Resources: Posters

Multi-Modal Single-Cell Phenotyping Resolves bona fide Senescent Cells in Human Preadipocytes

October 6, 2026

Cell Press Symposia: Hallmarks of Aging

Keywords: Cellular senescence, human preadipocytes, senolytics, SenMayo, p21/CDKN1A, SA-β-gal, multimodal single-cell profiling

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This poster, developed in collaboration with Nathan K. LeBrasseur of the Robert and Arlene Kogod Center on Aging at Mayo Clinic, presents a multimodal single-cell workflow for finding bona fide senescent cells. No single biomarker can do this reliably. Primary human preadipocytes were cultured in CellCage^TM enclosures on the Cellanome R3200 and treated with etoposide to induce senescence. Each cell was then profiled across several readouts at once: longitudinal brightfield imaging, cell morphology, proliferation history, SA-β-gal activity, p21/CDKN1A expression, and the SenMayo transcript signature from whole-transcriptome RNA-seq. Combining these per cell showed a multimodally senescent population, about 8% of etoposide-treated cells, compared with 1.1% or less in vehicle controls. In a follow-up experiment, senolytic treatment with dasatinib, quercetin, or both reduced the large, p21-positive cell fraction from 19% to as low as 5%. That makes the approach a foundation for high-content senolytic and senomorphic screening and senescence atlas efforts.

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Case Study: Functional Profiling of Microglia in Neuroinflammation

Link microglial behavior to gene expression at single-cell resolution, for insight into neuroinflammation, drug response, and immune dysfunction in CNS disease.

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Phagocytosis assay in CellCage enclosures - (click to expand image).

Researchers used the Cellanome R3200 to enclose individual microglia with fluorescent particles and track phagocytosis over 12 hours via fluorescent imaging. Each cell’s transcriptome was then sequenced, linking activity levels to gene expression.

What They Found:

High-activity microglia upregulated genes in complement signaling, lipid metabolism, and lysosomal function — key pathways in neuroinflammation and repair.

Why it Matters:

This approach overcomes key limitations in standard assays by capturing phagocytic function and gene expression in the same individual cells without dissociation, pooling, or inference. It enables a direct, scalable readout of immune heterogeneity, and reveals the transcriptional programs driving effective or impaired microglial responses.

‍What’s Next:

Extend to co-cultures by layering enclosed microglia over intact neuronal networks. Study how cell-cell interactions shape phagocytic behavior and fate. Combine with cytokines, CRISPR libraries, or immunotherapies to generate longitudinal datasets linking live-cell behavior with molecular readouts for MoA analysis, early biomarker discovery, and AI-guided modeling in CNS disease.

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Case Study: Modeling Synapse Formation and Developmental Trajectories in 3D

Track development, function, and gene expression in intact neurospheres, a human-relevant 3D model increasingly vital as regulators move away from animal studies.

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Neurospheres in windowed cages that allow them to reach out to form a synapse - (click to expand image).

Stem-cell-derived neurospheres offer a robust 3D model of early brain development, but standard assays disrupt their structure and miss critical dynamics.

Approach:

Using the Cellanome R3200, the research team explored:

Hundreds of intact neurospheres (100–200 cells each) were cultured inside individual CellCage™ enclosures.
Axon extension, synapse formation and calcium activity were tracked over multiple days.
End-point RNA-Seq was linked back to each neurosphere’s functional behavior.
UMAP clustering revealed lineage-specific gene programs, validated by fluorescent markers.

‍What's Next:

This approach supports CRISPR-based screens to probe mechanisms of development, degeneration, and repair by linking perturbations to longitudinal functional and molecular readouts within preserved 3D architecture.

‍Why it Matters:

As the FDA and others move to reduce reliance on animal models, human-relevant in vitro systems like this are increasingly essential.

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FAQ's

Why is it difficult to identify senescent cells?

No single biomarker is both sensitive and specific for senescence. Most single-cell methods also measure different features in separate samples, so you can’t tell whether multiple hallmarks appear in the same cell. In this study, Cellanome scientists and Mayo Clinic aging researcher Nathan K. LeBrasseur measured imaging and transcriptomic hallmarks on the same individual cells, so markers could be required together.

Which senescence readouts were measured in each cell?

Each cell got its whole transcriptome plus SA-β-gal activity, cell size and shape, image-based proliferation history, p21/CDKN1A mRNA, and a SenMayo gene signature score. All of it came from the same cell inside its own CellCage enclosure.

How was senescence induced and tracked on the platform?

Early-passage human preadipocytes were loaded onto fibronectin-coated flow cells and enclosed one cell per CellCage. They were treated with 20 μM etoposide for 2 days and then grown for 5 more days. Brightfield images were taken over the 7 days, followed by fluorescent staining and RNA capture on day 7.

Can this workflow be used for senolytic drug screening?

Yes. Dasatinib and quercetin each reduced the large, p21-positive senescent fraction, and the combination cut it from 19% to 5%. Because the drug response is read in imaging and transcriptomics together, the approach can help clarify how specific a senolytic is.

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