Therapeutic Activities of Multipotent Stromal Cells for Islet Regeneration

TL;DR

This paper explores how multipotent stromal cells may help regenerate insulin-producing cells in diabetes treatment.

Contribution

The paper provides an in-depth analysis of the potential regenerative mechanisms of multipotent stromal cells in beta cell regeneration.

Findings

MSC transplantation reduces hyperglycemia and aids islet repair in diabetes models.

MSC secretome has immunomodulatory and pro-regenerative properties for pancreatic tissues.

The mechanisms behind MSC-induced beta cell regeneration remain unclear and require further study.

Abstract

Diabetes mellitus is a global healthcare issue of epidemic proportions. At the root of these disorders, characterized by poor glucose regulation and insulin deficiencies, is the pancreatic beta cell and insufficient insulin signal transduction in peripheral tissues. Residual c-peptide secretion and persisting beta cells have been found in patients who have been living with type 1 diabetes for over 50 years. Thus, beta cell regeneration has been vastly studied in rodents, and many agents to expand beta cell mass are under rigorous investigation for the treatment of diabetes. Multipotent stromal cells (MSC), isolated from human bone marrow, have an immunomodulatory and pro-regenerative secretome that can aid in repairing damaged tissues, including pancreatic islets. MSC transplantation has been shown to reduce hyperglycemia and orchestrate islet repair in experimental diabetes models and is currently being assessed in clinical trials. While the immunomodulatory mechanisms of MSC are well-studied, the beta-cell-regenerative mechanisms are unknown. MSC likely play a regenerative role by signaling to resident progenitor or precursor cells in the pancreas; however, the decades-long controversy surrounding the origin of regenerated adult beta cells remains unresolved. Herein, we take a deep dive into the role of MSC in the treatment of diabetes and the potential cellular mechanisms behind the MSC stimulation of beta cell regeneration.

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