Key result
Antiphospholipid antibodies showed no association with heart valve pathology, as thickened heart valves were present in 68% of MRL-lpr/lpr mice and 80% of Balb/c controls.
Why the study?
Does the presence of antiphospholipid antibodies associate with heart valve lesions in MRL-lpr/lpr mice?
Does the presence of antiphospholipid antibodies associate with heart valve lesions in MRL-lpr/lpr mice?
In a murine model of antiphospholipid syndrome, antiphospholipid antibodies were not associated with heart valve pathology.
Answers are grounded in this paper and cite their sources.
No association in this murine model; leaves open whether antiphospholipid antibodies drive valve lesions in human disease.
Our objective in this study was to determine possible associations between antiphospholipid antibodies (aPL) and histologically defined heart valve lesions in the MRL-lpr/lpr mouse, a suitable model for the antiphospholipid syndrome (APS). At monthly intervals, from 2 to 6 months of age, three MRL-lpr/lpr mice (two with anticardiolipin antibodies, one without) and two sex- and age-matched Balb/c mice (controls) were sacrificed for histological studies. Serum binding to phospholipids and DNA was studied at this time. We found thickened heart valves in 68% of MRL-lpr/lpr mice and in 80% of Balb/c mice, and no association with any of the antibodies tested was found. No evidence of coronary vasculitis or thrombi was found in any of the mice studied. Platelet counts in MRL-lpr/lpr mice were significantly lower (640.550 +/- 211.818 x 10(6)/ml) than in Balb/c mice (780.0 + 112.5 x 10(6)/ml) (p < 0.05), and no association was found between platelet counts and aPL. In this model of murine APS, aPL bear no importance in heart valve pathology.
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Vianna et al. (1992) studied Antiphospholipid syndrome (APS). Antiphospholipid antibodies (aPL) vs. Balb/c mice (controls) / absence of aPL was evaluated on Thickened heart valves. Antiphospholipid antibodies showed no association with heart valve pathology, as thickened heart valves were present in 68% of MRL-lpr/lpr mice and 80% of Balb/c controls.
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