Andrew C. Newby, MA, PhD, Mark Bond, PhD  Journal of Vascular Surgery  Volume 50, Issue 5, Pages (November 2009) DOI: /j.jvs Copyright © 2009 Society for Vascular Surgery Terms and Conditions

2 Fig 1 Neointimal thickening 28 days after common carotid ligation in Skp2+/+ and Skp2−/− mice. Carotid ligation was performed on wild-type or homozygous Skp2-null mice. A, Representative longitudinal sections of from both groups 28 days post-ligation. Arrows locate ligation position. B, Quantification of neointimal areas. The comparison was made using Mann-Whitney test. Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2009 Society for Vascular Surgery Terms and Conditions

3 Fig 2 DN-Skp2 up regulates p27Kip1 levels, inhibits VSMC proliferation and neointima formation in balloon-injured rat common carotid arteries. Balloon-injured rat common carotid arteries were infected with either Ad:βGal (control) or Ad:DN-Skp2 by the luminal retention of 100 μl adenoviral solution (1 × 109 pfu/mL) for 30 minutes. The animals were injected with BrdU (25 mg/kg) at 17, 9, and 1 hour before euthanasia on the day 4 post balloon-injury. A, Representative pictures of arterial sections undergoing staining for p27Kip1, BrdU, phospho-Rb, p21Cip1, 4 days post injury and hematoxylin and eosin staining 14 days post injury, as indicated. Scale bars = 50 μm. Arrows indicate labeled cells. B, Quantified results of the immunohistochemistry and I/M ratios. Data are expressed as % of labeled cells. ** indicates P < .01, * indicates P < .02. Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2009 Society for Vascular Surgery Terms and Conditions

4 Fig 3 Skp2 over expression down regulates p27Kip1 levels and increases VSMC proliferation in minimally-injured rat common carotid arteries. After filament de-endothelialization, carotid arteries were infected with Ad:βGal or Ad:Skp2. A, Representative pictures of both groups. Carotid arterial sections were subjected to immunohistochemistry for the staining of Skp2, p27Kip1, phospho-Rb, p21Cip1 and BrdU 4 days post infection. Of note, Skp2- and BrdU-labeled cells were detected in Ad:βGal infected vessels mostly over the superficial layer of media (arrows), whereas those infected with Ad:Skp2 tended to have Skp2 and BrdU-positive cells trans-medially. Scale bars = 50 μm. Arrows indicate labeled cells. B, Quantification of the immunohistochemistry. Data are expressed as the percentage of labeled cells. ** indicates P < .01, * indicates P < .02. Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2009 Society for Vascular Surgery Terms and Conditions

5 Fig 4 Wild-type Skp2 enhances neointimal thickening in minimally-injured rat carotid arteries. Carotid arteries were treated as in Fig 4. Eight days after filament de-endothelialization, the carotids from both treatment groups were subjected to hematoxylin and eosin staining as described in Fig 2. A, Representative pictures of both groups. Scale bar = 100 μm. B, Quantified results of I/M ratios. Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2009 Society for Vascular Surgery Terms and Conditions

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