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Epac1-mediated Rap1 activation is not required for the production of nitric oxide in BV2, murine microglial cells.
J Neurosci Res. 2005 Jul 01; 81(1):38-44.JN

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.

Authors+Show Affiliations

Laboratory of Human Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Taejeon, Korea. eunyi@kribb.re.krNo 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

15931667

Citation

Moon, Eun-Yi, et al. "Epac1-mediated Rap1 Activation Is Not Required for the Production of Nitric Oxide in BV2, Murine Microglial Cells." Journal of Neuroscience Research, vol. 81, no. 1, 2005, pp. 38-44.
Moon EY, Oh SY, Han GH, et al. Epac1-mediated Rap1 activation is not required for the production of nitric oxide in BV2, murine microglial cells. J Neurosci Res. 2005;81(1):38-44.
Moon, E. Y., Oh, S. Y., Han, G. H., Lee, C. S., & Park, S. K. (2005). Epac1-mediated Rap1 activation is not required for the production of nitric oxide in BV2, murine microglial cells. Journal of Neuroscience Research, 81(1), 38-44.
Moon EY, et al. Epac1-mediated Rap1 Activation Is Not Required for the Production of Nitric Oxide in BV2, Murine Microglial Cells. J Neurosci Res. 2005 Jul 1;81(1):38-44. PubMed PMID: 15931667.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epac1-mediated Rap1 activation is not required for the production of nitric oxide in BV2, murine microglial cells. AU - Moon,Eun-Yi, AU - Oh,Su-Young, AU - Han,Gyoon-Hee, AU - Lee,Chul-Sang, AU - Park,Song-Kyu, PY - 2005/6/3/pubmed PY - 2005/11/4/medline PY - 2005/6/3/entrez SP - 38 EP - 44 JF - Journal of neuroscience research JO - J Neurosci Res VL - 81 IS - 1 N2 - 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. SN - 0360-4012 UR - https://www.unboundmedicine.com/medline/citation/15931667/Epac1_mediated_Rap1_activation_is_not_required_for_the_production_of_nitric_oxide_in_BV2_murine_microglial_cells_ L2 - https://doi.org/10.1002/jnr.20535 DB - PRIME DP - Unbound Medicine ER -