Pancreatic function and diabetes
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It is demonstrated that mRNA-based delivery of cell cycle regulators can overcome the intrinsic cell cycle block in beta cells and may provide a controllable approach for beta-cell regeneration.
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Pancreatic beta cells exhibit marked resistance to proliferation, posing a barrier to therapeutic strategies aimed at restoring beta-cell mass in diabetes. Here, we present a transient, non-integrative approach to stimulate beta-cell proliferation using in vitro transcribed (IVT) mRNAs encoding cell cycle regulators. In rodent beta cells and human-beta cell derived EndoC-BH5 cells, chemically modified IVT mRNAs activated cell cycle entry and subsequent mitosis. A single dose of cyclin D1 and CDK4 IVT mRNAs nearly doubled the number of rat beta cells. However, achieving cell division in human beta cells required co-delivery of MYC IVT mRNA. The mitogenic response of beta cells peaked within 36-60 hours, and declined thereafter, reflecting the transient nature of IVT mRNA. Transcriptomic profiling revealed temporary activation of proliferative pathways and reversible downregulation of beta-cell maturation markers. Importantly, we detected no evidence of sustained proliferation. Our findings demonstrate that mRNA-based delivery of cell cycle regulators can overcome the intrinsic cell cycle block in beta cells and may provide a controllable approach for beta-cell regeneration.
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@article{Koblas2026Stimulation,
title = {Stimulation of rodent and human beta-cell proliferation using synthetic modified mRNAs encoding cell cycle regulators},
author = {Tomas Koblas and Katerina Bittenglova and Pavel Abaffy and K. Zacharovová and Peter Girman and Lukáš Valihrach and Jan Kriz and Frantisek Saudek},
journal = {bioRxiv (Cold Spring Harbor Laboratory)},
year = {2026},
doi = {10.64898/2026.08.21.746224},
url = {https://doi.org/10.64898/2026.08.21.746224}
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