Magnetic Resonance Imaging and Invasive Evaluation of Development of Heart Failure in Transgenic Mice With Myocardial Expression of Tumor Necrosis Factor-α

Abstract

Background-Transgenic mice expressing tumor necrosis factor-␣ (TNF-␣) in cardiac myocytes develop dilated cardiomyopathy, but the temporal progression to cardiac dysfunction is not well characterized. We asked (1) Does magnetic resonance imaging (MRI) provide a reproducible assessment of cardiac output in mice that correlates with invasive measurements obtained with thermodilution? (2)

Application of cardiac gated magnetic resonance imaging in murine Chagas' disease.

“…Previous studies have focused on measuring LV mass or volume in normal and hypertrophied mouse hearts 4,5,26 or ejection fraction and chamber dilation in mice overexpressing tumor necrosis factor-␣ in the myocardium. [27][28][29] In the present study, we performed serial MRI experiments on mice infected with T. cruzi and demonstrated the utility of MRI in examining morphologic correlates in chronic cardiac disease associated with this infection. We performed several studies on individual mice over a prolonged period of time.…”

“…Magnetic resonance imaging will prove to be an important tool in the evaluation of murine models of Chagas' disease and other experimental cardiomyopathies. 22,[26][27][28][29] …”

Dual in vivo magnetic resonance evaluation of magnetically labeled mouse embryonic stem cells and cardiac function at 1.5 t

“…While previous MR investigations of mouse heart using a 1.5 T clinical scanner have been performed, application of a small-animal coil to image the transplanted mESC and their restorative effects on mouse myocardial infarction model has not been reported (18). This study demonstrated significant restoration of the injured myocardium by transplantation of mESC.…”

Animal models of rheumatoid arthritis: How informative are they?

“…Under the same conditions there was no evidence for any cardiac pathologies or complications (Schurgers et al, 2012). The hTNF model has high systemic inflammation due to over expression of TNF with some evidence that there is lung and cardiac inflammation but this seems to be after targeting these tissues directly rather than an effect of the arthritis model (Franco et al, 1999;Fujita et al, 2001;Tang et al, 2004). Little is known about extra-articular manifestations in the K/BxN model, however there are reports of spontaneous endocarditis alongside arthritis in these mice, interestingly via different pathways (Binstadt et al, 2009).…”