The role of the prostaglandin E2 receptors in vulnerability of oligodendrocyte precursor cells to death View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-05-23

AUTHORS

Noel G. Carlson, Satya Bellamkonda, Linda Schmidt, Jonathan Redd, Thomas Huecksteadt, Lauren Marissa Weber, Ethan Davis, Blair Wood, Takayuki Maruyama, John W. Rose

ABSTRACT

BACKGROUND: Activity of cyclooxygenase 2 (COX-2) in mouse oligodendrocyte precursor cells (OPCs) modulates vulnerability to excitotoxic challenge. The mechanism by which COX-2 renders OPCs more sensitive to excitotoxicity is not known. In the present study, we examined the hypothesis that OPC excitotoxic death is augmented by COX-2-generated prostaglandin E2 (PGE2) acting on specific prostanoid receptors which could contribute to OPC death. METHODS: Dispersed OPC cultures prepared from mice brains were examined for expression of PGE2 receptors and the ability to generate PGE2 following activation of glutamate receptors with kainic acid (KA). OPC death in cultures was induced by either KA, 3'-O-(Benzoyl) benzoyl ATP (BzATP) (which stimulates the purinergic receptor P2X7), or TNFα, and the effects of EP3 receptor agonists and antagonists on OPC viability were examined. RESULTS: Stimulation of OPC cultures with KA resulted in nearly a twofold increase in PGE2. OPCs expressed all four PGE receptors (EP1-EP4) as indicated by immunofluorescence and Western blot analyses; however, EP3 was the most abundantly expressed. The EP3 receptor was identified as a candidate contributing to OPC excitotoxic death based on pharmacological evidence. Treatment of OPCs with an EP1/EP3 agonist 17 phenyl-trinor PGE2 reversed protection from a COX-2 inhibitor while inhibition of EP3 receptor protected OPCs from excitotoxicity. Inhibition with an EP1 antagonist had no effect on OPC excitotoxic death. Moreover, inhibition of EP3 was protective against toxic stimulation with KA, BzATP, or TNFα. CONCLUSION: Therefore, inhibitors of the EP3 receptor appear to enhance survival of OPCs following toxic challenge and may help facilitate remyelination. More... »

PAGES

101

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12974-015-0323-7

DOI

http://dx.doi.org/10.1186/s12974-015-0323-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044809922

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25997851


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84 kainic acid
85 mechanism
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87 mouse oligodendrocyte precursor cells
88 oligodendrocyte precursor cells
89 pharmacological evidence
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92 present study
93 prostaglandin E2
94 prostaglandin E2 receptor
95 prostanoid receptors
96 protection
97 receptor agonist
98 receptors
99 remyelination
100 renders OPCs
101 role
102 specific prostanoid receptor
103 stimulation
104 study
105 survival
106 survival of OPCs
107 toxic challenge
108 toxic stimulation
109 treatment
110 twofold increase
111 viability
112 vulnerability
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