AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 282: H1521-H1533, 2002. First published December 20, 2001; doi:10.1152/ajpheart.00844.2001
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Vol. 282, Issue 4, H1521-H1533, April 2002

Increased expression of alternatively spliced dominant-negative isoform of SRF in human failing hearts

Francesca J. Davis1, Madhu Gupta2,3, Steven M. Pogwizd3,4, Emile Bacha1, Valluan Jeevanandam1, and Mahesh P. Gupta1

1 Department of Surgery (Cardiac and Thoracic), University of Chicago, Chicago 60637; 2 The Heart Institute for Children, Hope Children's Hospital, OakLawn 60453; and Departments of 3 Physiology and Biophysics and 4 Medicine (Cardiology), University of Illinois at Chicago, Chicago, Illinois 60612

Serum response factor (SRF) has been shown to play a key role in cardiac cell growth and muscle gene regulation. To understand the role of SRF in heart failure, we compared its expression pattern between control and failing human heart samples. Western blot analysis of control samples showed expression of four different isoforms of SRF, with ~67-kDa full-length SRF being the predominant isoform. Interestingly, in failing hearts we found robust expression of a low-molecular-mass (~52 kDa) SRF isoform, accompanied by decreased expression of full-length SRF. By RT-PCR and Southern blot analyses, we characterized this ~52-kDa SRF isoform as being encoded by an alternatively spliced form of SRF lacking exons 4 and 5 of the SRF primary RNA transcript (SRF-Delta 4,5 isoform). We cloned SRF-Delta 4,5 cDNA and showed that overexpression of this isoform into cells inhibits SRF-dependent activation of cardiac muscle genes. These results suggest that expression of SRF-Delta 4,5 in failing hearts may in part contribute to impaired cardiac gene expression and consequently to the pathogenesis of heart failure.

serum response factor; cardiac hypertrophy; cardiac gene regulation; alternative gene splicing


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