Contribution of the delayed-rectifier potassium channel Kv2.1 to acute spinal cord injury in rats
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Recent studies have reported that delayed-rectifier Kv channels regulate apoptosis in the nervous system. Herein, we investigated changes in the expression of the delayed-rectifier Kv channels Kv1.2, Kv2.1, and Kv3.1 after acute spinal cord injury (SCI) in rats. We performed RT-PCR analysis and found an increase in the level of Kv2.1 mRNA after SCI but no significant changes in the levels of Kv1.2 and Kv3.1 mRNA. Western blot analysis revealed that Kv2.1 protein levels rapidly decreased and then dramatically increased from 1 day,whereas Kv3.1b protein levels gradually and sharply decreased at 5 days. Kv1.2 protein levels did not change significantly. In addition, Kv2.1 clusters were disrupted in the plasma membranes of motor neurons after SCI. Interestingly, the expressional changes and translocation of Kv2.1 were consistent with the apoptotic changes on day 1. Therefore, these results suggest that Kv2.1 channels probably contribute to neuronal cell responses to SCI.
Abstract
Recent studies have reported that delayed-rectifier Kv channels regulate apoptosis in the nervous system. Herein, we investigated changes in the expression of the delayed-rectifier Kv channels Kv1.2, Kv2.1, and Kv3.1 after acute spinal cord injury (SCI) in rats. We performed RT-PCR analysis and found an increase in the level of Kv2.1 mRNA after SCI but no significant changes in the levels of Kv1.2 and Kv3.1 mRNA. Western blot analysis revealed that Kv2.1 protein levels rapidly decreased and then dramatically increased from 1 day,whereas Kv3.1b protein levels gradually and sharply decreased at 5 days. Kv1.2 protein levels did not change significantly. In addition, Kv2.1 clusters were disrupted in the plasma membranes of motor neurons after SCI. Interestingly, the expressional changes and translocation of Kv2.1 were consistent with the apoptotic changes on day 1. Therefore, these results suggest that Kv2.1 channels probably contribute to neuronal cell responses to SCI.
참고문헌 (21)
- Keane, R. W., "Inflammatory and apoptotic signaling after spinal cord injury", J. Neurotrauma., 23, pp.335~344 (2006)
- Liu, X. Z., "Neuronal and glial apoptosis after traumatic spinal cord injury", J. Neurosci., 17, pp.5395~5406 (1997)
- Thuret, S., "Therapeutic interventions after spinal cord injury", Nat. Rev. Neurosci., 7, pp.628~643 (2006)
- Lapointe, N. P., "Plasticity in sublesionally located neurons following spinal cord injury", J. Neurophysiol., 98, pp.2497~2500 (2007)
- Vacher, H., "Localization and targeting of voltage-dependent ion channels in mammalian central neurons", Physiol. Rev., 88, pp.1407~1447 (2008)
- Yao, H., "The Kv2.1 channels mediate neuronal apoptosis induced by excitotoxicity", J. Neurochem., 108, pp.909~919 (2009)
- Shen, Q. J., "Contribution of Kv channel subunits to glutamate-induced apoptosis in cultured rat hippocampal neurons", J. Neurosci. Res., 87, pp.3153~3160 (2009)
- Redman, P. T., "Apoptotic surge of potassium currents is mediated by p38 phosphorylation of Kv2.1", Proc. Natl. Acad. Sci. U.S.A., 통권 : 104, pp.3568~3573 (2007)
- Jiao, S., "cAMP", protein kinase A signalling pathway protects against neuronal apoptosis and is associated with modulation of Kv2.1 in cerebellar granule cells, 2007, pp.100, 979~991
- Pal, S. K., "Apoptotic surface delivery of K+ channels", Cell Death Differ., 13, pp.661~667 (2006)
- Preussat, K., "Expression of voltage-gated potassium channels Kv1.3 and Kv1.5 in human gliomas", Neurosci. Lett., 346, pp.33~36 (2003)
- Liu, N. K., "beta-tubulin is a more suitable internal control than beta-actin in western blot analysis of spinal cord tissues after traumatic injury", J. Neurotrauma, 23, pp.1794~1801 (2006)
- Misonou, H., "Calcium- and metabolic state-dependent modulation of the voltage-dependent Kv2.1 channel regulates neuronal excitability in response to ischemia", J. Neurosci., 25, pp.11184~11193 (2005)
- Muennich, E. A., "Focal aggregation of voltage-gated, Kv2.1 subunit-containing, potassium channels at synaptic sites in rat spinal motoneurones", J. Physiol., 554, pp.673~685 (2004)
- Yu, S. P., "Regulation and critical role of potassium homeostasis in apoptosis", Prog. Neurobiol., 70, pp.363~386 (2003)
- Yu, S. P., "Mediation of neuronal apoptosis by enhancement of outward potassium current", Science, 278, pp.114~117 (1997)
- Pal, S., "Mediation of neuronal apoptosis by Kv2.1-encoded potassium channels", J. Neurosci., 23, pp.4798~4802 (2003)
- McBride, J. M., "4-Aminopyridine derivatives enhance impulse conduction in guinea-pig spinal cord following traumatic injury", Neuroscience, 148, pp.44~52 (2007)
- Burg, E. D., "K+ channels in apoptosis", J. Membr. Biol., 209, pp.3~20 (2006)
- Misonou, H., "Regulation of ion channel localization and phosphorylation by neuronal activity", Nat. Neurosci., 7, pp.711~718 (2004)
- Gruner, J. A., "A monitored contusion model of spinal cord injury in the rat", J. Neurotrauma, 9, pp.123~126 (1992)