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Articles in PresS, published online ahead of print December 20, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00844.2001
Submitted on September 27, 2001
Accepted on December 13, 2001
* To whom correspondence should be addressed. E-mail: mgupta{at}surgery.bsd.uchicago.edu.
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 analysis of control samples showed expression of four different isoforms of SRF, with ~67kD full-length SRF being the predominant isoform. Interestingly, in failing hearts we found robust expression of a low molecular weight (~52kD) SRF isoform, accompanied by decreased expression of full-length SRF. By RT-PCR and Southern-blot analyses, we characterized this ~52kd SRF isoform as being encoded by an alternatively spliced form of SRF lacking exons 4 and 5 of the SRF primary RNA transcript, so named as SRF-
4,5 isoform. We cloned SRF-4,5 cDNA and showed that over expression of this isoform in cells inhibits SRF-dependent activation of cardiac muscle genes. These results suggest that expression of SRF-4,5 in failing hearts may in part contribute to impaired cardiac gene expression and consequently to the pathogenesis of heart failure.
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