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Optimizing beta cell function through mesenchymal stromal cell-mediated mitochondria transfer.

Chloe L Rackham1, Ella L Hubber1, Anna Czajka1

  • 1Department of Diabetes, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.

Stem Cells (Dayton, Ohio)
|January 9, 2020
PubMed
Summary
This summary is machine-generated.

Mesenchymal stromal cells (MSCs) transfer mitochondria to islet beta-cells, enhancing insulin secretion. This mitochondrial transfer, partly via tunneling nanotubes, is crucial for improving islet function and holds promise for clinical islet transplantation therapies.

Keywords:
diabetesislet transplantationmesenchymal stromal cellsmitochondrial transfer

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Area of Science:

  • Cell Biology
  • Immunology
  • Endocrinology

Background:

  • Pretransplant islet culture often leads to reduced islet cell mass and impaired insulin secretion.
  • Mesenchymal stromal cells (MSCs) can improve islet function in vitro, correlating with better in vivo graft outcomes.
  • Insulin secretion is tightly regulated by mitochondrial ATP production in beta-cells.

Purpose of the Study:

  • To investigate if improved islet function after coculture with MSCs is due to mitochondrial transfer from MSCs to islets.
  • To elucidate the mechanism and extent of mitochondrial transfer between MSCs and islet beta-cells.

Main Methods:

  • Coculture of human adipose-derived MSCs with human islet beta-cells.
  • Fluorescence imaging to visualize and confirm mitochondrial transfer.
  • Comparison of mitochondrial transfer efficiency between human and mouse islets under various conditions (e.g., hypoxia).

Main Results:

  • Demonstrated direct mitochondrial transfer from human MSCs to human islet beta-cells in coculture.
  • Identified tunneling nanotube (TNT)-like structures as a mechanism for mitochondrial transfer.
  • Observed greater mitochondrial transfer to human islets compared to mouse islets, potentially due to greater cellular stress in human islets.
  • Showed increased MSC-mediated mitochondrial transfer to hypoxia-exposed mouse islets.

Conclusions:

  • Mesenchymal stromal cells effectively transfer mitochondria to islet beta-cells, enhancing their function.
  • Mitochondrial transfer, potentially via TNTs, is a key mechanism by which MSCs support islet health.
  • Optimizing MSC-derived mitochondrial transfer could enhance the therapeutic potential of MSCs for clinical islet transplantation, especially for compromised beta-cells.