[TRPM8 mediates PC-12 neuronal cell apoptosis induced by oxygen-glucose deprivation through cAMP-PKA/UCP4 signaling].
To explore the molecular mechanism responsible for apoptosis of PC-12 neuronal cells induced by oxygen-glucose deprivation (OGD).



PC12 cells were exposed to OGD for 24 h to simulate ischemia-reperfusion injury. Flow cytometry was employed detect the cell apoptosis, and the expresions of TRPM8, UCP4, cAMP and PKA in the exposed cells were detected with RT-PCR and Western blotting. The changes in the expressions of Bax, Bcl-2, cAMP, PKA and UCP4 proteins were detected in the exposed cells in resposne to inhibition of TRPM8 and cAMP-PKA signal or over-expression of UCP4.



OGD for 24 induced obvious apoptosis in PC-12 cells and caused TRPM8 over-expression and inhibition of UCP4 and cAMP-PKA signaling. Inhibiting TRPM8 expression reduced the cell apoptosis and up-regulated cAMP, p-PKA and UCP4 in the cells exposed to OGD. In cells exposed to OGD, inhibition of TRPM8 and cAMP-PKA signaling suppressed the expressio of UCP4 and increased the cell apoptosis.



TRPM8 mediates OGD-induced PC12 cell apoptosis through cAMP-PKA/UCP4 signaling.
Orthopaedics Key Laboratory of Gansu Province, Second Hospital of Lanzhou University, Lanzhou 730000, China.E-mail: 754867290@qq.com.
Hong-Wei
HW
Li
Bin
B
Zhou
Hai-Hong
HH
Zhang
D000818:Animals; D017209:Apoptosis; D000242:Cyclic AMP / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D000071245:Mitochondrial Uncoupling Proteins / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D016716:PC12 Cells; D051381:Rats; D015427:Reperfusion Injury; D015398:Signal Transduction; D050053:TRPM Cation Channels / Q000378:metabolism*
D000071245:Mitochondrial Uncoupling Proteins; C494853:Slc25a27 protein, rat; D050053:TRPM Cation Channels; C498947:Trpm8 protein, rat; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D005947:Glucose; D010100:Oxygen