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BMC Neuroscience

, 8:82

First Online: 03 October 2007Received: 17 January 2007Accepted: 03 October 2007


BackgroundInterleukin-3 IL-3 is an important glycoprotein involved in regulating biological responses such as cell proliferation, survival and differentiation. Its effects are mediated via interaction with cell surface receptors. Several studies have demonstrated the expression of IL-3 in neurons and astrocytes of the hippocampus and cortices in normal mouse brain, suggesting a physiological role of IL-3 in the central nervous system. Although there is evidence indicating that IL-3 is expressed in some neuronal populations, its physiological role in these cells is poorly known.

ResultsIn this study, we demonstrated the expression of IL-3 receptor in cortical neurons, and analyzed its influence on amyloid β Aβ-treated cells. In these cells, IL-3 can activate at least three classical signalling pathways, Jak-STAT, Ras-MAP kinase and the PI 3-kinase. Viability assays indicated that IL-3 might play a neuroprotective role in cells treated with Aβ fibrils. It is of interest to note that our results suggest that cell survival induced by IL-3 required PI 3-kinase and Jak-STAT pathway activation, but not MAP kinase. In addition, IL-3 induced an increase of the anti-apoptotic protein Bcl-2.

ConclusionAltogether these data strongly suggest that IL-3 neuroprotects neuronal cells against neurodegenerative agents like Aβ.

AbbreviationsThe abbreviations used areIL-3, Interleukin 3


JAKsJanus kinases

STATsignal transducers and activators of transcription

MAPKmitogen-activated protein kinase

ERKextracellular signal-regulated protein kinases

PI 3kphosphatidylinositol 3-kinase

PKBprotein kinase B

ADAlzheimer-s disease

PBSphosphate buffered saline

BSAbovine serum albumin

MTT3- 4,5-dimethylthiazol 2-yl-2,5 diphenyltetrazolium bromide

TUNELterminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2202-8-82 contains supplementary material, which is available to authorized users.

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Autor: Angara Zambrano - Carola Otth - Lorena Mujica - Ilona I Concha - Ricardo B Maccioni


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