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KMID : 0613820100200121820
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Journal of Life Science
2010 Volume.20 No. 12 p.1820 ~ p.1828
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Endoplasmic Reticulum Stress Response and Apoptosis via the CoCl₂-Induced Hypoxia in Neuronal Cells
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Kim Seon-Hwan
Kwon Hyon-Jo
Koh Hyeon-Song
Song Shi-Hun
Kwon Ki-Sang
Kwon O-Yu
Choi Seung-Won
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Abstract
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Cobalt(Ⅱ) chloride, a chemical compound with the formula CoCl₂, has been widely used in the treatment of anemia, as a chemical agent for the induction of hypoxia in cell cultures, and is known to activate hypoxic signaling. However, excessive exposure to cobalt is associated with several clinical conditions, including asthma, pneumonia, and hematological abnormalities, and can lead to tissue and cellular toxicity. It is also known to induce apoptosis. One of the questions was that of whether CoCl₂ might induce apoptosis via endoplasmic reticulum (ER) stress in neurons. To address this question, first, the level of DNA fragmentation was measured for assay of apoptotic rates using CoCl₂ with neuron PC12 cells. After confirmation of apoptosis inductions, under the same conditions, the expression levels of ER stress associated factors [ER chaperones Bip, calnexin, ERp72, ERp29, PDI, and ER membrane kinases (IRE1, ATF6, PERK)] were examined by RT-PCR and Western blotting. These results indicated that apoptosis is induced through activation of ER membrane kinases via ER stress. In conclusion, during induction of apoptosis through CoCl₂-induced hypoxia in neuron PC12 cells, ER membrane kinase of IRE1 was dominantly up-expressed, and, consecutively, TRAF2, which has been suggested to be one of the links connecting apoptosis and ER stress, was strongly up-expressed.
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KEYWORD
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CoCl₂, apoptosis, hypoxia, endoplasmic reticulum(ER)
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