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Bone marrow transplantation stimulates pancreatic β-cell replication after tissue damage.

Rosengren, Anders LU ; Taneera, Jalal LU ; Rymo, Simin and Renström, Erik LU (2009) In Islets 1(1). p.10-18
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Islets
volume
1
issue
1
pages
10 - 18
publisher
Landes Bioscience
external identifiers
  • wos:000207900400003
  • pmid:21084844
  • scopus:79953247251
ISSN
1938-2022
DOI
10.4161/isl.1.1.8529
language
English
LU publication?
yes
id
b40f7c20-1ada-4228-890d-5016f54db4a7 (old id 1731844)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21084844?dopt=Abstract
date added to LUP
2010-12-01 12:52:43
date last changed
2017-01-01 07:32:19
@article{b40f7c20-1ada-4228-890d-5016f54db4a7,
  abstract     = {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.},
  author       = {Rosengren, Anders and Taneera, Jalal and Rymo, Simin and Renström, Erik},
  issn         = {1938-2022},
  language     = {eng},
  number       = {1},
  pages        = {10--18},
  publisher    = {Landes Bioscience},
  series       = {Islets},
  title        = {Bone marrow transplantation stimulates pancreatic β-cell replication after tissue damage.},
  url          = {http://dx.doi.org/10.4161/isl.1.1.8529},
  volume       = {1},
  year         = {2009},
}