Project description:The effect of C1q knockout on brain gene expression was examined in non-transgenic and TauP301S mice. Complement pathway has been shown to play an important role in neurodegenerative diseases, and in-house data show that C1QC KO protects against neurodegeneration in Alzheimer's disease (AD) model. TauP301S mice have neuroinflammation and neurodegeneration in the brain and is AD model. The most severe pathology of this disease model is in hippocampus.
Project description:Microarray analysis of cortices, hippocampi and brainstems of Nrf2 knockout mice, Three independent RNAs from cortices, hippocampi and brainstems of Nrf2 knockout and wild-type control mice were used for the microarray analyses.
Project description:We have data from a previous microarray experiment which shows that C1q elicits macrophages to express genes important for clearance of dead (apoptotic) cells. In this experiment we want to determine the signaling mechanism by which C1q is turning on macrophage gene expression. For our control (sample 1-3) we heated C1q to denature it so it is inactive. We also want to know which portion of C1q is responsible for activation the macrophage so we generated C1qtails (samples 4-5). We also have macrophages treated with the whole C1q molecule (7-9). And finally we have a cell line (J774) treated with C1q but does not activate the cells (samples 10-12). Bone marrow derived macrophages or J774 cells were adhered to heat inactivated C1q, C1q tails or C1q for 18 hours. Cells were harvested and RNA was isolated and converted to double stranded cDNA and subsequently labeled and hybridized onto NimbleGen mouse gene expression array [100718_MM9_EXP] using Nimblegen Hybridization system 4 according to manufacturerM-bM-^@M-^Ys instructions (Roche)