Volume 9, Issue 5 pp. 911-915

Tendon-derived stem/progenitor cell aging: defective self-renewal and altered fate

Zuping Zhou

Zuping Zhou

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Takintope Akinbiyi

Takintope Akinbiyi

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Lili Xu

Lili Xu

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Melissa Ramcharan

Melissa Ramcharan

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Daniel J. Leong

Daniel J. Leong

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Stephen J. Ros

Stephen J. Ros

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Alexis C. Colvin

Alexis C. Colvin

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Mitchell B. Schaffler

Mitchell B. Schaffler

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Robert J. Majeska

Robert J. Majeska

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Evan L. Flatow

Evan L. Flatow

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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Hui B. Sun

Hui B. Sun

Department of Orthopaedics, Mount Sinai School of Medicine, New York, NY, USA

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First published: 16 September 2010
Citations: 165
Dr Hui B. Sun and Dr Evan L. Flatow, Department of Orthopaedics, Box 1188, Mount Sinai, School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA. Tel.: +1(212) 241 3767; fax: +1(212) 876 3168; e-mail: [email protected]or[email protected]

Summary

Aging is a major risk factor for tendon injury and impaired tendon healing, but the basis for these relationships remains poorly understood. Here we show that rat tendon-derived stem/progenitor cells (TSPCs) differ in both self-renewal and differentiation capability with age. The frequency of TSPCs in tendon tissues of aged animals is markedly reduced based on colony formation assays. Proliferation rate is decreased, cell cycle progression is delayed and cell fate patterns are also altered in aged TSPCs. In particular, expression of tendon lineage marker genes is reduced while adipocytic differentiation increased. Cited2, a multi-stimuli responsive transactivator involved in cell growth and senescence, is also downregulated in aged TSPCs while CD44, a matrix assembling and organizing protein implicated in tendon healing, is upregulated, suggesting that these genes participate in the control of TSPC function.

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