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Regulation of the cyclooxygenase-2 system by interleukin-1beta through mitogen-activated protein kinase signaling pathways: a comparative study of human neuroglioma and neuroblastoma cells.
Brain Res Mol Brain Res. 2005 Jun 13; 137(1-2):202-12.BR

Abstract

Glial activation and inflammation following brain injury may initiate and maintain the process of neurodegeneration. Both glia and neurons synthesize proinflammatory mediators such as interleukin 1 beta (IL-1beta), cytosolic phospholipase A2 (cPLA2), cyclooxygenase-2 (COX-2), and prostaglandins. The molecular mechanisms by which IL-1beta regulates inflammatory genes such as cPLA2 and COX-2 in glial and neuronal cells are poorly understood. We have studied IL-1beta-mediated gene regulation in an established glial and neuronal human cell lines. We report that IL-1beta induced cPLA2 and COX-2 mRNA and protein expression and subsequent prostaglandin E2 (PGE2) release in a time-dependent manner in H4 neuroglioma cells. Both SB203580 and PD98059 [p38 and p42/44 mitogen-activated protein kinase (MAPKs) inhibitors, respectively] reduced IL-1beta-induced PGE2 production, while only SB203580 reduced both cPLA2 and COX-2 expression. Similarly, in SKNSH neuroblastoma cells, both SB203580 and PD98059 reduced IL-1beta-induced PGE2 release, with no detectable COX-2 and cPLA2 protein expression in these cells. Our results indicate that the signaling mechanisms of p38 and p42/44 MAPKs play a role in IL-1beta-mediated PGE2 release in both of these cell lines, with differences upstream at the level of cPLA(2)/COX-2 expression. IL-1beta-induced cPLA2 and COX-2 gene expression is modulated through the p38 MAPK pathway in both neuroglioma and neuroblastoma cells. Understanding the signaling mechanisms involved in IL-1beta-mediated inflammatory processes in both glia and neuronal cells may provide potential targets for therapeutic intervention for neurological disorders.

Authors+Show Affiliations

M3-104, Division of Pharmacology, 2411 Holmes, UMKC School of Medicine, University of Missouri-Kansas City, MO 64108, USA.No affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15950779

Citation

Moolwaney, Anju S., and Orisa J. Igwe. "Regulation of the Cyclooxygenase-2 System By Interleukin-1beta Through Mitogen-activated Protein Kinase Signaling Pathways: a Comparative Study of Human Neuroglioma and Neuroblastoma Cells." Brain Research. Molecular Brain Research, vol. 137, no. 1-2, 2005, pp. 202-12.
Moolwaney AS, Igwe OJ. Regulation of the cyclooxygenase-2 system by interleukin-1beta through mitogen-activated protein kinase signaling pathways: a comparative study of human neuroglioma and neuroblastoma cells. Brain Res Mol Brain Res. 2005;137(1-2):202-12.
Moolwaney, A. S., & Igwe, O. J. (2005). Regulation of the cyclooxygenase-2 system by interleukin-1beta through mitogen-activated protein kinase signaling pathways: a comparative study of human neuroglioma and neuroblastoma cells. Brain Research. Molecular Brain Research, 137(1-2), 202-12.
Moolwaney AS, Igwe OJ. Regulation of the Cyclooxygenase-2 System By Interleukin-1beta Through Mitogen-activated Protein Kinase Signaling Pathways: a Comparative Study of Human Neuroglioma and Neuroblastoma Cells. Brain Res Mol Brain Res. 2005 Jun 13;137(1-2):202-12. PubMed PMID: 15950779.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of the cyclooxygenase-2 system by interleukin-1beta through mitogen-activated protein kinase signaling pathways: a comparative study of human neuroglioma and neuroblastoma cells. AU - Moolwaney,Anju S, AU - Igwe,Orisa J, Y1 - 2005/04/15/ PY - 2004/05/18/received PY - 2005/03/07/revised PY - 2005/03/13/accepted PY - 2005/6/14/pubmed PY - 2005/9/20/medline PY - 2005/6/14/entrez SP - 202 EP - 12 JF - Brain research. Molecular brain research JO - Brain Res. Mol. Brain Res. VL - 137 IS - 1-2 N2 - Glial activation and inflammation following brain injury may initiate and maintain the process of neurodegeneration. Both glia and neurons synthesize proinflammatory mediators such as interleukin 1 beta (IL-1beta), cytosolic phospholipase A2 (cPLA2), cyclooxygenase-2 (COX-2), and prostaglandins. The molecular mechanisms by which IL-1beta regulates inflammatory genes such as cPLA2 and COX-2 in glial and neuronal cells are poorly understood. We have studied IL-1beta-mediated gene regulation in an established glial and neuronal human cell lines. We report that IL-1beta induced cPLA2 and COX-2 mRNA and protein expression and subsequent prostaglandin E2 (PGE2) release in a time-dependent manner in H4 neuroglioma cells. Both SB203580 and PD98059 [p38 and p42/44 mitogen-activated protein kinase (MAPKs) inhibitors, respectively] reduced IL-1beta-induced PGE2 production, while only SB203580 reduced both cPLA2 and COX-2 expression. Similarly, in SKNSH neuroblastoma cells, both SB203580 and PD98059 reduced IL-1beta-induced PGE2 release, with no detectable COX-2 and cPLA2 protein expression in these cells. Our results indicate that the signaling mechanisms of p38 and p42/44 MAPKs play a role in IL-1beta-mediated PGE2 release in both of these cell lines, with differences upstream at the level of cPLA(2)/COX-2 expression. IL-1beta-induced cPLA2 and COX-2 gene expression is modulated through the p38 MAPK pathway in both neuroglioma and neuroblastoma cells. Understanding the signaling mechanisms involved in IL-1beta-mediated inflammatory processes in both glia and neuronal cells may provide potential targets for therapeutic intervention for neurological disorders. SN - 0169-328X UR - https://www.unboundmedicine.com/medline/citation/15950779/Regulation_of_the_cyclooxygenase_2_system_by_interleukin_1beta_through_mitogen_activated_protein_kinase_signaling_pathways:_a_comparative_study_of_human_neuroglioma_and_neuroblastoma_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0169-328X(05)00122-1 DB - PRIME DP - Unbound Medicine ER -