Modulation of ERK and JNK activity by transient forebrain ischemia in rats

Deborah A. Shackelford; Richard Y. Yeh

doi:10.1002/jnr.20747

journal article Jan 05, 2006

Modulation of ERK and JNK activity by transient forebrain ischemia in rats

Deborah A. Shackelford Richard Y. Yeh

Journal of Neuroscience Research Vol. 83 No. 3 pp. 476-488 · Wiley

View at Publisher Save 10.1002/jnr.20747

Abstract

AbstractThe mitogen‐activated protein (MAP) kinase families of ERK and JNK participate in numerous intracellular signaling pathways and are abundantly expressed in the CNS. Activation of ERK and JNK during reperfusion of ischemic tissue is implicated in promoting cell death, insofar as inhibition of either pathway reduces neuronal cell death. However, ERK or JNK activation provides protection in other neuronal injury models. In this study, we monitored the concurrent modulation of ERK and JNK activity in the hippocampus, neocortex, and striatum during ischemia and immediately upon reperfusion in a rat model of transient global ischemia. All three regions incur a similar reduction in blood flow during occlusion but show different extents and temporal patterns of injury following reperfusion. ERK and JNK were active in the normal rat forebrain, and phosphorylation was reduced by ischemia. Upon reperfusion, ERK was rapidly activated in the hippocampus, neocortex, and striatum, whereas JNK phosphorylation increased in the hippocampus and striatum but not in the neocortex. The response of JNK vs. ERK more closely reflects the susceptibility of these regions. JNK1 was the predominant phosphorylated isoform. A minor pool of phosphorylated JNK3 increased above the control level after reperfusion in hippocampal but not in neocortical particulate fractions. In addition, a novel 32–35‐kDa c‐Jun kinase activity was detected in the hippocampus, neocortex, and striatum. The results show that ERK and JNK activities are rapidly, but not identically, modulated by ischemia and reperfusion and indicate that the MAP kinase pathways contribute to regulating the response to acute CNS injury. © 2006 Wiley‐Liss, Inc.

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References

61

[1]

10.1073/pnas.96.22.12866

[2]

10.1038/ncb1005

[3]

10.1002/(sici)1097-0029(19990515/01)45:4/5<276::aid-jemt11>3.0.co;2-4

[4]

10.1038/nm911

[5]

10.1111/j.1460-9568.2005.03857.x

[6]

10.1046/j.1471-4159.2001.00400.x

[7]

10.1016/s1474-4422(03)00532-5

[8]

10.1124/jpet.103.064246

[9]

10.1111/j.1471-4159.2004.02925.x

[10]

10.1074/jbc.m312363200

[11]

10.1111/j.1432-1033.2004.04131.x

[12]

Mammalian MAP kinase signalling cascades

Lufen Chang, Michael Karin

Nature 10.1038/35065000

[13]

10.1016/s1534-5807(03)00094-7

[14]

10.1111/j.1432-1033.2004.04132.x

[15]

10.1089/neu.2004.21.1168

[16]

10.1016/s0962-8924(01)01980-8

[17]

Signal Transduction by the JNK Group of MAP Kinases

Roger J Davis

Cell 10.1016/s0092-8674(00)00116-1

[18]

10.1038/sj.jcbfm.9600062

[19]

10.1097/00004647-200102000-00001

[20]

Gu Z "c‐Jun N‐terminal kinase activation in hippocampal CA1 region was involved in ischemic injury" Mol Neurosci (2001)

[21]

10.1016/s0006-8993(01)02275-2

[22]

10.1016/j.brainres.2004.11.050

[23]

10.1111/j.1432-1033.2004.04133.x

[24]

10.1101/gad.7.11.2135

[25]

Hsu M "Vulnerability of mossy fiber targets in the rat hippocampus to forebrain ischemia" J Neurosci (1993) 10.1523/jneurosci.13-09-03964.1993

[26]

Role of Mitogen- and Stress-Activated Kinases in Ischemic Injury

Elaine A. Irving, Mark Bamford

Journal of Cerebral Blood Flow & Metabolism 10.1097/00004647-200206000-00001

[27]

10.1016/s0896-6273(00)80727-8

[28]

10.1073/pnas.2336254100

[29]

10.1128/mcb.22.13.4929-4942.2002

[30]

10.1002/bies.10204

[31]

10.1038/sj.cr.7290262

[32]

10.1007/s11064-004-7040-4

[33]

PROTEIN MEASUREMENT WITH THE FOLIN PHENOL REAGENT

OliverH. Lowry, NiraJ. Rosebrough, A. Lewis Farr et al.

Journal of Biological Chemistry 10.1016/s0021-9258(19)52451-6

[34]

10.1089/neu.2000.17.899

[35]

10.1016/s0301-0082(99)00042-8

[36]

10.1089/089771502320914642

[37]

10.1097/00004647-200204000-00008

[38]

10.1073/pnas.181213498

[39]

10.1523/jneurosci.22-18-07923.2002

[40]

10.1385/mn:23:1:01

[41]

10.1523/jneurosci.1745-04.2004

[42]

10.1161/01.str.10.3.267

[43]

10.1111/j.1471-4159.1983.tb13599.x

[44]

10.1002/ana.410110509

[45]

10.1002/ana.410110510

[46]

10.1016/s0896-6273(03)00355-6

[47]

10.1016/s0925-4773(99)00213-0

[48]

10.1023/a:1021004525979

[49]

10.1096/fasebj.9.9.7601337

[50]

Shackelford DA (1997)

Showing 50 of 61 references

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Details

Published: Jan 05, 2006
Vol/Issue: 83(3)
Pages: 476-488
License: View

Authors

D

Deborah A. Shackelford

R

Richard Y. Yeh

Cite This Article

Deborah A. Shackelford, Richard Y. Yeh (2006). Modulation of ERK and JNK activity by transient forebrain ischemia in rats. Journal of Neuroscience Research, 83(3), 476-488. https://doi.org/10.1002/jnr.20747

Modulation of ERK and JNK activity by transient forebrain ischemia in rats

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