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RISS 인기검색어
- 검색키워드
- 발행기관 : The University of Texas Graduate School of Biomedi (검색결과 2 건)
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PLASMALEMMAL REPAIR OF INJURED MAMMALIAN CELL LINES
유순문 THE UNIVERSITY OF TEXAS GRADUATE SCHOOL OF BIOMEDI 2002 해외박사
To understand repair mechanisms (plasma membrane sealing and cell survival) of injured neurons, I used extensively characterized in vitro mammalian neuron models, i.e., the differentiated PC12 cell line derived from rat adrenal medullary cells (PNS) and the B104 cell line derived from rat brain (CNS), in which I assessed restoration of a barrier (plasma membrane seal) and subsequent cell survival after mechanical transection of neurites. I showed that Ca^(2+) plays multiple, essential roles in the initiation of phylogenetically conserved processes that restore a plasma membrane barrier. Specifically, as shown previously in invertebrate axons, Ca^(2+) activation of cysteine proteases (m-calpain) or application of exogenous m-calpain was necessary for rapid formation of a barrier (exclusion of dye entry) in transected neurites of PC12 and B104 cells. Furthermore, by use of antibodies that inactivate synaptotagmin, syntaxin and synaptobrevin, which mediate Ca^(2+)-initiated exocytosis at synapses, I found that these fusion-promoting proteins are also necessary for the repair of injured cells. I obtained data that explains retrograde degeneration following neurite transection near (<50μm) the soma in contrast to cell survival of injury far (>100μm) from the soma. I hypothesized that cells with a neurite transected near their soma degenerate due to incomplete restoration of a barrier at the site of injury. Instead, I found that barrier formation occurs but too slowly to prevent sufficient Ca^(2+) entry and build up in the cell body, which initiates degeneration before a seal (Ca^(2+) impermeant barrier) is restored. By imaging the fluorescence of preloaded Ca^(2+)-indicator dye, I measured the rise of [Ca^(2+)]I within the cell body after neurite transection near the soma. I determined that Ca^(2+) entry is mainly through the site of injury. Furthermore, the extent of the [Ca^(2+)]i increase in the cell body after neurite transection near the soma correlated with cell degeneration. Finally, cell survival of injury near the soma could be increased by preloading the cells with a Ca^(2+) buffer (BAPTA) before injury.
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