Effects of Estrogen on Chondrocyte Proliferation and Collagen Synthesis in Skeletally Mature Articular Cartilage

Talwar, Reena M.; Wong, Brendan S.; Svoboda, Kathy K.H.; Harper, Richard P.

doi:10.1016/j.joms.2005.12.006

Cited by 76 publications

(58 citation statements)

References 36 publications

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“…Thus, the level of estrogen may have had an influence on chondrocyte proliferation and differentiation. As reported by previous studies (12)(13)(14), ovariectomy significantly stimulates chondrocyte proliferation and matrix synthesis in the growth plate cartilage, probably through IGF-I (13). This may be one of the reasons contributing to chondrocyte proliferation and inhibition of the removal of hypertrophic chondrocytes.…”

Section: Discussionsupporting

confidence: 66%

Osteoporosis increases chondrocyte proliferation without a change in apoptosis during fracture healing in an ovariectomized rat model

Chen

2011

Mol Med Report

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Abstract. Osteoporotic fractures commonly occur in the elderly. Current studies regarding cell proliferation and apoptosis during osteoporotic fracture healing are limited. In this study, we established an osteoporotic fracture healing model. Bone loss and callus formation were monitored with DXA, cell proliferation was examined using immunohistochemistry with BrdU monoclonal antibody and apoptotic cells were detected using the TUNEL method. Both cell proliferation and apoptosis occurred during the entire period of the study. BrdU immunostaining showed a decreasing tendency in the process of fracture healing. On days 20 and 30 post-fracture, the percentage of BrdU-positive cells in ovariectomized rats was significantly higher compared to sham-operated rats. TUNEL-positive chondrocytes reached a peak on day 20 postfracture. There was no significant difference between the two groups. Our results indicate that osteoporosis markedly delays the fracture healing process, mostly due to increased chondrocyte proliferation without a change in chondrocyte apoptosis.

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Section: Discussionsupporting

confidence: 66%

Osteoporosis increases chondrocyte proliferation without a change in apoptosis during fracture healing in an ovariectomized rat model

Chen

2011

Mol Med Report

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“…One limitation of this approach is the potential confounding effects of tamoxifen. As an estrogen metabolite, tamoxifen promotes growth plate chondrocyte apoptosis and reduces the proliferation of articular chondrocytes (33,34). We did not observe any changes in growth plate depth or proliferative growth plate chondrocytes in tamoxifeninjected C57 animals.…”

Section: Discussioncontrasting

confidence: 51%

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

Bradley

Carpio

Olson

et al. 2015

Journal of Biological Chemistry

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Background: Hdac7 is a transcriptional co-repressor in skeletal tissues, but its role in chondrocytes is undefined. Results: Proteasomal degradation reduced Hdac7 levels during chondrogenic maturation and conditional deletion of Hdac7 in chondrocytes increased proliferation and ␤-catenin levels. Conclusion: Hdac7 degradation enhances ␤-catenin transcriptional activity in growth plate chondrocytes. Significance: Suppressing Hdac7 levels increases chondrocyte proliferation and promotes cartilage formation and regeneration.

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“…Growth hormone, for example, has been shown to stimulate growth of the mandibular condyle while estrogen reduces it. 9,10 Growth factors and cytokines are local mediators which are rapidly degraded or inactivated. They can be secreted in response to mechanical and inflammatory stimuli.…”

Section: Introductionmentioning

confidence: 99%

Role of Growth Factors in the Development of Mandible

Leander¹

2011

JIOS

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The exhaustive research over the past four decades has focused on the natural growth of the mandibular condyle and growth changes during the use of different orthopedic appliances on experimental animals. Cartilage growth is partly genetically determined but is strongly influenced by epigenetic factors. The latter includes systemic factors and local factors, such as growth factors and mechanical stimuli. Growth factors and cytokines are local mediators which are rapidly degraded or inactivated. They can be secreted in response to mechanical and inflammatory stimuli.Growth factors are a large family of polypeptide molecules that regulate cell division in many tissues by autocrine or paracrine mechanisms.Depending on what receptors are activated, growth factors can initiate mitogenic, antiproliferative or trophic effects, that is growth factors act as positive or negative modulators of cell proliferation. The synergistic and orchestrated influences of various growth factors and other regulatory factors that are endogenously expressed in the condyle have been well documented. Growth factors do not only play an important role in embryonic development and adult tissue homeostasis but also in pathological situations, like infection and wound healing. Consequently, the applications of growth factors have therapeutic applications.

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Effects of Estrogen on Chondrocyte Proliferation and Collagen Synthesis in Skeletally Mature Articular Cartilage

Cited by 76 publications

References 36 publications

Osteoporosis increases chondrocyte proliferation without a change in apoptosis during fracture healing in an ovariectomized rat model

Osteoporosis increases chondrocyte proliferation without a change in apoptosis during fracture healing in an ovariectomized rat model

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

Role of Growth Factors in the Development of Mandible

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