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J Thorac Cardiovasc Surg 2006;132:1270-1271
© 2006 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease

Discussion

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

Dr Robert C. Robbins (Stanford, Calif). You went through it very quickly, but this is a tour de force; technically it is a very difficult model and you are to be congratulated for getting the animals through this. Also impressive is the sophisticated use of molecular genetics that you used here to help answer important questions. Certainly heart failure is an important public health issue. Finally, the experimental therapeutic approach to try to identify potential targets for developing small molecules or other strategies to treat heart failure is impressive.

I have just a couple of comments and questions for you.

GATA-4 and NKx2.5 are things that we are looking at as embryonic stem cells differentiate into cardiac myocytes. I thought it was interesting that you targeted these particular transcription factors. You mentioned the isoform shift of cardiac myosin in your manuscript, and a lot of work has been done by Jeff Robbins in this area. I would like to note that you mentioned cardiac myosin. Because it is so important in allograft rejection and autoimmune disease, can you comment on what you found with cardiac myosin specifically?

Dr Azakie. We used the MF20 antibody, which selects . . . [Full Text of this Article]


Related Article

Myocardial transcription factors are modulated during pathologic cardiac hypertrophy in vivo
Anthony Azakie, Jeffrey R. Fineman, and Youping He
J. Thorac. Cardiovasc. Surg. 2006 132: 1262-1271. [Abstract] [Full Text] [PDF]





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