PMID- 28586025
OWN - NLM
STAT- MEDLINE
DCOM- 20180409
LR  - 20181113
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 16
IP  - 2
DP  - 2017 Aug
TI  - Protective role of 17beta-estradiol on tumor necrosis factor-alpha-induced apoptosis in 
      human nucleus pulposus cells.
PG  - 1093-1100
LID - 10.3892/mmr.2017.6690 [doi]
AB  - The molecular mechanisms underlying protection and pathogenesis in spinal 
      degenerative diseases remain unclear. Tumor necrosis factor-alpha (TNF-alpha) has been 
      demonstrated to induce apoptosis of inte rvertebral disc (IVD) cells during IVD 
      degeneration, and 17beta‑estradiol (17beta‑E2) has a protective effect against IVD cell 
      apoptosis. However, the underlying molecular mechanism by which 17beta‑E2 protects 
      nucleus pulposus (NP) cells remains to be investigated. The aim of the present 
      study was to evaluate whether 17beta‑E2 modulates apoptosis of human NP cells 
      induced by TNF‑alpha. In addition, the concentration‑response effect of 17beta‑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‑alpha for 48 h, with or without pretreatment with 
      various concentrations of 17beta‑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‑alpha treatment. These effects of 
      TNF‑alpha were abolished by pretreatment with 17beta‑E2 in a concentration‑dependent 
      manner. The results of the present study indicated that 17beta‑E2 serves a critical 
      role in the survival of degenerative human NP cells.
FAU - Liu, Huan
AU  - Liu H
AD  - Department of Spine Surgery, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei 050051, P.R. China.
FAU - Yang, Si-Dong
AU  - Yang SD
AD  - Department of Spine Surgery, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei 050051, P.R. China.
FAU - Xu, Ying
AU  - Xu Y
AD  - Department of Cardiology, The Traditional Chinese Medicine Hospital of Hebei 
      Medical University, Shijiazhuang, Hebei 050011, P.R. China.
FAU - Ning, Sheng-Hua
AU  - Ning SH
AD  - Department of Spine Surgery, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei 050051, P.R. China.
FAU - Wang, Tao
AU  - Wang T
AD  - Department of Spine Surgery, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei 050051, P.R. China.
FAU - Yang, Da-Long
AU  - Yang DL
AD  - Department of Spine Surgery, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei 050051, P.R. China.
FAU - Ding, Wen-Yuan
AU  - Ding WY
AD  - Department of Spine Surgery, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei 050051, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20170606
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Protective Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 4TI98Z838E (Estradiol)
RN  - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Apoptosis/*drug effects
MH  - Blotting, Western
MH  - Caspase 3/metabolism
MH  - Cell Proliferation/drug effects
MH  - Cell Shape/drug effects
MH  - Estradiol/*pharmacology
MH  - Humans
MH  - Nucleus Pulposus/drug effects/enzymology/*pathology
MH  - Poly(ADP-ribose) Polymerases/metabolism
MH  - Protective Agents/*pharmacology
MH  - Tumor Necrosis Factor-alpha/*toxicity
PMC - PMC5561935
EDAT- 2017/06/07 06:00
MHDA- 2018/04/10 06:00
PMCR- 2017/06/06
CRDT- 2017/06/07 06:00
PHST- 2016/04/27 00:00 [received]
PHST- 2017/03/23 00:00 [accepted]
PHST- 2017/06/07 06:00 [pubmed]
PHST- 2018/04/10 06:00 [medline]
PHST- 2017/06/07 06:00 [entrez]
PHST- 2017/06/06 00:00 [pmc-release]
AID - mmr-16-02-1093 [pii]
AID - 10.3892/mmr.2017.6690 [doi]
PST - ppublish
SO  - Mol Med Rep. 2017 Aug;16(2):1093-1100. doi: 10.3892/mmr.2017.6690. Epub 2017 Jun 
      6.