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Updated: May 15, 2026
09:25
A Protocol to Acquire the Degenerative Tenocyte from Humans
Published on: June 9, 2018
In vitro tenocyte metabolism in aging and oestrogen deficiency
P Torricelli1, F Veronesi, S Pagani
1Preclinical and Surgical Studies Laboratory, Codivilla Putti Research Institute, Rizzoli Orthopaedic Institute, via di Barbiano, 1/10, 40136, Bologna, Italy, paola.torricelli@ior.it.
Age (Dordrecht, Netherlands)
|January 1, 2013
Summary
Aging and estrogen deficiency impair tendon healing. This study found reduced tenocyte proliferation, collagen, and healing rates in older and ovariectomized rats, highlighting risks for tendon injuries.
Area of Science:
- Biomedical Science
- Cell Biology
- Musculoskeletal Research
Background:
- Tendon aging and estrogen deficiency effects on tenocyte behavior are poorly understood.
- Estrogen plays a role in maintaining tendon health and function.
- Aging and hormonal changes can increase susceptibility to tendon injuries.
Purpose of the Study:
- To investigate the in vitro effects of aging and estrogen deficiency on rat tenocyte proliferation and metabolism.
- To assess differences in tendon healing using an in vitro micro-wound model.
- To elucidate the impact of senescence and estrogen loss on tenocyte function.
Main Methods:
- Isolation and culture of tenocytes from young, aged, and ovariectomized (OVX) rat Achilles tendons.
- Assessment of tenocyte proliferation, collagen I, aggrecan, elastin, fibronectin, vascular endothelial growth factor, and metalloproteinase-13.
- Utilizing an in vitro micro-wound healing model to evaluate healing rate, cell migration, collagen III, and nitric oxide production.
Main Results:
- Aged and OVX tenocytes exhibited significantly lower proliferation rates and reduced levels of collagen I, aggrecan, and elastin compared to young tenocytes.
- OVX tenocytes showed decreased fibronectin and elastin, but increased vascular endothelial growth factor and metalloproteinase-13 compared to young and aged groups.
- In the micro-wound model, aged and OVX tenocytes demonstrated impaired healing rates, proliferation, collagen I, and nitric oxide production, with OVX tenocytes showing further deficits in elastin and cell migration.
Conclusions:
- Aging and, particularly, estrogen deficiency significantly impair tenocyte metabolism and tendon healing capacity.
- These findings underscore the negative impact of senescence and estrogen loss on tendon health.
- Further research is warranted to develop strategies for preventing tendon injuries in aging and menopausal populations.
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