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Author Correction: Targeted pharmacological therapy restores β-cell function for diabetes remission

Authors:
Stephan Sachs
Stephan Sachs
Stephan Sachs
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Aimée Bastidas-Ponce
Aimée Bastidas-Ponce
Aimée Bastidas-Ponce
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Sophie Tritschler
Sophie Tritschler
Sophie Tritschler
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Mostafa Bakhti at Helmholtz Zentrum München Deutsches Forschungszentrum für Gesundheit und Umwelt (GmbH)
Mostafa Bakhti
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Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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AmendmenTs
https://doi.org/10.1038/s42255-020-0201-1
Author Correction: Targeted pharmacological therapy restores β-cell function for
diabetes remission
Stephan Sachs, Aimée Bastidas-Ponce, Sophie Tritschler, Mostafa Bakhti , Anika Böttcher, Miguel A. Sánchez-Garrido,
Marta Tarquis-Medina, Maximilian Kleinert, Katrin Fischer, Sigrid Jall, Alexandra Harger, Erik Bader, Sara Roscioni,
Siegfried Ussar , Annette Feuchtinger, Burcak Yesildag, Aparna Neelakandhan, Christine B. Jensen, Marion Cornu,
Bin Yang, Brian Finan , Richard D. DiMarchi, Matthias H. Tschöp , Fabian J. Theis , Susanna M. Hofmann ,
Timo D. Müller  and Heiko Lickert
Correction to: Nature Metabolism https://doi.org/10.1038/s42255-020-0171-3, published online 20 February 2020.
In the version of this article initially published, in Fig. 7c, in the ‘Day 25’ panels, the ‘GLP-1–oestrogen’ image mistakenly duplicated the
‘PEG–insulin’ image. The error has been corrected in the HTML and PDF versions of the article.
Published online: 14 April 2020
https://doi.org/10.1038/s42255-020-0201-1
© The Author(s), under exclusive licence to Springer Nature Limited 2020
Original
Day 25
No STZ mSTZ PEG–insulin GLP-1–oes + PEG–ins
Corrected
Day 25
No STZ mSTZ GLP-1–oes + PEG–insPEG–insulinGLP-1–oestrogen
GLP-1–oestrogen
Fig 7c | Original and corrected Day 25 panels.
Nature MetabolisM | VOL 2 | APRIL 2020 | 380 | www.nature.com/natmetab
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... Diabetes mellitus is a complex metabolic disorder that results from the malfunction of the endocrine pancreas. In both type 1 (T1D) and type 2 diabetes (T2D), autoimmunity and glucolipotoxicity respectively lead to dedifferentiation, dysfunction and ultimately loss of insulin-producing β-cells, key events in the disease progression [1][2][3]. These glucose-/nutrient-sensing and insulin-secreting cells are central for glucose homeostasis and exist as a heterogeneous population in health and disease [4,5]. ...
... In healthy islets, β-cells contain immature and mature subpopulations. Furthermore, upon exposure to stress, β-cells upregulate a stress response and undergo dedifferentiation along a developmental trajectory, partially overlapping with the transcriptome of embryonic and neonatal β-cells [1,2]. Therefore, successful regenerative strategies can be achieved by stopping the stress and redifferentiation of dedifferentiated β-cells. ...
... Differential gene expression between β-cell subclusters were determined with scanpy's rank_genes_groups function. For other analyses, processed, normalized, and annotated single cell RNA sequencing data were downloaded from the following databases with the accession number GSE132188 [41], GSE128565 [2], GSE117770 [42], GSE114412 [43] and GSE84133 [44]. The scRNA-seq count data (10X Genomics Chromium protocol) from GSE117770 [41] were downloaded, filtered, normalized by library size (CPM normalization with target sum 10,000) and log+1 scaled. ...
CD81 marks immature and dedifferentiated pancreatic β-cells
Article
Full-text available
  • Feb 2021
Objective The islets of Langerhans contain heterogeneous populations of insulin-producing β-cells. Surface markers and respective antibodies for isolation, tracking and analysis are urgently needed to study β-cell heterogeneity and to explore the mechanisms to harness the regenerative potential of immature β-cells. Methods We performed single-cell mRNA profiling of early postnatal mouse islets and re-analyzed several single-cell mRNA sequencing datasets from mouse and human pancreas and islets. We used mouse primary islets, iPSC-derived endocrine cells, Min6 insulinoma and human EndoC-βH1 β-cell lines and performed FAC sorting, western blotting and imaging to support and complement the findings from the data analyses. Results We found that all endocrine cell types expressed the cluster of differentiation 81 (CD81) during pancreas development, but the expression levels of this protein were gradually reduced in β-cells during postnatal β-cell maturation. Single cell gene expression profiling and high-resolution imaging revealed an immature signature of β-cells expressing high levels of CD81 (CD81high) compared to a more mature population expressing no or low levels of this protein (CD81low/-). Analysis of β-cells from different diabetic mouse models and in vitro β-cell stress assays indicated an upregulation of CD81 expression levels in stressed and dedifferentiated β-cells. Similarly, CD81 is upregulated and marks stressed human β-cells in vitro. Conclusions Here, we identified CD81 as a novel surface marker that labels immature, stressed and dedifferentiated β-cells in the adult mouse and human islets. This novel surface marker will allow to better study β-cell heterogeneity in healthy and diabetes progression.
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... This would involve delivery of small molecules or transcription factors to the target population and specificity of the delivery would be of major importance to ensure both efficiency and elimination of side effects. There are several promising avenues for targeting b cells (163)(164)(165)(166) but knowledge of the receptors present on the surface of other target cells will be essential. This necessitates the unequivocal identification and thorough characterization of the target cells, but this remains elusive even in mouse models. ...
Debates in Pancreatic Beta Cell Biology: Proliferation Versus Progenitor Differentiation and Transdifferentiation in Restoring β Cell Mass
Article
Full-text available
  • Aug 2021
In all forms of diabetes, β cell mass or function is reduced and therefore the capacity of the pancreatic cells for regeneration or replenishment is a critical need. Diverse lines of research have shown the capacity of endocrine as well as acinar, ductal and centroacinar cells to generate new β cells. Several experimental approaches using injury models, pharmacological or genetic interventions, isolation and in vitro expansion of putative progenitors followed by transplantations or a combination thereof have suggested several pathways for β cell neogenesis or regeneration. The experimental results have also generated controversy related to the limitations and interpretation of the experimental approaches and ultimately their physiological relevance, particularly when considering differences between mouse, the primary animal model, and human. As a result, consensus is lacking regarding the relative importance of islet cell proliferation or progenitor differentiation and transdifferentiation of other pancreatic cell types in generating new β cells. In this review we summarize and evaluate recent experimental approaches and findings related to islet regeneration and address their relevance and potential clinical application in the fight against diabetes.
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