Protective role of 17β-estradiol on tumor necrosis factor-α-induced apoptosis in human nucleus pulposus cells.
In: Molecular Medicine Reports, Jg. 16 (2017-08-01), Heft 2, S. 1093-1100
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Zugriff:
The molecular mechanisms underlying protection and pathogenesis in spinal degenerative diseases remain unclear. Tumor necrosis factor-α (TNF-α) has been demonstrated to induce apoptosis of inte rvertebral disc (IVD) cells during IVD degeneration, and 17β-estradiol (17β-E2) has a protective effect against IVD cell apoptosis. However, the underlying molecular mechanism by which 17β-E2 protects nucleus pulposus (NP) cells remains to be investigated. The aim of the present study was to evaluate whether 17β-E2 modulates apoptosis of human NP cells induced by TNF-α. In addition, the concentration-response effect of 17β-E2 on human NP cells was investigated. Human NP cells were cultured in complete medium, which was replaced every three days until the culture was ~80% confluent. Cells were treated with 100 ng/ml TNF-α for 48 h, with or without pretreatment with various concentrations of 17β-E2, and ICI 182,780, for 30 min. Morphologic alterations characteristic of apoptosis were observed by inverted phase-contrast microscopy and Hoechst 33258 staining; the apoptosis rate was analyzed by flow cytometry. A Cell Counting kit-8 assay was used to assess cell proliferation. Furthermore, caspase-3 activity was determined and proteins associated with apoptosis were analyzed by western blotting. The level of apoptosis and caspase-3 activity in human NP cells increased, whereas proliferation and the expression of poly ADP-ribose polymerase decreased following TNF-α treatment. These effects of TNF-α were abolished by pretreatment with 17β-E2 in a concentration-dependent manner. The results of the present study indicated that 17β-E2 serves a critical role in the survival of degenerative human NP cells. [ABSTRACT FROM AUTHOR]
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Protective role of 17β-estradiol on tumor necrosis factor-α-induced apoptosis in human nucleus pulposus cells.
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Autor/in / Beteiligte Person: | HUAN, LIU ; SI-DONG, YANG ; YING, XU ; SHENG-HUA, NING ; TAO, WANG ; DA-LONG, YANG ; WEN-YUAN, DING |
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Zeitschrift: | Molecular Medicine Reports, Jg. 16 (2017-08-01), Heft 2, S. 1093-1100 |
Veröffentlichung: | 2017 |
Medientyp: | academicJournal |
ISSN: | 1791-2997 (print) |
DOI: | 10.3892/mmr.2017.6690 |
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