Cardioprotective effects of phosphoramidon on myocardial structure and function in murine Chagas' disease

Jelicks, Linda A.; Chandra, Madhulika; Shirani, Jamshid; Shtutin, Vitaliy; Tang, Bin; Christ, George J.; Factor, Stephen M.; Wittner, Murray; Huang, Huan; Weiss, Louis M.; Mukherjee, Shankar; Bouzahzah, Boumediene; Petkova, Stefka B.; Teixeira, Mauro Martins; Douglas, Stephen A.; Loredo, Maria; D’Orléans-Juste, Pedro; Tanowitz, Herbert B.

doi:10.1016/s0020-7519(02)00136-4

Cited by 42 publications

(45 citation statements)

References 43 publications

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“…There was no significant difference in the RVID between infected and uninfected MIP-1α null mice. This result supports the hypothesis that the absence of chemokines such as MIP-1α prevents inflammation and limits the cardiac remodeling that is typically observed in infected mice [13][14][15][16]. Although fractional shortening was not significantly different in the infected C57BL/6×129sv mice, these mice had abnormal wall motion, primarily in the apical region (as described in more detail below).…”

Section: Discussionsupporting

confidence: 83%

“…As predicted based on our previous studies [13][14][15][16], the RV chamber of infected C57BL/ 6×129sv mice exhibited significant dilatation as compared with uninfected C57BL/×6 129sv mice [see RV inner diameter (RVID) in Table 1]. There was no significant difference in the RVID between infected and uninfected MIP-1α null mice.…”

Section: Discussionsupporting

confidence: 64%

“…Many infected individuals remain free of symptoms, but 10−30% of patients will ultimately develop defined clinical syndromes, including chronic myocarditis, cardiomegaly, congestive heart failure, arrhythmias and destruction of skeletal muscles and/or the digestive tract. Mice infected with T. cruzi develop progressive chronic cardiomyopathy similar to that observed in humans [13][14][15][16].…”

Section: Introductionmentioning

confidence: 56%

“…It was also shown that pharmacological blockade of the chemokine receptor, CCR5, prevents chronic inflammation in T. cruzi-infected mice [20]. These studies suggest that the absence of chemokines such as MIP-1α may prevent inflammation during acute and chronic experimental T. cruzi infections and thus limit the cardiac remodeling that is typically observed in infected mice [13][14][15][16].…”

Section: Introductionmentioning

confidence: 88%

“…Acquisition of several multislice imaging data sets at different time points of the cardiac cycle during a 30-to 45-min period of anesthesia was possible under these conditions. Cardiac-gated MRI was performed as described in previous work [11,[13][14][15]. A GE Omega 9.4-T vertical bore MR system (Fremont, CA, USA) with a gradient strength of 75 G/cm provided by an S50 shielded gradient microimaging accessory and a homebuilt 35-mm-inner diameter linear cosine litz coil constructed specifically for mice [11,21] were used for the MRI experiments.…”

Section: Mrimentioning

confidence: 99%

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Dyskinesis in chagasic myocardium: centerline analysis of wall motion using cardiac-gated magnetic resonance images of mice

Durand

Tang

Gutstein

et al. 2006

Magnetic Resonance Imaging

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We report on the use of centerline analysis of cardiac-gated magnetic resonance images to measure wall motion abnormalities in mice infected with Trypanosoma cruzi. To our knowledge, this is the first report of segmental wall motion abnormalities in an animal model of Chagas' disease. Chagas' disease patients with severe cardiac involvement exhibit mild hypokinesis in an extensive region of the left ventricle and dyskinesis in the apical region. We observed dyskinetic segments in a similar region of the hearts of infected wild-type mice. Dyskinesis was not observed in infected mice lacking macrophage inflammatory protein-1α, a chemokine that may play an important role in the cardiac remodeling that is normally observed in mouse models of Chagas' disease and in human patients. This study aimed to demonstrate the utility of cardiac-gated magnetic resonance imaging and centerline analysis as a straightforward method for monitoring regional left ventricular wall motion in transgenic and/or diseased mice.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 56%

Section: Introductionmentioning

confidence: 88%

Section: Mrimentioning

confidence: 99%

See 3 more Smart Citations

Dyskinesis in chagasic myocardium: centerline analysis of wall motion using cardiac-gated magnetic resonance images of mice

Durand

Tang

Gutstein

et al. 2006

Magnetic Resonance Imaging

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Current understanding of immunity to Trypanosoma cruzi infection and pathogenesis of Chagas disease

et al. 2012

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Chagas disease caused by Trypanosoma cruzi remains an important neglected tropical disease and a cause of significant morbidity and mortality. No longer confined to endemic areas of Latin America, it is now found in non-endemic areas due to immigration. The parasite may persist in any tissue, but in recent years there has been increased recognition of adipose tissue both as an early target of infection and a reservoir of chronic infection. The major complications of this disease are cardiomyopathy and megasyndromes involving the gastrointestinal tract. The pathogenesis of Chagas disease is complex and multifactorial involving many interactive pathways. The significance of innate immunity, including the contributions of cytokines, chemokines, reactive oxygen species, and oxidative stress, has been emphasized. The role of the components of the eicosanoid pathway such as thromboxane A2 and the lipoxins has been demonstrated to have profound effects as both pro-and anti-inflammatory factors. Additionally, we discuss the vasoconstrictive actions of thromboxane A2 and endothelin-1n Chagas disease. Human immunity to T. cruzi infection and its role in pathogen control and disease progression have not been fully investigated. However, recently, it was demonstrated that a reduction in the anti-inflammatory cytokine IL-10 was associated with clinically significant chronic chagasic cardiomyopathy.

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Microarray analysis of changes in gene expression in a murine model of chronic chagasic cardiomyopathy

Mukherjee

Belbin

Spray

et al. 2003

Parasitology Research

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Chagas' disease, caused by infection with Trypanosoma cruzi, is a major cause of cardiomyopathy in endemic regions. Infection leads to cardiac remodeling associated with congestive heart failure and dilated cardiomyopathy. In order to study the changes in the gene expression profile due to infection, C57BL/6 x 129sv male mice were infected with 1 x 10(3) trypomastigotes of the Brazil strain of T. cruzi. Histopathological examination of the myocardium revealed chronic inflammation, vasculitis and fibrosis 100 days post-infection. Cardiac magnetic resonance imaging revealed a significantly dilated heart compared with uninfected mice. The relative abundance or depletion of myocardial mRNAs was evaluated using high-density microarrays consisting of 27,400 mouse cDNAs, which were hybridized with fluorescent probes generated from mRNAs of T. cruzi infected and uninfected hearts. Differentially expressed genes were sorted according to their normalized expression patterns and functional groups including those involved in transcription, intracellular transport, structure/junction/adhesion or extracellular matrix, signaling, host defense, energetics, metabolism, cell shape and death. The regulated genes are interpreted in the pathogenesis of chagasic heart disease.

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Cardioprotective effects of phosphoramidon on myocardial structure and function in murine Chagas' disease

Cited by 42 publications

References 43 publications

Dyskinesis in chagasic myocardium: centerline analysis of wall motion using cardiac-gated magnetic resonance images of mice

Dyskinesis in chagasic myocardium: centerline analysis of wall motion using cardiac-gated magnetic resonance images of mice

Current understanding of immunity to Trypanosoma cruzi infection and pathogenesis of Chagas disease

Microarray analysis of changes in gene expression in a murine model of chronic chagasic cardiomyopathy

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