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Title 

Epac1-mediated Rap1 activation is not required for the production of nitric oxide in BV2, murine microglial cells

Authors 

Eun Yi MoonSu Young OhG H HanC S LeeSong Kyu Park

Publisher 

Wiley-Blackwell

Issue Date 

2005

Citation 

Journal of Neuroscience Research, vol. 81, no. 1, pp. 38-44

Keywords 

BV2cAMPEpac1lipopolysaccharide (LPS)nitric oxide (NO)PKARAP1nitric oxideanimal cellenzyme activation

Abstract 

This study demonstrates that cyclic AMP (cAMP) production is induced by lipopolysaccharide (LPS) stimulation and activates two different pathways in murine BV2 microglial cells. Two principal effector proteins for cAMP are protein kinase A (PKA) and cAMP-responsive guanine nucleotide exchange factor (Epac), a Rap GDP exchange factor. When cells were treated with various cAMP level modulators, nitric oxide (NO) production increased as the result of posttreatment with Type IV phosphodiesterase (PDE4) inhibitor, rolipram or dibutyryl-cAMP (dbcAMP), at 2 hr after LPS stimulation. Intracellular cAMP increased due to LPS stimulation and the cAMP modulators phosphorylate transcription factor CREB, which is enhanced in turn by posttreatment with dbcAMP. In contrast, the Epac-specific cAMP analog 8-(4-chloro-phenylthio)- 2′-O-methyladenosine-3′,5′-cyclic monophosphate (8CPT-2Me-cAMP) activates Rap1 in the BV2 cells, but does not induce PKA activation, as judged by CREB phosphorylation. NO production was enhanced by posttreatment with dbcAMP but not by treatment with 8CPT-2Me-cAMP. This suggests that LPS-stimulated NO production is mainly PKA-dependent and also that Epac1-mediated Rap1 activation is not required for the induction of NO production.

ISSN 

0360-4012

Link 

http://dx.doi.org/10.1002/jnr.20535

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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