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Estrogen reduces cellular aging in human mesenchymal stem cells and chondrocytes
Author(s) -
Breu Anita,
Sprinzing Benedikt,
Merkl Katharina,
Bechmann Volker,
Kujat Richard,
JeneiLanzl Zsuzsa,
Prantl Lukas,
Angele Peter
Publication year - 2011
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.21424
Subject(s) - telomere , mesenchymal stem cell , chondrogenesis , estrogen , chondrocyte , senescence , tamoxifen , microbiology and biotechnology , endocrinology , cartilage , stem cell , medicine , cell growth , estrogen receptor , biology , chemistry , anatomy , cancer , biochemistry , dna , breast cancer
Chondrocyte aging is associated with cartilage degeneration and senescence impairs the regenerative potential of mesenchymal stem cells (MSCs). Estrogen exerts profound effects on human physiology including articular cartilage and MSCs. The present study should analyze the effects of pre‐ and postmenopausal estrogen concentrations on chondrogenic cells. Physiologic premenopausal concentrations of 17β‐estradiol (E 2 ) significantly decelerated telomere attrition in MSCs and chondrocytes while postmenopausal E 2 concentration had no significant effects. The estrogen agonist–antagonist tamoxifen did not affect telomere biology, but inhibited the E 2 ‐stimulated reduction in telomere shortening. E 2 and tamoxifen did not influence cell proliferation, cell morphology, and β‐galactosidase staining in chondrogenic cells. E 2 treatment did not affect the telomere‐associated proteins TRF1 and TRF2. E 2 had no regulatory effects on the expression rates of the cell cycle regulator p21 and the DNA repair proteins SIRT1 and XRCC5. In spite of reducing telomere shortening in aging MSCs and chondrocytes, estrogen is not able to prevent somatic cells from replicative exhaustion and from finally entering senescence. The fade of telomere shortening under pre‐ to postmenopausal estrogen concentrations suggests, at least in part, a senescence‐dependent cause for the onset of osteoarthritis in women after menopause. © 2011 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29: 1563–1571, 2011