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Jauneau AC, Ischenko A, Chatagner A, et al. Interleukin-1beta and anaphylatoxins exert a synergistic effect on NGF expression by astrocytes. J Neuroinflammation. 2006;3:8doi: 10.1186/1742-2094-3-8.
Jauneau, A. C., Ischenko, A., Chatagner, A., Benard, M., Chan, P., Schouft, M. T., Patte, C., Vaudry, H., & Fontaine, M. (2006). Interleukin-1beta and anaphylatoxins exert a synergistic effect on NGF expression by astrocytes. Journal of neuroinflammation, 38. https://doi.org/10.1186/1742-2094-3-8
Jauneau, Anne-christine, et al. "Interleukin-1beta and anaphylatoxins exert a synergistic effect on NGF expression by astrocytes." Journal of neuroinflammation vol. 3 (2006): 8. doi: https://doi.org/10.1186/1742-2094-3-8
Jauneau AC, Ischenko A, Chatagner A, Benard M, Chan P, Schouft MT, Patte C, Vaudry H, Fontaine M. Interleukin-1beta and anaphylatoxins exert a synergistic effect on NGF expression by astrocytes. J Neuroinflammation. 2006 Apr 04;3:8. doi: 10.1186/1742-2094-3-8. PMID: 16594997; PMCID: PMC1482689.
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J Neuroinflammation. 2006 Apr 04;3:8. doi: 10.1186/1742-2094-3-8.

Interleukin-1beta and anaphylatoxins exert a synergistic effect on NGF expression by astrocytes.

Journal of neuroinflammation

Anne-christine Jauneau, Alexander Ischenko, Alexandra Chatagner, Magalie Benard, Philippe Chan, Marie-therese Schouft, Christine Patte, Hubert Vaudry, Marc Fontaine

Affiliations

  1. Institut Fédératif de Recherche Multidisciplinaire sur les Peptides no23, INSERM U413, Faculté des Sciences, 76130 Mont-St-Aignan, France. [email protected]

PMID: 16594997 PMCID: PMC1482689 DOI: 10.1186/1742-2094-3-8

Abstract

C3a and C5a anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that anaphylatoxins could mediate neuroprotection. In this study, we used RT-PCR and ribonuclease protection assays (RPA) to investigate the role of anaphylatoxins on neurotrophin expression by the human glioblastoma cell line T98G and by rat astrocytes. Our data show that for both cell types, anaphylatoxins upregulate expression of NGF mRNA. This response depended on a G protein-coupled pathway since pre-treatment of cells with pertussis toxin (PTX) completely blocked NGF mRNA increases. This effect was anaphylatoxin-specific since pre-incubation with anti-C3a or anti-C5aR antibodies abolished the effects of C3a and C5a, respectively. The regulation of NGF mRNA by anaphylatoxins was not accompanied by translation into protein expression, but there was a significant synergic effect of anaphylatoxins/IL-1b costimulation. Our demonstration of involvement of anaphylatoxins in the NGF release process by astrocytes suggests that C3a and C5a could modulate neuronal survival in the CNS.

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