Association of matrix metalloproteinase-9 and Purkinje cell degeneration in mouse cerebellum caused by Angiostrongylus cantonensis

Angiostrongylosis is a neurological disorder caused by invasion of the central nervous system by developing larvae of Angiostrongylus cantonensis. Purkinje cells in infected mouse cerebellums are small and irregular with degenerative atrophy or partial loss. Ultrastructural changes in degenerative c...

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Published inInternational journal for parasitology Vol. 34; no. 10; pp. 1147 - 1156
Main Authors Chen, Ke-Min, Lee, Hsiu-Hsiung, Lu, Kuang-Hui, Tseng, Yu-Kai, Hsu, Li-Sung, Chou, Hui-Lin, Lai, Shih-Chan
Format Journal Article
LanguageEnglish
Published Oxford Elsevier Ltd 01.09.2004
Elsevier Science
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ISSN0020-7519
1879-0135
DOI10.1016/j.ijpara.2004.07.004

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Summary:Angiostrongylosis is a neurological disorder caused by invasion of the central nervous system by developing larvae of Angiostrongylus cantonensis. Purkinje cells in infected mouse cerebellums are small and irregular with degenerative atrophy or partial loss. Ultrastructural changes in degenerative cells included enlarged vacuolar structures and swollen mitochondria within the cytoplasm. The matrix metalloproteinase-9 mRNA which is low in normal cerebellums was expressed in A. cantonensis-infected mice cerebellum prior to Purkinje cell degeneration. Matrix metalloproteinase-9 protein level and enzyme activity increased when the Purkinje cells appeared degenerated. Using immunohistochemistry, matrix metalloproteinase-9 was localised within degenerative Purkinje cells. In addition, when the specific matrix metalloproteinase inhibitor, GM6001, was added, matrix metalloproteinase-9 enzyme activity was reduced by 41.6%. The numbers of degenerative Purkinje cells increased significantly upon establishment of infection but subsided upon inhibition. These results suggested that the expression of matrix metalloproteinase-9 may be associated with degeneration of Purkinje cells in mouse cerebellum infected by A. cantonensis.
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ISSN:0020-7519
1879-0135
DOI:10.1016/j.ijpara.2004.07.004