doi: 10.1161/CIRCRESAHA.109.199232
© 2009 American Heart Association, Inc.
Letters to the Editor |
Response to the Letter by Frantz and Bauersachs
Experimental Cardiology Laboratory, University Medical Center, Utrecht, The Netherlands, E-mail d.dekleijn@umcutrecht.nl
An extract of the first 100% of the full text is provided, because this article has no abstract. |
We thank Frantz and Bauersachs for their letter. Although 9.4 Tesla MRI is currently the most accurate means to assess cardiac function in mice, we agree that the superiority of MRI alone may not explain the differences in functional outcome. In addition to different imaging techniques, different mouse backgrounds were used in our study (129Bl61) and in the studies referred to in the letter (c57Bl62 and FVB3,4). Because we used the mixed 129Bl6 background, together with the appropriate background controls, the functional outcome in our study was not influenced by any other factor than the genetic deletion of p50.
In general, the p50/p50 homodimer is considered as a repressor of nuclear factor (NF)
B activity.5–7 Deletion of the repressor in the p50 knockout leads to increased expression of tumor necrosis factor-
and interleukin-6 in the infarct area and to increased expression of interleukin-6 after lipopolysaccharide stimulation in vitro. In addition to our study,1 this has also been found in the studies referenced by Frantz and Bauersachs.2–4 This suggests that p50 acts as a repressor in all backgrounds mentioned above and that NF-B activity is in fact increased in p50 knockout mice. Therefore, our functional results and inflammatory data are in line with previous studies demonstrating that the NF-B-mediated inflammatory response following myocardial infarction is involved in cardiac remodeling.8–10
Sources of Funding
None.
Disclosures
None.
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