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Engineered vasculature induces functional maturation of pluripotent stem cell-derived islet organoids

ABSTRACT: Engineered vasculature induces functional maturation of pluripotent stem cell-derived islet organoids

PROVIDER: PRJNA1159163 | ENA |

REPOSITORIES: ENA

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Engineered vasculature induces functional maturation of pluripotent stem cell-derived islet organoids

Project description:Blood vessels play a critical role in pancreatic islet function, yet current methods for deriving islet organoids from human pluripotent stem cells (SC-islets) lack vasculature. We engineered 3D vascularized SC-islet organoids by assembling SC-islet cells, human primary endothelial cells (ECs) and fibroblasts in a non-perfused model and a microfluidic device with perfused vessels. Vasculature improved stimulus-dependent Ca2+ influx into SC-β-cells, a hallmark of β-cell function that is blunted in non-vascularized SC-islets. Furthermore, vascularization accelerated diabetes reversal post-engraftment of a subtherapeutic SC-islet dose. We show that vasculature leads to formation of an islet-like basement membrane that contributes to functional improvement of SC-β-cells. Furthermore, scRNA-seq data predicted BMP2/4-BMPR2 signaling from ECs to SC-β cells, and correspondingly, BMP4 enhanced the SC-β cell Ca2+ response and insulin secretion. Vascularized SC-islets will enable further studies of crosstalk between β-cells and ECs and will serve as an in vitro platform for disease modeling and therapeutic testing.

2025-08-20 | GSE276815 | GEO

Vascularization of pluripotent stem cell-derived islet organoids improves β-cell function

Project description:Blood vessels play a critical role in pancreatic islet health and function, yet current culture methods to generate islet organoids from human pluripotent stem cells (SC-islets) lack a vascular component. Here, we engineered 3D vascularized SC-islet organoids by assembling SC-islet cells, human primary endothelial cells (ECs) and fibroblasts both in a non-perfused model and a microfluidic device with perfused vessels. Vasculature improved stimulus-dependent Ca2+ influx into SC-β-cells; a hallmark of β-cell function that is blunted in non-vascularized SC-islets. We show that an islet-like basement membrane is formed by vasculature and contributes to the functional improvement of SC-β-cells. Furthermore, cell-cell communication networks based on scRNA-seq data predicted BMP2/4-BMPR2 signaling from ECs to SC-β-cells. Correspondingly, BMP4 augmented the SC-β-cell Ca2+ response and insulin secretion. The here-described vascularized SC-islet models will enable further studies of crosstalk between β-cells and ECs and serve as an in vivo-mimicking platform for disease modeling and therapeutic testing.

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Project description:Repositioning the early pathology of type 1 diabetes to the extra-islet vasculature.

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Islet-specific microRNA changes driven by nutrient shift trigger postnatal beta-cell maturation - intact islet microRNAs

Project description:We found that in rodents, postnatal beta-cell maturation is associated with changes in the expression of several islet microRNAs and discovered that these modifications are driven by changes in the nutrient supply. Mimicking the microRNA changes observed during ?-cell maturation in newborn rat islet cells was sufficient to promote glucose-induced insulin release and to achieve a mature ?-cell secretory phenotype. Moreover, the modifications in the level of some of these microRNAs reduced the proliferation of newborn ?-cells, suggesting that they contribute to the limited proliferative capacity of adult ?-cells. These findings demonstrated that miRNAs contribute to postnatal beta-cell maturation and development. Their role is likely to promote beta-cell adaptation to fule supply and to maintain glucose homeostasis by regulating insulin release and proliferation. Islets from 10-day-old rats (P10) (n=5) or 3-month-old male rat (n=6) were taken. Total RNA was extracted and microRNA profiling was performed using the Illumina TruSeq small RNA kit and single-end sequencing.

2014-09-06 | E-GEOD-61180 | biostudies-arrayexpress

Islet-specific microRNA changes driven by nutrient shift trigger postnatal beta-cell maturation - intact islet mRNAs

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2014-09-06 | E-GEOD-61179 | biostudies-arrayexpress

LncRNA and mRNA changes during postnatal islet maturation

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Proteomic profiling of intra-islet features reveals substructure-specific protein signatures

Project description:LCM-coupled nanoPOTS proteomics using FAIMS of intra-islet microstructures. 5 acinar samples, 5 whole islets, 5 islet interface vasculature pools, 5 islet inner microvasculature pools, 3 islets after microsvasculature removed.

2022-01-25 | MSV000088730 | MassIVE

Single-cell RNA-seq of engineered healthy human kidney organoids

Project description:Single-cell RNA-seq of engineered healthy human kidney organoids. These data are part of a larger investigation (data not provided here) showing that SARS-CoV-2 can directly infect engineered human blood vessel organoids and human kidney organoids which can be inhibited by human recombinant soluble ACE2 (hrsACE2), demonstrating that hrsACE2 can significantly block early stages of SARS-CoV-2 infections.

2020-04-05 | GSE147863 | GEO

Islet-specific microRNA changes driven by nutrient shift trigger postnatal beta-cell maturation - intact islet mRNAs

Project description:We found that in rodents, postnatal beta-cell maturation is associated with changes in the expression of several islet microRNAs and discovered that these modifications are driven by changes in the nutrient supply. Mimicking the microRNA changes observed during β-cell maturation in newborn rat islet cells was sufficient to promote glucose-induced insulin release and to achieve a mature β-cell secretory phenotype. Moreover, the modifications in the level of some of these microRNAs reduced the proliferation of newborn β-cells, suggesting that they contribute to the limited proliferative capacity of adult β-cells. These findings demonstrated that miRNAs contribute to postnatal beta-cell maturation and development. Their role is likely to promote beta-cell adaptation to fule supply and to maintain glucose homeostasis by regulating insulin release and proliferation.

2014-09-06 | GSE61179 | GEO

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