Bone marrow transplantation stimulates pancreatic β-cell replication after tissue damage.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1731844
- author
- Rosengren, Anders LU ; Taneera, Jalal LU ; Rymo, Simin and Renström, Erik LU
- organization
- publishing date
- 2009
- 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
- pmid:21084844
- 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
- 2016-04-04 07:37:35
- date last changed
- 2024-04-12 18:49:26
@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}},
doi = {{10.4161/isl.1.1.8529}},
volume = {{1}},
year = {{2009}},
}