Melatonin attenuates decrease of protein phosphatase 2A subunit B in ischemic brain injury
Article first published online: 26 JUL 2011
© 2011 John Wiley & Sons A/S
Journal of Pineal Research
Volume 52, Issue 1, pages 57–61, January 2012
How to Cite
Koh, P.-O. (2012), Melatonin attenuates decrease of protein phosphatase 2A subunit B in ischemic brain injury. Journal of Pineal Research, 52: 57–61. doi: 10.1111/j.1600-079X.2011.00918.x
- Issue published online: 12 DEC 2011
- Article first published online: 26 JUL 2011
- Accepted manuscript online: 27 JUN 2011 11:35AM EST
- Received May 3, 2011; Accepted June 16, 2011.
- protein phosphatase 2A subunit B
Abstract: Melatonin is an antioxidant that has neuroprotective functions in ischemic brain injury. Protein phosphatase 2A (PP2A) is a serine and threonine phosphatase that modulates cell metabolism and cell survival. This study investigated whether melatonin modulates PP2A subunit B in focal cerebral ischemia and glutamate toxicity-induced neuronal cell death in a rat model. Middle cerebral artery occlusion (MCAO) was performed to induce permanent cerebral ischemic injury. Adult male rats were treated with vehicle or melatonin (5 mg/kg) prior to MCAO, and cerebral cortex tissues were collected 24 hr after MCAO. A proteomic approach elucidated the decrease in PP2A subunit B in MCAO-operated animals. Melatonin treatment attenuated injury-induced reductions in PP2A subunit B levels. Western blot analyses indicated that melatonin prevents injury-induced decrease in PP2A subunit B levels. In neuronal cells, glutamate toxicity induced a lowering of PP2A subunit B, while melatonin treatment attenuated the glutamate exposure-induced decreases in PP2A subunit B. These results suggest that the maintenance of PP2A subunit B by melatonin in ischemic injury is critical to the neuroprotective function of melatonin during neuronal cell damage.