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Related Concept Videos

Mesenchymal Stem Cells01:19

Mesenchymal Stem Cells

Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into most connective tissue cell types, except for hematopoietic cells, depending upon the source of MSCs. For example, bone-marrow-derived MSCs (BM-MSCs) can differentiate into osteocytes, hepatocytes, and pancreatic and neuronal cells. MSCs can be isolated from various sources such as bone marrow, placenta, adipose tissue, teeth, and Wharton’s jelly, a gelatinous substance in the umbilical cord. The ease of their access...

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Isolation of Rat Adipose Tissue Mesenchymal Stem Cells for Differentiation into Insulin-producing Cells
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Diabetes induced changes in rat mesenchymal stem cells.

Alexandra Stolzing1, Donna Sellers, Owen Llewelyn

  • 1Kroto Research Institute, Centre for Biomaterials and Tissue Engineering, North Campus, University of Sheffield, Sheffield, UK. alexandra.stolzing @ izi.fraunhofer.de

Cells, Tissues, Organs
|February 5, 2010
PubMed
Summary

Diabetes impairs bone health by affecting mesenchymal stem cells (MSCs). Diabetic rats showed reduced MSCs, leading to bone loss and impaired healing, suggesting MSC exhaustion as a cause of diabetes-related osteoporosis.

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Area of Science:

  • Endocrinology
  • Stem Cell Biology
  • Orthopedics

Background:

  • Diabetes mellitus is a major cause of vascular disease and is linked to bone loss and poor fracture healing.
  • Mesenchymal stem cells (MSCs) are crucial for bone formation and repair due to their differentiation potential.
  • The direct impact of diabetes on MSCs in vivo remains an area of investigation for understanding diabetes-induced bone complications.

Purpose of the Study:

  • To investigate the direct effects of diabetes on mesenchymal stem cells (MSCs) in vivo.
  • To determine if diabetes-induced alterations in MSCs contribute to bone loss and impaired healing.
  • To explore the cellular mechanisms underlying diabetes-related orthopedic issues.

Main Methods:

  • Isolated MSCs from rats with streptozotocin-induced diabetes for ex vivo analysis.
  • Assessed MSC proliferation and differentiation using the fibroblastic colony-forming unit assay.
  • Quantified bone metabolism in vivo by analyzing tibiae using quantitative computerized tomography.

Main Results:

  • Diabetic rats exhibited a significant reduction in the number and size of MSC colonies.
  • Osteoblastic differentiation potential of MSCs was markedly decreased in diabetic animals.
  • Advanced glycation end products (AGEs) and increased receptor for AGEs (RAGE) appeared to mediate MSC apoptosis and senescence, correlating with trabecular bone loss.

Conclusions:

  • Diabetes directly impacts MSCs, leading to their exhaustion and reduced differentiation capacity.
  • MSC dysfunction is a potential cellular mechanism contributing to diabetes-induced osteoporosis and impaired bone repair.
  • Targeting MSCs may offer therapeutic strategies for managing orthopedic complications in diabetes mellitus.