Molecular insights from a novel cardiac troponin I mouse model of familial hypertrophic cardiomyopathy

Tsoutsman, Tatiana; Chung, Jessica; Doolan, Alessandra; Nguyen, Lan Thi Ngoc; Williams, Iwan A.; Tu, Emily; Lam, Lien; Bailey, Charles G.; Rasko, John E.J.; Allen, David G.; Semsarian, Christopher

doi:10.1016/j.yjmcc.2006.07.016

Cited by 32 publications

(64 citation statements)

References 37 publications

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“…8B) (565). Transgenic mouse models corroborate this model of stoichiometric myofilament replacement as transgenic animals also maintain myofilament protein stoichiometry despite an overabundance of sarcomeric transgene transcripts (151, 258,403,567,621,735,872,874,903,999).…”

Section: A Protein Turnover and Stoichiometrymentioning

confidence: 82%

Designing Heart Performance by Gene Transfer

Davis¹,

Westfall²,

Townsend³

et al. 2008

Physiological Reviews

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The birth of molecular cardiology can be traced to the development and implementation of high-fidelity genetic approaches for manipulating the heart. Recombinant viral vector-based technology offers a highly effective approach to genetically engineer cardiac muscle in vitro and in vivo. This review highlights discoveries made in cardiac muscle physiology through the use of targeted viral-mediated genetic modification. Here the history of cardiac gene transfer technology and the strengths and limitations of viral and nonviral vectors for gene delivery are reviewed. A comprehensive account is given of the application of gene transfer technology for studying key cardiac muscle targets including Ca2+handling, the sarcomere, the cytoskeleton, and signaling molecules and their posttranslational modifications. The primary objective of this review is to provide a thorough analysis of gene transfer studies for understanding cardiac physiology in health and disease. By comparing results obtained from gene transfer with those obtained from transgenesis and biophysical and biochemical methodologies, this review provides a global view of cardiac structure-function with an eye towards future areas of research. The data presented here serve as a basis for discovery of new therapeutic targets for remediation of acquired and inherited cardiac diseases.

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Section: A Protein Turnover and Stoichiometrymentioning

confidence: 82%

Designing Heart Performance by Gene Transfer

Davis¹,

Westfall²,

Townsend³

et al. 2008

Physiological Reviews

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show abstract

“…Standard curves were constructed using a serial dilution of the plasmid with the gene of interest inserted. In each case, the gene of interest expression level was normalized to 18s ribosomal RNA and related to the relevant control, as previously described (45,46) and as indicated in the text.…”

Section: Methodsmentioning

confidence: 99%

Adverse effects of high glucose and free fatty acid on cardiomyocytes are mediated by connective tissue growth factor

Wang

McLennan

Allen

et al. 2009

American Journal of Physiology-Cell Physiology

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“…An in vivo study with a cTnI R145G transgenic mouse model also confirmed these results (James et al, 2000). Other animal models recapitulate human FHC findings of myocellular dysfunction preceding structural phenotype; young transgenic cTnI G203S mice display abnormal Ca 2+ cycling with prolonged decay rates of Ca 2+ transients long before phenotypic expression of hypertrophy, fibrosis and myocyte disarray (Tsoutsman et al, 2006). Transgenic rabbits expressing low protein levels of R145G cTnI displayed apical myocyte disarray, interstitial fibrosis, but with only mild ventricular hypertrophy at later ages (1.5 to 2 years of age) (Sanbe et al, 2005).…”

Section: In Vitro and In Vivo Approachesmentioning

confidence: 61%