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Disruption of Striated Preferentially Expressed Gene Locus Leads to Dilated Cardiomyopathy in Mice

Disruption of Striated Preferentially Expressed Gene Locus Leads to Dilated Cardiomyopathy in Mice Heart Failure Disruption of Striated Preferentially Expressed Gene Locus Leads to Dilated Cardiomyopathy in Mice Xiaoli Liu, MD, PhD*; Tripurasundari Ramjiganesh, PhD*; Yen-Hsu Chen, MD, PhD; Su Wol Chung, PhD; Sean R. Hall, PhD; Scott L. Schissel, MD, PhD; Robert F. Padera, Jr, MD, PhD; Ronglih Liao, PhD; Kate G. Ackerman, MD; Jan Kajstura, PhD; Annarosa Leri, MD; Piero Anversa, MD; Shaw-Fang Yet, PhD; Matthew D. Layne, PhD; Mark A. Perrella, MD Background—The striated preferentially expressed gene (Speg) generates 4 different isoforms through alternative promoter use and tissue-specific splicing. Depending on the cell type, Speg isoforms may serve as markers of striated or smooth muscle differentiation. Methods and Results—To elucidate function of Speg gene isoforms, we disrupted the Speg gene locus in mice by replacing common exons 8, 9, and 10 with a lacZ gene. -Galactosidase activity was detected in cardiomyocytes of the developing heart starting at day 11.5 days post coitum (dpc). -Galactosidase activity in other cell types, including vascular smooth muscle cells, did not begin until 18.5 dpc. In the developing heart, protein expression of only Speg and Speg isoforms was present in cardiomyocytes. Homozygous Speg mutant hearts began to enlarge by 16.5 dpc, and by 18.5 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Circulation Wolters Kluwer Health

Disruption of Striated Preferentially Expressed Gene Locus Leads to Dilated Cardiomyopathy in Mice

Circulation , Volume 119 (2) – Jan 1, 2009

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References (47)

ISSN
0009-7322
eISSN
1524-4539
DOI
10.1161/CIRCULATIONAHA.108.799536
pmid
19118250
Publisher site
See Article on Publisher Site

Abstract

Heart Failure Disruption of Striated Preferentially Expressed Gene Locus Leads to Dilated Cardiomyopathy in Mice Xiaoli Liu, MD, PhD*; Tripurasundari Ramjiganesh, PhD*; Yen-Hsu Chen, MD, PhD; Su Wol Chung, PhD; Sean R. Hall, PhD; Scott L. Schissel, MD, PhD; Robert F. Padera, Jr, MD, PhD; Ronglih Liao, PhD; Kate G. Ackerman, MD; Jan Kajstura, PhD; Annarosa Leri, MD; Piero Anversa, MD; Shaw-Fang Yet, PhD; Matthew D. Layne, PhD; Mark A. Perrella, MD Background—The striated preferentially expressed gene (Speg) generates 4 different isoforms through alternative promoter use and tissue-specific splicing. Depending on the cell type, Speg isoforms may serve as markers of striated or smooth muscle differentiation. Methods and Results—To elucidate function of Speg gene isoforms, we disrupted the Speg gene locus in mice by replacing common exons 8, 9, and 10 with a lacZ gene. -Galactosidase activity was detected in cardiomyocytes of the developing heart starting at day 11.5 days post coitum (dpc). -Galactosidase activity in other cell types, including vascular smooth muscle cells, did not begin until 18.5 dpc. In the developing heart, protein expression of only Speg and Speg isoforms was present in cardiomyocytes. Homozygous Speg mutant hearts began to enlarge by 16.5 dpc, and by 18.5

Journal

CirculationWolters Kluwer Health

Published: Jan 1, 2009

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