Bone marrow transplantation stimulates pancreatic β−cell replication after tissue damage

Bone marrow transplantation has been shown to normalize hyperglycemia but the mechanisms underlying pancreatic β-cell regeneration remain elusive. Here, we investigate the capacity of transplanted bone marrow cells to engraft into the pancreas, to adopt an endothelial cell phenotype and to stimulate...

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Bibliographic Details
Published in:	Islets Vol. 1; no. 1; pp. 10 - 18
Main Authors:	Rosengren, Andres H., Taneera, Jalal, Rymo, Simin, Renström, Erik
Format:	Journal Article
Language:	English
Published:	United States Taylor & Francis 01-07-2009
Subjects:	Algorithms Animals Binding Biology Bioscience Bone Marrow Transplantation - physiology Calcium Cancer Cell Cell Proliferation Clinical Medicine Cycle Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - pathology Diabetes Mellitus, Experimental - physiopathology Endocrinology and Diabetes Endokrinologi och diabetes Humans Insulin-Secreting Cells - pathology Insulin-Secreting Cells - physiology Klinisk medicin Landes Medical and Health Sciences Medicin och hälsovetenskap Mice Mice, Inbred C57BL Mice, Transgenic Organogenesis Pancreas - drug effects Pancreas - pathology Pancreas - physiopathology Pancreatic Diseases - chemically induced Pancreatic Diseases - pathology Pancreatic Diseases - physiopathology Pancreatic Diseases - therapy Proteins Receptor Protein-Tyrosine Kinases - genetics Receptor, TIE-2 Streptozocin Up-Regulation - physiology
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Summary:	Bone marrow transplantation has been shown to normalize hyperglycemia but the mechanisms underlying pancreatic β-cell regeneration remain elusive. Here, we investigate the capacity of transplanted bone marrow cells to engraft into the pancreas, to adopt an endothelial cell phenotype and to stimulate β-cell regeneration after islet damage. Genetically marked whole bone marrow from Tie2-Cre/ZEG mice was transplanted into lethally irradiated wild-type mice. The fate of the transplanted cells, as well as blood glucose levels and β-cell mass dynamics, was investigated in normal and hyperglycemic recipient mice. Bone marrow transplantation significantly increased β-cell mass and reduced the hyperglycemia of mice subjected to β-cell damage by streptozotocin (STZ). This was associated with enhanced replication of pre-existing β-cells, proportional to the degree of β-cell damage, whereas no evidence was obtained for islet neogenesis. The engrafted bone marrow-derived cells in the pancreas showed little capacity to differentiate into blood vessel endothelium but retained a myeloid cell fate. By contrast, the transplantation evoked pronounced proliferation of recipient endothelial cells. These findings illuminate an important adjuvant function of transplanted bone marrow cells in both angiogenesis and β-cell regeneration. This may have interesting clinical implications, not least for human islet transplantation endeavours, where co-transplantation of islets with bone marrow cells might represent a simple means to improve islet survival and function.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1938-2014 1938-2022 1938-2022
DOI:	10.4161/isl.1.1.8529