Identification of unique cell type responses in pancreatic islets to stress

Marlie M. Maestas, Matthew Ishahak, Punn Augsornworawat, Daniel A. Veronese-Paniagua, Kristina G. Maxwell, Leonardo Velazco-Cruz, Erica Marquez, Jiameng Sun, Mira Shunkarova, Sarah E. Gale, Fumihiko Urano and Jeffrey R. Millman ()
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Marlie M. Maestas: Washington University School of Medicine
Matthew Ishahak: Washington University School of Medicine
Punn Augsornworawat: Mahidol University
Daniel A. Veronese-Paniagua: Washington University School of Medicine
Kristina G. Maxwell: Washington University School of Medicine
Leonardo Velazco-Cruz: Washington University School of Medicine
Erica Marquez: Washington University School of Medicine
Jiameng Sun: Washington University School of Medicine
Mira Shunkarova: Washington University School of Medicine
Sarah E. Gale: Washington University School of Medicine
Fumihiko Urano: Washington University School of Medicine
Jeffrey R. Millman: Washington University School of Medicine

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Diabetes involves the death or dysfunction of pancreatic β-cells. Analysis of bulk sequencing from human samples and studies using in vitro and in vivo models suggest that endoplasmic reticulum and inflammatory signaling play an important role in diabetes progression. To better characterize cell type-specific stress response, we perform multiplexed single-cell RNA sequencing to define the transcriptional signature of primary human islet cells exposed to endoplasmic reticulum and inflammatory stress. Through comprehensive pair-wise analysis of stress responses across pancreatic endocrine and exocrine cell types, we define changes in gene expression for each cell type under different diabetes-associated stressors. We find that β-, α-, and ductal cells have the greatest transcriptional response. We utilize stem cell-derived islets to study islet health through the candidate gene CIB1, which was upregulated under stress in primary human islets. Our findings provide insights into cell type-specific responses to diabetes-associated stress and establish a resource to identify targets for diabetes therapeutics.

Date: 2024
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DOI: 10.1038/s41467-024-49724-w

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