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J Thorac Cardiovasc Surg 2006;132:1355
© 2006 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Discussion

The first 20% of the full text of this article appears below.

Dr Robert M. Mentzer (Detroit, Mich). Dr Mieno, I congratulate you and your colleagues on your efforts to help us better understand the impact of aging on VEGF-stimulated angiogenesis. The magnitude of your work should not be underestimated. The use of a preparation that allows one to assess the effect of various stimuli in the presence and absence of VEGF on the microcirculation of human atrial tissue is quite innovative and represents a significant achievement in itself.

The first question I have for you relates to your findings in regard to the intracellular signaling events. As you are aware, there are numerous signaling molecules that have been associated with VEGF. I am curious to learn more about the rationale you used for the selection of the molecules you elected to study, since there are numerous other distant pathway signaling molecules that have been implicated in VEGF-stimulated angiogenesis. These include the mitogen-activated protein kinases, the p38 MAPK, phospholipase C, and protein kinase C.

Dr Mieno. In this study, we looked at specific VEGFR2 signaling pathways, because the VEGFR2 signaling pathway is more important for the development of angiogenesis . . . [Full Text of this Article]


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Aging is associated with an impaired coronary microvascular response to vascular endothelial growth factor in patients
Shigetoshi Mieno, Munir Boodhwani, Richard T. Clements, Basel Ramlawi, Neel R. Sodha, Jian Li, and Frank W. Sellke
J. Thorac. Cardiovasc. Surg. 2006 132: 1348-1355. [Abstract] [Full Text] [PDF]





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