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The heart and antiphospholipid antibodies in MRL-lpr/lpr mice
J L Vianna1, S Trotter, M A Khamashta
1Lupus & Arthritis Research Unit, Rayne Institute, St Thomas' Hospital, London, UK.
Abstract:
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.
Insights
Antiphospholipid antibodies (aPL) do not appear to cause heart valve lesions in a mouse model of antiphospholipid syndrome (APS). This study found no link between aPL and valve thickening or other cardiac issues in MRL-lpr/lpr mice.
Area of Science:
- Immunology
- Cardiology
- Pathology
Background:
- Antiphospholipid syndrome (APS) is an autoimmune disorder associated with aPL.
- Heart valve lesions are a potential complication of APS, but their direct link to aPL is not fully understood.
- The MRL-lpr/lpr mouse model offers a platform to study APS-related pathology.
Purpose of the Study:
- To investigate the association between antiphospholipid antibodies (aPL) and heart valve lesions in MRL-lpr/lpr mice.
- To determine if aPL contribute to valvular pathology in a murine model of APS.
Main Methods:
- Histological examination of heart valves in MRL-lpr/lpr mice and Balb/c controls from 2 to 6 months of age.
- Assessment of serum binding to phospholipids and DNA.
- Analysis of platelet counts in both mouse groups.
Main Results:
- Thickened heart valves were observed in both MRL-lpr/lpr (68%) and Balb/c (80%) mice, with no correlation to tested antibodies.
- No evidence of coronary vasculitis or thrombi was detected in any mice.
- MRL-lpr/lpr mice exhibited significantly lower platelet counts than controls, independent of aPL presence.
Conclusions:
- Antiphospholipid antibodies do not play a significant role in the development of heart valve pathology in this murine model of APS.
- The observed valve thickening in MRL-lpr/lpr mice is likely independent of aPL.
- Further research may be needed to elucidate other factors contributing to cardiac findings in this APS model.