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Modulation of gene expression by complement protein C1q in amyloid-beta injured neurons

ABSTRACT: Complement protein C1q is induced after injury in the brain and during Alzheimer's disease and has been shown to protect against amyloid-beta induced neuronal death. In this study, we used microarray approach to identify the pathways modulated by C1q that are associated with neuroprotection. Immature rat cortical primary neurons are treated with fibrillar amyloid-beta peptides and/or C1q for 3h before RNA extraction and hybridization on rat Affymetrix microarrays. Supplementary file: Processed/normalized, probe-level signal intensities from neurons treated with amyloid-beta or C1q. Median signal intensity used as global normalization method, done with JMP genomics (v5.0) software.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Marie Benoit 

PROVIDER: E-GEOD-28886 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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C1q-induced LRP1B and GPR6 proteins expressed early in Alzheimer disease mouse models, are essential for the C1q-mediated protection against amyloid-β neurotoxicity.

Benoit Marie E ME   Hernandez Michael X MX   Dinh Minhan L ML   Benavente Francisca F   Vasquez Osvaldo O   Tenner Andrea J AJ  

The Journal of biological chemistry 20121113 1

Complement protein C1q is induced in the brain in response to a variety of neuronal injuries, including Alzheimer disease (AD), and blocks fibrillar amyloid-β (fAβ) neurotoxicity in vitro. Here, we show that C1q protects immature and mature primary neurons against fAβ toxicity, and we report for the first time that C1q prevents toxicity induced by oligomeric forms of amyloid-β (Aβ). Gene expression analysis reveals C1q-activated phosphorylated cAMP-response element-binding protein and AP-1, two  ...[more]

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