Transgenic animal models for hypertension research

Paul, Martin; Franz, Wolfgang-Michael

doi:10.1016/1050-1738(95)00053-c

Cited by 3 publications

(3 citation statements)

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“…In terms of altered functional activity, the final yield is low, and consequently, the financial cost is usually rather high. Transgenic animals are becoming a new tool accessible to physiologists and pharmacologists because there are now a number of transgenic animals commercially available such as the transgenic strains of hypertensive rats [Reviewed in [1][2][3][4][5][6]. The microinjected DNA can be a complete, already present gene, including its own promoter, used to induce overexpression by multiplying the coding sequences.…”

Section: Gene Transfers Using Transgenic Technologymentioning

confidence: 99%

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Transgenic models of myocardial dysfunction

Swynghedauw

1997

Heart Failure Rev

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Transgenic Technology (TT), is an important tool in the molecular biology arena. It allows one to generate new strains of mice in which a genetic construct is expressed. The construct can be made with a promoter that allows for the targeted expression of a gene of interest to a given part of the cardiovascular system. By so doing, it is possible to modify a given physiologic function and to better understand the structural and functional relationships. This so-called "reverse physiology" is becoming extensively utilized in cardiac research. Another possibility is to use this technology to analyze which part of a promoter is responsible for the transcriptional regulation. In that case, the coding sequence is a gene not normally expressed in the tissue and is called the reporter. Mice are generally used for such a purpose because of their cost. Consequently the physiology of the mouse has been developed using microtechnologies.Several models of cardiac hypertrophy or tumors have been developed using genes encoding various transcriptional factors, such as oncoproteins or skeletal myogenic regulators. The overexpression of the two ~-Adrenergic Receptors (AR), did not generate hypertrophy, while that of al~-AR did. Myocardial function has been studied after disruption or overexpression of genes known to be vital to the functioning of the myocardium. Disruption of phospholamban results in increased relaxation and contractility. The overexpression of both the ~1-and ~2-AR increases basal contractility, which becomes insensitive to isoproterenol. We have also found in our laboratory that the enhanced ~I-AR model has an impaired heart rate variability without arrhythmias or shortening of the life span. An overexpression of Gs~ or ~-AR kinase does not have any inotropic effect per se, but results in an enhanced inotropic and chronotropic effect of isoproterenol. Such experiments have been the basis of new concepts in receptology. Several transgenic models of arterial hypertension with cardiac hypertrophy are now available. Most of them have been created by transgenic manipulations of the renin-angiotensin system. For the moment, there are only a few transgenic models of cardiac failure available.can synthesize DNA or RNA fragments and use them to make proteins or detect rapid changes in the cardiac or vascular structures. Soon after, molecular biologists could not resist the fascinating experiment inherent in introducing a new genetic material into germinal, autosomal, and even in adult cells. This was done in order to change genetic expression, with the ultimate goal of either permanently or transiently, modifying the phenotype of a cell, of a group of cells, and finally of an entire organism.Gene transfer technologies are currently a source of heated debate in cardiovascular research. These technologies offer promising areas for therapeutic approaches, such as the prevention of restenosis after coronary angioplasty. Nevertheless, the time when DNA can be a real drug is unpredictable. In contrast, these technologies, and ...

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Section: Gene Transfers Using Transgenic Technologymentioning

confidence: 99%

“…The genetic studies have failed to demonstrate any association with renin, but have evidenced a linkage with angiotensinogen, and ACE. Transgenic technology has confirmed genetic analysis (Table 5) [Reviewed in 4,11,78,79].…”

Section: Transgenic Models In Hypertension Researchmentioning

confidence: 99%

Transgenic models of myocardial dysfunction

Swynghedauw

1997

Heart Failure Rev

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“…A number of transgenic animal models of the reninangiotensin system have been developed to date, using rat and murine models [44]. However, not all the experimental manipulations undertaken in these animals have resulted in hypertension, despite expression of the transgene.…”

Section: Animal Modelsmentioning

confidence: 99%