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Possible roles of JNK pathway in the regulation of hippocampal proenkephalin and immediate early gene expression induced by kainic acid.
Mol Cells. 2001 Apr 30; 11(2):144-50.MC

Abstract

Mitogen-activated protein kinases (MAPKs) may play crucial roles in the kainic acid (KA)-evoked excitotoxic effect and the regulation of transcription factors (e.g. c-Fos and c-Jun) in hippocampus, but their exact role in the regulation of KA-induced opioid peptides expression has not been well characterized in vivo. Therefore, we examined possible involvement of the phosphorylated form of JNK, as well as CREB, in the regulation of KA-induced proenkephalin and immediate early genes (IEGs) expression in the rat hippocampus. KA increased proenkephalin mRNA expression in rat hippocampus, which was decreased by pre-administration with cycloheximide (CHX, a protein synthesis inhibitor). KA alone increased c-fos as well as c-jun mRNA levels. CHX further enhanced KA-induced c-fos and c-jun mRNA levels. Additionally, KA increased the phosphorylation of JNK, especially JNK1, which was attenuated by CHX. CHX decreased KA-induced c-Fos protein expression. Interestingly, CHX itself increased the phosphorylation of CREB, which was abolished by KA administration. Our results suggest that the phosphorylation of JNK is involved in the up-regulation of the proenkephalin gene expression via c-Fos and c-Jun that is induced by KA in rat hippocampus. However, the phosphorylation of CREB is not associated with the up-regulation of the proenkephalin mRNA level induced by KA in the rat hippocampus.

Authors+Show Affiliations

Department of Pharmacology, Institute of Natural Medicine, College of Medicine, Hallym University, Chunchon, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11355693

Citation

Kim, Y H., et al. "Possible Roles of JNK Pathway in the Regulation of Hippocampal Proenkephalin and Immediate Early Gene Expression Induced By Kainic Acid." Molecules and Cells, vol. 11, no. 2, 2001, pp. 144-50.
Kim YH, Choi SS, Lee JK, et al. Possible roles of JNK pathway in the regulation of hippocampal proenkephalin and immediate early gene expression induced by kainic acid. Mol Cells. 2001;11(2):144-50.
Kim, Y. H., Choi, S. S., Lee, J. K., Won, J. S., Choi, M. R., & Suh, H. W. (2001). Possible roles of JNK pathway in the regulation of hippocampal proenkephalin and immediate early gene expression induced by kainic acid. Molecules and Cells, 11(2), 144-50.
Kim YH, et al. Possible Roles of JNK Pathway in the Regulation of Hippocampal Proenkephalin and Immediate Early Gene Expression Induced By Kainic Acid. Mol Cells. 2001 Apr 30;11(2):144-50. PubMed PMID: 11355693.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possible roles of JNK pathway in the regulation of hippocampal proenkephalin and immediate early gene expression induced by kainic acid. AU - Kim,Y H, AU - Choi,S S, AU - Lee,J K, AU - Won,J S, AU - Choi,M R, AU - Suh,H W, PY - 2001/5/18/pubmed PY - 2002/1/5/medline PY - 2001/5/18/entrez SP - 144 EP - 50 JF - Molecules and cells JO - Mol Cells VL - 11 IS - 2 N2 - Mitogen-activated protein kinases (MAPKs) may play crucial roles in the kainic acid (KA)-evoked excitotoxic effect and the regulation of transcription factors (e.g. c-Fos and c-Jun) in hippocampus, but their exact role in the regulation of KA-induced opioid peptides expression has not been well characterized in vivo. Therefore, we examined possible involvement of the phosphorylated form of JNK, as well as CREB, in the regulation of KA-induced proenkephalin and immediate early genes (IEGs) expression in the rat hippocampus. KA increased proenkephalin mRNA expression in rat hippocampus, which was decreased by pre-administration with cycloheximide (CHX, a protein synthesis inhibitor). KA alone increased c-fos as well as c-jun mRNA levels. CHX further enhanced KA-induced c-fos and c-jun mRNA levels. Additionally, KA increased the phosphorylation of JNK, especially JNK1, which was attenuated by CHX. CHX decreased KA-induced c-Fos protein expression. Interestingly, CHX itself increased the phosphorylation of CREB, which was abolished by KA administration. Our results suggest that the phosphorylation of JNK is involved in the up-regulation of the proenkephalin gene expression via c-Fos and c-Jun that is induced by KA in rat hippocampus. However, the phosphorylation of CREB is not associated with the up-regulation of the proenkephalin mRNA level induced by KA in the rat hippocampus. SN - 1016-8478 UR - https://www.unboundmedicine.com/medline/citation/11355693/Possible_roles_of_JNK_pathway_in_the_regulation_of_hippocampal_proenkephalin_and_immediate_early_gene_expression_induced_by_kainic_acid_ L2 - http://www.molcells.org/journal/view.html?year=2001&volume=11&number=2&spage=144 DB - PRIME DP - Unbound Medicine ER -