skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Oxidative stress induces senescence in human mesenchymal stem cells

Abstract

Mesenchymal stem cells (MSCs) contribute to tissue repair in vivo and form an attractive cell source for tissue engineering. Their regenerative potential is impaired by cellular senescence. The effects of oxidative stress on MSCs are still unknown. Our studies were to investigate into the proliferation potential, cytological features and the telomere linked stress response system of MSCs, subject to acute or prolonged oxidant challenge with hydrogen peroxide. Telomere length was measured using the telomere restriction fragment assay, gene expression was determined by rtPCR. Sub-lethal doses of oxidative stress reduced proliferation rates and induced senescent-morphological features and senescence-associated {beta}-galactosidase positivity. Prolonged low dose treatment with hydrogen peroxide had no effects on cell proliferation or morphology. Sub-lethal and prolonged low doses of oxidative stress considerably accelerated telomere attrition. Following acute oxidant insult p21 was up-regulated prior to returning to initial levels. TRF1 was significantly reduced, TRF2 showed a slight up-regulation. SIRT1 and XRCC5 were up-regulated after oxidant insult and expression levels increased in aging cells. Compared to fibroblasts and chondrocytes, MSCs showed an increased tolerance to oxidative stress regarding proliferation, telomere biology and gene expression with an impaired stress tolerance in aged cells.

Authors:
 [1]; ;  [2];  [1];  [2]
  1. Department of Anesthesiology, University Medical Center Regensburg, Franz-Josef-Strauss-Allee 11, 93042 Regensburg (Germany)
  2. Department of Trauma Surgery, University Medical Center Regensburg, Franz-Josef-Strauss-Allee 11, 93042 Regensburg (Germany)
Publication Date:
OSTI Identifier:
22212151
Resource Type:
Journal Article
Resource Relation:
Journal Name: Experimental Cell Research; Journal Volume: 317; Journal Issue: 11; Other Information: Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; AGING; CELL PROLIFERATION; DNA DAMAGES; FIBROBLASTS; GALACTOSIDASE; HYDROGEN PEROXIDE; IN VIVO; LETHAL DOSES; MONOCLINIC LATTICES; OXIDATION; PHOSPHATES; SODIUM COMPOUNDS; STEM CELLS

Citation Formats

Brandl, Anita, Meyer, Matthias, Bechmann, Volker, Nerlich, Michael, and Angele, Peter, E-mail: Peter.Angele@klinik.uni-regensburg.de. Oxidative stress induces senescence in human mesenchymal stem cells. United States: N. p., 2011. Web. doi:10.1016/J.YEXCR.2011.02.015.
Brandl, Anita, Meyer, Matthias, Bechmann, Volker, Nerlich, Michael, & Angele, Peter, E-mail: Peter.Angele@klinik.uni-regensburg.de. Oxidative stress induces senescence in human mesenchymal stem cells. United States. doi:10.1016/J.YEXCR.2011.02.015.
Brandl, Anita, Meyer, Matthias, Bechmann, Volker, Nerlich, Michael, and Angele, Peter, E-mail: Peter.Angele@klinik.uni-regensburg.de. Fri . "Oxidative stress induces senescence in human mesenchymal stem cells". United States. doi:10.1016/J.YEXCR.2011.02.015.
@article{osti_22212151,
title = {Oxidative stress induces senescence in human mesenchymal stem cells},
author = {Brandl, Anita and Meyer, Matthias and Bechmann, Volker and Nerlich, Michael and Angele, Peter, E-mail: Peter.Angele@klinik.uni-regensburg.de},
abstractNote = {Mesenchymal stem cells (MSCs) contribute to tissue repair in vivo and form an attractive cell source for tissue engineering. Their regenerative potential is impaired by cellular senescence. The effects of oxidative stress on MSCs are still unknown. Our studies were to investigate into the proliferation potential, cytological features and the telomere linked stress response system of MSCs, subject to acute or prolonged oxidant challenge with hydrogen peroxide. Telomere length was measured using the telomere restriction fragment assay, gene expression was determined by rtPCR. Sub-lethal doses of oxidative stress reduced proliferation rates and induced senescent-morphological features and senescence-associated {beta}-galactosidase positivity. Prolonged low dose treatment with hydrogen peroxide had no effects on cell proliferation or morphology. Sub-lethal and prolonged low doses of oxidative stress considerably accelerated telomere attrition. Following acute oxidant insult p21 was up-regulated prior to returning to initial levels. TRF1 was significantly reduced, TRF2 showed a slight up-regulation. SIRT1 and XRCC5 were up-regulated after oxidant insult and expression levels increased in aging cells. Compared to fibroblasts and chondrocytes, MSCs showed an increased tolerance to oxidative stress regarding proliferation, telomere biology and gene expression with an impaired stress tolerance in aged cells.},
doi = {10.1016/J.YEXCR.2011.02.015},
journal = {Experimental Cell Research},
number = 11,
volume = 317,
place = {United States},
year = {Fri Jul 01 00:00:00 EDT 2011},
month = {Fri Jul 01 00:00:00 EDT 2011}
}