Introduction: We previously reported that atherosclerotic plaque formation was severely retarded in the Ldlr^-/-/Apobec1^-/-/Plasminogen^-/- (L^-/-/A^-/-/Plg^-/-) triple knockout mice compared with L^-/-/A^-/- mice, which a murine model of type IIa human familial hypercholesterolemia. Therefore, it is inferred that tPA or uPA (tissue-type plasminogen activator or urokinase-type plasminogen activator) involved in the activation of Plg is deeply involved in the development of atherosclerotic plaque formation. In this study, we investigated the effect of tPA on type IIa human familial hypercholesterolemia.
Results and discussion: We produced L^-/-/A^-/-/Plat^-/- mice by crossing L^-/-/A^-/- mouse with Plat^-/- knockout mouse. L^-/-/A^-/-/Plat^-/- and L^-/-/A^-/- Mice were fed a normal diet for 24, 36, 48 weeks, and then the aortic sinus was collected from the mice. Then, the aorta was stained with HE or Masson's trichrome, and the size of the atherosclerotic lesion was measured using ImageJ. As a result, the size of atherosclerotic lesions in 36-week-old and 48-week-old L^-/-/A^-/-/Plat^-/- mice was significantly smaller than that in L^-/-/A^-/-mice. The results of this study suggest that tPA is involved in the suppression of arteriosclerosis.