Key result
Infection of NOS-null mice with T. cruzi revealed distinct roles for NOS isoforms, with NOS1-null mice showing increased mortality and LVID, while NOS3-null mice exhibited reduced LVID and RVID.
Why the study?
Does the knockout of specific NO synthase isoforms affect the development of Trypanosoma cruzi-induced cardiomyopathy in mice?
Does the knockout of specific NO synthase isoforms affect the development of Trypanosoma cruzi-induced cardiomyopathy in mice?
Different NO synthase isoforms play distinct roles in the development of Trypanosoma cruzi-induced cardiomyopathy, with NOS1 deficiency worsening outcomes and NOS3 deficiency reducing ventricular dilation.
NOS1 deficiency worsens while NOS3 deficiency attenuates T. cruzi cardiomyopathy in mice; leaves open isoform-specific targeting in human Chagas disease.
Trypanosoma cruzi infection results in an increase in myocardial NO and intense inflammation. NO modulates the T. cruzi-induced myocardial inflammatory reaction. NO synthase (NOS)1-, NOS2-, and NOS3-null mice were infected with T. cruzi (Brazil strain). Infected NOS1-null mice had increased parasitemia, mortality, and left ventricular inner diameter (LVID). Chronically infected NOS1- and NOS2-null and wild-type mice (WT) exhibited increased right ventricular internal diameter (RVID), although the fold increase in the NOS2-null mice was smaller. Infected NOS3-null mice exhibited a significant reduction both in LVID and RVID. Reverse transcriptase-polymerase chain reaction showed expression of NOS2 and NOS3 in hearts of infected NOS1-null and WT mice, whereas infected NOS2-null hearts showed little change in expression of other NOS isoforms. Infected NOS3-null hearts showed an increase only in NOS1 expression. These results may indicate different roles for NOS isoforms in T. cruzi-induced cardiomyopathy.
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Durand et al. (2009) studied Trypanosoma cruzi-induced cardiomyopathy. NOS1, NOS2, and NOS3 gene knockout vs. Wild-type mice was evaluated on Parasitemia, mortality, left ventricular inner diameter (LVID), and right ventricular internal diameter (RVID). Infection of NOS-null mice with T. cruzi revealed distinct roles for NOS isoforms, with NOS1-null mice showing increased mortality and LVID, while NOS3-null mice exhibited reduced LVID and RVID.
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