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Tbx5-dependent pathway regulating diastolic function in congenital heart disease

Zhu, Yonghong, Gramolini, Anthony O., Walsh, Mark A., Zhou, Yu-Qing, Slorach, Cameron, Friedberg, Mark K., Takeuchi, Jun K., Sun, Hui, Henkelman, R. Mark, Backx, Peter H., Redington, Andrew N., MacLennan, David H., Bruneau, Benoit G.·2008·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.0801779105
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Abstract

At the end of every heartbeat, cardiac myocytes must relax to allow filling of the heart. Impaired relaxation is a significant factor in heart failure, but all pathways regulating the cardiac relaxation apparatus are not known. Haploinsufficiency of the T-box transcription factor Tbx5 in mouse and man causes congenital heart defects (CHDs) as part of Holt–Oram syndrome (HOS). Here, we show that haploinsufficiency of Tbx5 in mouse results in cell-autonomous defects in ventricular relaxation. Tbx5 dosage modulates expression of the sarco(endo)plasmic reticulum Ca 2+ -ATPase isoform 2a encoded by Atp2a2 and Tbx5 haploinsufficiency in ventricular myocytes results in impaired Ca 2+ uptake dynamics and Ca 2+ transient prolongation. We also demonstrate that Tbx5 can activate the Atp2a2 promoter. Furthermore, we find that patients with HOS have significant diastolic filling abnormalities. These results reveal a direct genetic pathway that regulates cardiac diastolic function, implying that patients with structural CHDs may have clinically important underlying anomalies in heart function that merit treatment.

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Research works printed but not linked: 37

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Metadata

Authors
Zhu, Y., Gramolini, A. O., Walsh, M. A., Zhou, Y.-Q., Slorach, C., Friedberg, M. K., Takeuchi, J. K., Sun, H., Henkelman, R. M., Backx, P. H., Redington, A. N., MacLennan, D. H., & Bruneau, B. G.
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2008-04-08
Volume
105
Issue
14
Pages
5519-5524
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.0801779105
Cited by
65
References
0
Language
en

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