References
Query Results -- Details
MGI Accession ID: MGI:1927022
J Number: J:65660
Other Accession IDs:
Title: Apolipoprotein J/clusterin limits the severity of murine autoimmune myocarditis
Authors: McLaughlin L; Zhu G; Mistry M; Ley-Ebert C; Stuart WD; Florio CJ; Groen PA; Witt SA; Kimball TR; Witte DP; Harmony JA; Aronow BJ
Journal: J Clin Invest
Volume: 106
Issue: 9
Date: 2000 Nov
Year: 2000
Pages: 1105-13
Review Status: Peer Reviewed
Abstract:
Apolipoprotein J/clusterin (apoJ/clusterin), an intriguing protein with unknown function, is induced in myocarditis and numerous other inflammatory injuries. To test its ability to modify myosin-induced autoimmune myocarditis, we generated apoJ-deficient mice. ApoJ-deficient and wild-type mice exhibited similar initial onset of myocarditis, as evidenced by the induction of two early markers of the T cell-mediated immune response, MHC-II and TNF receptor p55. Furthermore, autoantibodies against the primary antigen cardiac myosin were induced to the same extent. Although the same proportion of challenged animals exhibited some degree of inflammatory infiltrate, inflammation was more severe in apoJ-deficient animals. Inflammatory lesions were more diffuse and extensive in apoJ-deficient mice, particularly in females. In marked contrast to wild-type animals, the development of a strong generalized secondary response against cardiac antigens in apoJ-deficient mice was predictive of severe myocarditis. Wild-type mice with a strong Ab response to secondary antigens appeared to be protected from severe inflammation. After resolution of inflammation, apoJ-deficient, but not wild-type, mice exhibited cardiac function impairment and severe myocardial scarring. These results suggest that apoJ limits progression of autoimmune myocarditis and protects the heart from postinflammatory tissue destruction.
Additional Information:
