JNK signalling mediates aspects of maternal immune activation: importance of maternal genotype in relation to schizophrenia risk.

ABSTRACT:

Background

Important insight into the mechanisms through which gene-environmental interactions cause schizophrenia can be achieved through preclinical studies combining prenatal immune stimuli with disease-related genetic risk modifications. Accumulating evidence associates JNK signalling molecules, including MKK7/MAP2K7, with genetic risk. We tested the hypothesis that Map2k7 gene haploinsufficiency in mice would alter the prenatal immune response to the viral mimetic polyriboinosinic-polyribocytidylic acid (polyI:C), specifically investigating the impact of maternal versus foetal genetic variants.

Methods

PolyI:C was administered to dams (E12.5), and cytokine/chemokine levels were measured 6 h later, in maternal plasma, placenta and embryonic brain.

Results

PolyI:C

SUBMITTER: Openshaw RL 

PROVIDER: S-EPMC6350402 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature