ArticleCell & bioscience2021
Changes to the identity of EndoC-βH1 beta cells may be mediated by stress-induced depletion of HNRNPD.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- RNA binding proteins (RBPs) on genetic stability and diseases.Global medical genetics · 2025Review
- Differences in gene expression between high and low tolerance rainbow trout (Oncorhynchus mykiss) to acute thermal stress.PloS one · 2025Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundBeta cell identity changes occur in the islets of donors with diabetes, but the molecular basis of this remains unclear. Protecting residual functional beta cells from cell identity changes may be beneficial for patients with diabetes.
resultsA somatostatin-positive cell population was induced in stressed clonal human EndoC-βH1 beta cells and was isolated using FACS. A transcriptomic characterisation of somatostatin-positive cells was then carried out. Gain of somatostatin-positivity was associated with marked dysregulation of the non-coding genome. Very few coding genes were differentially expressed. Potential candidate effector genes were assessed by targeted gene knockdown. Targeted knockdown of the HNRNPD gene induced the emergence of a somatostatin-positive cell population in clonal EndoC-βH1 beta cells comparable with that we have previously reported in stressed cells.
conclusionsWe report here a role for the HNRNPD gene in determination of beta cell identity in response to cellular stress. These findings widen our understanding of the role of RNA binding proteins and RNA biology in determining cell identity and may be important for protecting remaining beta cell reserve in diabetes.
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