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SURFACE EXPRESSION OF CPN60: IMPLICATIONS FOR NEURODEGENERATION R. D. Martinus
Understanding the death of neuronal cells in the brains of Alzheimer’s and Parkinson’s disease patients remains an important goal of neurobiology. Mitochondrial involvement and inflammatory responses are thought to play key roles in the pathogenecity of neurodegeneration. In this study an in vitro cellular model system with impaired mitochondrial bioenergetic functions has been developed to investigate the relationship between mitochodrial dysfunction and inflammation. The ability to grow mitochondrially compromised cells in growth media supplemented with pyruvate and uridine was exploited in this study. Western blot analysis indicated that exposure of primary cortical and hippocampal neuronal cells to AZT (a mitochondrial g-polymerase inhibitor) resulted in specific up-regulation of mitochondrial molecular chaperonins cpn60 and cpn10. Interestingly, the levels of over-expression of cpn60 was such that significant surface expression was detected in the mitochondrially compromised neuronal cells by indirect immunofluorescence microscopy using an anti cpn60 polyclonal antibody. Since surface expression of cpn60 is implicated to play a key role in humoral immune responses, it is proposed that cell surface expression of cpn60, which is released in response to damage to the mitochondrion, could provide a link between mitochondria and inflammatory responses in neurodegeneration.
For further information contact...Carmen Mannella: carmen@wadsworth.org |
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