R-Ras is a global regulator of vascular regeneration that suppresses intimal hyperplasia and tumor angiogenesis (Nat Med, 2005, 11:1346-1350)

報告日期: 2006/03/24
報告時間: 16:00/16:50
報告學生: 黃議賢
講評老師: 呂增宏
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R-Ras is a global regulator of vascular regeneration that suppresses intimal hyperplasia and tumor angiogenesis

Nat Med. 2005 Dec;11(12):1346-50.

 

Time: Mar. 24. 2006, 16:00-16:50

Place: Room 602

Speaker: 黃議賢

Commentator: 呂增宏 老師

 

Abstract:

R-Ras is a GTP-binding protein highly and homologus to H-Ras protein.  Previous studies shown that R-Ras promotes apoptosis induced by growth factors deprivation,   and the transforming activity of R-Ras was very low compared with H-Ras and K-Ras.  Thus, it seems that R-Ras may have activity distinct from the transforming Ras protein.  In this study, they used R-Ras-null mice to explore the function in vivo.  They found that the R-Ras-null mice were fertile and shown no obvious abnormalities and their tissues appear normal upon histological examination.  Through whole tissues screen the expression of R-Ras protein in wild-type mice, which was primarily confined to smooth muscle in various tissues and organs.  In artery injury and tumor implantation model, they found neointimal thickening was greatly increased and increased angiogenesis in tumor implantation in R-Ras-null mice.  This phenomena could be restore by exogenous activated R-Ras (R-Ras38V and R-Ras87L).  These results suggest that enhanced neointimal growth and tumor angiogenesis caused by loss of R-Ras expression may be related to the ability of R-Ras to promote cellular differentiation.

 

References:

1.         Komatsu M, Ruoslahti E.  R-Ras is a global regulator of vascular regeneration that suppresses intimal hyperplasia and tumor angiogenesis.  Nat Med. 2005 Dec;11(12):1346-50.

2.         Moiseeva EP.  Adhesion receptors of vascular smooth muscle cells and their functions.  Cardiovasc Res. 2001 Dec;52(3):372-86.