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KMID : 0848120070320020051
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International Journal of Oral Biology
2007 Volume.32 No. 2 p.51 ~ p.57
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Involvement of Antiapoptotic Signals in Rat PC12 Cells Proliferation by Cyclosporin A Treatment
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Park Ji-Il
Lee Kum-Sug
Jeong Yeon-Jin
Kim Byung-Gook
Kim Jae-Hyung
Lim Hoi-Soon
Kim Sun-Hun
Kim Won-Jae
Jeong Ji-Yeon
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Abstract
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Cyclosporin A (CsA) plays an important role in clinical medicine and basic biology as an immunosuppressant and a mitochondrial permeability blocker, respectively. It was reported that CsA has a protective role by preventing apoptosis and promoting the proliferation in severed neurons. However, the molecular mechanisms for CsA-induced neuronal cell proliferation are unclear. In this study, we examined the mechanisms underlying the CsA-induced proliferation of PC12 cells. CsA increased the viability of PC12 cells in a dose(over )-and time-dependent manner. The level of ROS generation was decreased in the CsA-treated PC12 cells. Expression of Bcl-2, an antiapoptotic molecule that inhibits the release of cytochrome c from the mitochondria into the cytosol, was upregulated, whereas Bax, a proapototic molecule, was not changed in the CsA-treated PC12 cells. CsA downregulated the mRNA expression of VDAC 1 and VDAC 3, but VDAC 2 was not changed in the CsA-treated PC12 cells. The level of cytosolic cytochrome c released from the mitochondria and the caspase-3 activity were attenuated in the CsA-treated PC12 cells. These results suggest that the mitochondria-mediated apoptotic signal and Bcl-2 family may play an important role in CsA-induced proliferation in PC12 cells.
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KEYWORD
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Cyclosporin A, PC12 cells, Cytochrome c, Caspase, Bcl-2 family
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