Nuclear factor-kappaB activation regulates Cyclooxygenase-2 induction in human astrocytes in response to CXCL12: Role in neuronal toxicity.

Nuclear factor-kappaB activation regulates Cyclooxygenase-2 induction in human astrocytes in response to CXCL12: Role in neuronal toxicity.

J Neurochem. 2010 Feb 17;

Authors: Alvarez S, Blanco A, Fresno M, Muñoz-Fernández MA

Abstract Neurodegenerative and neuroinflammatory disorders are commonly associated with local chemokine release. In other way, emerging data indicate that the prostaglandin E2 (PGE(2)), one of the major prostaglandins produced in the brain, play a central role in several pathological diseases. Here, we have investigated the relationship between CXCL12, cyclooxygenase-2 (COX-2) and PGE(2) in human brain cells. CXCL12 induced COX-2 and secretion of PGE(2) in a dose-dependent manner in human astrocytes. This induction was abolished by treatment with PTx and AMD3100, confirming the role of CXCR4 signaling. The NF-kappaB involvement was confirmed by using PDTC, and with transient transfection assays. Overexpression of IkappaBalpha abrogated COX-2 induction, and CXCL12 induced p65/relA translocation. Culture supernatants from CXCL12-treated astrocytes reduced viability of neuroblastoma cells, and COX inhibitors abrogated this toxicity. Therefore, the relationship between chemokines and PGs could differentially influence the pathogenic network responsible for neurodegeneration.

PMID: 20180883 [PubMed - as supplied by publisher]

Read the complete post at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&db=PubMed&cmd=Retrieve&list_uids=20180883&dopt=Abstract

Posted 26 Feb 2010 4:13 AM by pubmed: neuroblastoma
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