cat no | io1031, io1032
ioMicroglia APOE 4/4 C112R/C112R™
Human iPSC-derived Alzheimer's disease model
ioMicroglia APOE 4/4 are opti-ox™ precision reprogrammed microglia carrying a genetically engineered homozygous C112R mutation in the APOE gene, converting the wild-type APOE3 allele to APOE4, encoding the apolipoprotein E4. The APOE4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease (AD).
These cells offer a functional, rapidly maturing, and disease relevant system to study the role of APOE4 in late-onset AD, alongside a genetically matched wild-type control.
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Confidently investigate your phenotype of interest across multiple clones with our disease model clone panel. Detailed characterisation data (below) and bulk RNA sequencing data (upon request) help you select specific clones if required.
Benchtop benefits
Making True Comparisons
Pair the ioDisease Model Cells with the genetically matched wild-type ioMicroglia to directly investigate the effect of APOE4 on late-onset AD.
Quick
Rapidly maturing cells that are ready to use within 10 days post-revival, in mono- and co-cultures.
Functional
Disease model cells display key phagocytic and cytokine secretion functions.
Cells arrive ready to plate
ioMicroglia APOE 4/4 are delivered in a cryopreserved format and are programmed to rapidly mature upon revival in the recommended media. The protocol for the generation of these cells is a three-phase process: an Induction phase that is carried out at bit.bio, Phase 1: Stabilisation for 24 hours, Phase 2: Maturation for a further 9 days, Phase 3: the Maintenance phase. Cells are ready to use from day 10.
Highly characterised and defined
Disease model cells express key microglia markers comparably to the genetically matched wild-type control
Immunofluorescent staining on day 10 post-revival demonstrates similar homogenous expression of microglia markers IBA1 and P2RY12 and ramified morphology in both disease model clones compared to the genetically matched wild-type (WT) control. 100X magnification.
Disease model cells show expected ramified morphology by day 10
Both disease model clones mature rapidly and key ramified morphology can be identified by day 4 and continues through to day 10, similarly to the WT control. Day 1 to 10 post-thawing; 100x magnification.
Key phagocytic function
Disease model cells show a reduced proportion of phagocytosis of E. coli particles compared to the genetically matched wild-type control
Phagocytosis was analysed at day 10 post-revival after incubation with 1 µg/0.33 cm2 pHrodo™ RED labelled E. coli particles for 24 hours +/- cytochalasin D control. The graph displays the proportion of cells phagocytosing E. coli particles over 24 hours and shows that both disease model clones display a reduced proportion of phagocytosis compared to the WT control. Images were acquired every 30 mins on the Incucyte® looking at red fluorescence and phase contrast. Three technical replicates were performed experiment.
Disease model cells show a reduced degree of phagocytosis of E. coli particles compared to the genetically matched wild-type control
Phagocytosis was analysed at day 10 post-revival after incubation with 1 µg/0.33 cm2 pHrodo™ RED labelled E. coli particles for 24 hours +/- cytochalasin D control. The graph displays the fluorescence intensity per cell displaying degree of phagocytosis per cell and shows that both disease model clones display a reduced degree of phagocytosis per cell compared to the WT control. Images were acquired every 30 mins on the Incucyte® looking at red fluorescence and phase contrast. Three technical replicates were performed experiment.
Key cytokine secretion function
Disease model cells display reduced secretion of pro-inflammatory cytokines upon activation compared to the genetically matched wild-type control
Cytokine secretion was analysed at day 10 post-revival after stimulation with LPS 100 ng/ml and IFNɣ 20 ng/ml for 24 hours. This revealed that both disease model clones secrete the predominantly pro-inflammatory cytokines, IL-6, IL-8, IL-10, IL-12p70, IL-1β, and TNF⍺ at a lower-level compared to the WT control. Supernatants were harvested and analysed using MSD V-plex Proinflammatory Kit™. Three technical replicates were performed experiment.
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