A method of protecting against heart failure

A heart failure, cardiac troponin technology, applied in chemical instruments and methods, biochemical equipment and methods, cardiovascular system diseases, etc.

Inactive Publication Date: 2011-11-23
DUKE UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Thus, forward genetics approaches have had only limited success in identifying novel drug targets

Method used

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  • A method of protecting against heart failure
  • A method of protecting against heart failure
  • A method of protecting against heart failure

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Experimental program
Comparison scheme
Effect test

Embodiment 1

[0045] Experiment details

[0046] Animal care and handling: All mice were handled according to accepted protocols and animal welfare regulations of the Institutional Ethics Committee of Duke University Medical Center. All strains of inbred mice used during this study were obtained from the Jackson Laboratory (Bar Harbor, ME). Transgenic mice overexpressing CSQ (Jones et al, J. Clin. Invest. 101: 1385-1393 (1998), Cho et al, J. Biol. Chem. 274: 22251-22256 (1999)) in DBA / 2J Feeding on a genetic background.

[0047] DBA.AKR-Hrtfm2 congenic mice: Through continuous backcrossing with DBA / 2J, congenic mice harboring the AKR genome sequence at the Hrtfm2 locus were created in the DBA genetic background. In the N2 generation, litters were selected that were heterozygous for Hrtfm2 and homozygous for DBA at other mapped modification sites (Wheeler et al, Mamm. Genome 16:414-423 (2005)). Genotyping of genomic wild-type SNPs was performed with 1449 SNPs using a mouse MD linkage an...

Embodiment 2

[0073] As a first step in confirming the function of the Tnni3k protein in normal cardiomyocytes, its location in mouse heart tissue was investigated. Antiserum specific for human Tnni3k protein was used to probe the location of exogenous (transgenic) protein in Tnni3k transgenic mice. These mice express the human Tnni3k protein from the heart-specific cardiac myosin heavy chain promoter. Importantly, these transgenic mice had been backcrossed into a DBA / 2J background, which did not express detectable endogenous mouse Tnni3k protein. Therefore, any staining is dependent on the presence of the human protein in the mouse tissue. Tnni3k staining (red) showed a streaky staining pattern, consistent with its role as a constituent unit of cardiac sarcomeres ( Figure 13 ). This is the first description of Tnni3k as a structural protein. The sarcomere is the major structural unit of both cardiac and skeletal muscle and is directly responsible for the contractile action of the musc...

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PUM

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Abstract

The present invention relates, in general, to heart failure, and, in particular to a method of reducing the risk of heart failure, particularly in patents with established cardiomyopathy.

Description

[0001] This application claims priority to US Provisional Application No. 61 / 110,323, filed October 31, 2008, which is hereby incorporated by reference in its entirety. [0002] This invention was made with government support under Grant Nos. R01 HL083155, R01 HL68963, and 5 F32HL079863 awarded by the National Institutes of Health. The government has certain rights in this invention. technical field [0003] The present invention relates generally to heart failure, and in particular to methods of reducing the risk of heart failure, particularly in patients with established cardiomyopathy. Background technique [0004] Genetic factors responsible for the development and severity of heart disease have been difficult to identify, in large part because of the challenges posed by the normalization of clinical outcomes in populations. Thus, forward genetics approaches have had limited success in identifying novel drug targets. [0005] Cardiomyopathy model of troponin (CSQ) tran...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): G01N33/68G01N33/58C12Q1/68C07K14/47G01N33/15
CPCC12Q1/485G01N33/5008G01N2333/9121C07K14/47G01N33/5061A61P43/00A61P9/00A61P9/04
Inventor 道格拉斯·A·马尔丘克霍华德·A·罗克曼费林·C·惠勒
Owner DUKE UNIV
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