The Wilson lab new report describing a CRISPR-based platform to study COPD genes in iPSC-alveolar cells

Genome-wide association studies (GWAS) have identified dozens of loci associated with chronic obstructive
pulmonary disease (COPD) susceptibility; however, the function of associated genes in the cell type(s) affected in
disease remains poorly understood, partly due to a lack of cell models that recapitulate human alveolar biology.
Here, we apply CRISPR interference to interrogate the function of nine genes implicated in COPD by GWAS in
induced pluripotent stem cell–derived type 2 alveolar epithelial cells (iAT2s). We find that multiple genes
implicated by GWAS affect iAT2 function, including differentiation potential, maturation, and/or proliferation.
Detailed characterization of the GWAS gene DSP demonstrates that it regulates iAT2 cell-cell junctions, proliferation,
mitochondrial function, and response to cigarette smoke–induced injury. Our approach thus elucidates the
biological function, as well as disease-relevant consequences of dysfunction, of genes implicated in COPD by GWAS
in type 2 alveolar epithelial cells.

 

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My name is Gabrielle. I'm the Administrative Assistant at CReM. Leave us a short message down below. We will get back to you ASAP!

Our research focuses on understanding how lung epithelial progenitors interact with their supportive niche in the contexts of pulmonary disease and repair. We use cell culture, mouse models, and cell engraftment to study and augment these interactions with the ultimate goal of establishing novel therapies for pulmonary disease.

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