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Table of Contents
Vol. 191, No. 6, 2010
Issue release date: May 2010
Section title: Original Paper
Cells Tissues Organs 2010;191:453–465
(DOI:10.1159/000281826)

Diabetes Induced Changes in Rat Mesenchymal Stem Cells

Stolzing A.a, d · Sellers D.b · Llewelyn O.a · Scutt A.a, c
aKroto Research Institute, Centre for Biomaterials and Tissue Engineering, North Campus, University of Sheffield, bBiomedical Research Centre, Sheffield Hallam University, cSection of Musculoskeletal Science, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK; dFraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: September 16, 2009
Published online: February 03, 2010
Issue release date: May 2010

Number of Print Pages: 13
Number of Figures: 10
Number of Tables: 1

ISSN: 1422-6405 (Print)
eISSN: 1422-6421 (Online)

For additional information: http://www.karger.com/CTO

Abstract

Diabetes mellitus, the single most important cause of vascular disease in the industrialized world, is also associated with bone loss and impaired fracture healing. Mesenchymal stem cells (MSCs) have the potential to differentiate into osteoblasts, chondrocytes and adipocytes and other mesenchymal cells and play a central role in bone formation and repair. Because of this, we have investigated the possibility that diabetes has direct effects on MSCs in vivo and that this might represent a cellular basis for diabetes-induced osteoporosis. We isolated MSCs from rats with streptozotocin-induced diabetes and analysed them ex vivo for their ability to proliferate and differentiate in the fibroblastic colony-forming unit assay. Effects of diabetes on bone metabolism in vivo were determined by analysing tibiae from control and diabetic animals by quantitative computerized tomography. The total number of colonies and osteoblastic colonies staining positive for alkaline phosphatase were quantified and both colony size and number were found to be significantly reduced in diabetic rats. The changes appear to be mediated by the induction of apoptosis and senescence by advanced glycation end products (AGEs), together with an increase in the receptor for AGEs (RAGE). These changes were paralleled by extensive loss of trabecular bone in the tibiae of the diabetic animals. These data suggest that MSCs become exhausted during diabetes and lose their differentiation potential, leading to a net loss of trabecular bone. Therefore, direct effects on MSCs may be responsible for some of the orthopaedic effects associated with diabetes.

© 2010 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: September 16, 2009
Published online: February 03, 2010
Issue release date: May 2010

Number of Print Pages: 13
Number of Figures: 10
Number of Tables: 1

ISSN: 1422-6405 (Print)
eISSN: 1422-6421 (Online)

For additional information: http://www.karger.com/CTO


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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