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ISSN : 1226-7155(Print)
ISSN : 2287-6618(Online)
International Journal of Oral Biology Vol.32 No.2 pp.51-57

Involvement of Antiapoptotic Signals in Rat PC12 Cells Proliferation by Cyclosporin A Treatment

Ji-Yeon Jung, Park Ji-Il, Lee Guem-Sug, Jeong Yeon-Jin, Kim Byung-Kuk, Kim Jae-Hyung, Lim Hoi-Soon, Kim Sun-Hun, Kim Won-Jae
Dental Science Research Institute, Brain Korea 21 Project, School of Dentistry Chonnam National University
Department of Dental Hygiene, Gwangju Health Collage


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 0.1~10 μM)-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.