Abstract

Significant advances in the development of genetically engineered mice lacking or over-expressing specific proteins has proven to be a powerful research tool. As described in this SCOR proposal, a number of interesting transgenic and gene """"""""knockout"""""""" models will be developed to explore the role of specific enzymes and proteins in the physiology and pathophysiology of the cardiovascular system. The mouse cardiovascular Physiology Core will assist with the characterization of the mouse models. This Core will provide rigorous physiologic evaluation of mouse models including; 1) characterization of the structure and function of the heart and great vessels using trans-thoracic echocardiography, 2) cardiovascular hemodynamic measurements of the mouse circulatory system using open- and closed-chest cardiac catheterization, 3) identification and characterization of cardiac rhythm disturbances in mice using ambulatory telemetric electrocardiographic monitoring, and 4) to evaluate the responses to short-term and long-term exercise studies in mice. The Mouse Cardiovascular Physiology Core will accomplish these goals in dedicated space within the Clinical Sciences Research Building at Washington University School of Medicine. It is anticipated after the evaluation of the mouse models developed in this proposal will identify cardiovascular abnormalities relevant to the pathogenesis of pediatric cardiovascular disease.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Specialized Center (P50)
Project #
5P50HL061006-02
Application #
6302529
Study Section
Project Start
2000-01-01
Project End
2000-12-31
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
2
Fiscal Year
2000
Total Cost
$188,328
Indirect Cost

  Institution

Name
Washington University
Department
Type
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130

  Publications

Jay, Patrick Y; Bielinska, Malgorzata; Erlich, Jonathan M et al. (2007) Impaired mesenchymal cell function in Gata4 mutant mice leads to diaphragmatic hernias and primary lung defects. Dev Biol 301:602-14
Bielinska, M; Kiiveri, S; Parviainen, H et al. (2006) Gonadectomy-induced adrenocortical neoplasia in the domestic ferret (Mustela putorius furo) and laboratory mouse. Vet Pathol 43:97-117
Thomassin, Laetitia; Werneck, Claudio C; Broekelmann, Thomas J et al. (2005) The Pro-regions of lysyl oxidase and lysyl oxidase-like 1 are required for deposition onto elastic fibers. J Biol Chem 280:42848-55
Bielinska, Malgorzata; Genova, Elena; Boime, Irving et al. (2005) Gonadotropin-induced adrenocortical neoplasia in NU/J nude mice. Endocrinology 146:3975-84
Chiu, Hsiu-Chiang; Kovacs, Attila; Blanton, Robert M et al. (2005) Transgenic expression of fatty acid transport protein 1 in the heart causes lipotoxic cardiomyopathy. Circ Res 96:225-33
Broekelmann, Thomas J; Kozel, Beth A; Ishibashi, Hideaki et al. (2005) Tropoelastin interacts with cell-surface glycosaminoglycans via its COOH-terminal domain. J Biol Chem 280:40939-47
Ketola, Ilkka; Otonkoski, Timo; Pulkkinen, Mari-Anne et al. (2004) Transcription factor GATA-6 is expressed in the endocrine and GATA-4 in the exocrine pancreas. Mol Cell Endocrinol 226:51-7
Spiekerkoetter, Ute; Khuchua, Zaza; Yue, Zou et al. (2004) General mitochondrial trifunctional protein (TFP) deficiency as a result of either alpha- or beta-subunit mutations exhibits similar phenotypes because mutations in either subunit alter TFP complex expression and subunit turnover. Pediatr Res 55:190-6
Kozel, Beth A; Ciliberto, Christopher H; Mecham, Robert P (2004) Deposition of tropoelastin into the extracellular matrix requires a competent elastic fiber scaffold but not live cells. Matrix Biol 23:23-34
Peterson 2nd, R A; Kiupel, M; Bielinska, M et al. (2004) Transcription factor GATA-4 is a marker of anaplasia in adrenocortical neoplasms of the domestic ferret (Mustela putorius furo). Vet Pathol 41:446-9

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