Complement protein C1q-mediated neuroprotection is correlated with regulation of neuronal gene and microRNA expression.

ABSTRACT: Activation of the complement cascade, a powerful effector mechanism of the innate immune system, is associated with neuroinflammation but also with elimination of inappropriate synapses during development. Synthesis of C1q, a recognition component of the complement system, occurs in brain during ischemia/reperfusion and Alzheimer's disease, suggesting that C1q may be a response to injury. In vitro, C1q, in the absence of other complement proteins, improves neuronal viability and neurite outgrowth and prevents β-amyloid-induced neuronal death, suggesting that C1q may have a direct neuroprotective role. Here, investigating the molecular basis for this neuroprotection in vitro, addition of C1q to rat primary cortical neurons significantly upregulated expression of genes associated with choles

SUBMITTER: Benoit ME 

PROVIDER: S-EPMC3080046 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature