PMID- 32964956
OWN - NLM
STAT- MEDLINE
DCOM- 20210510
LR  - 20210510
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 17
DP  - 2020 Sep
TI  - HBP1 deficiency protects against stress-induced premature senescence of nucleus 
      pulposus.
PG  - 8685-8693
LID - 22805 [pii]
LID - 10.26355/eurrev_202009_22805 [doi]
AB  - OBJECTIVE: Senescence of nucleus pulposus (NP) cells is involved in the 
      pathological process of intervertebral disc degeneration (IVDD). HMG-box 
      transcription factor 1 (HBP1) is a transcriptional inhibitor that prevents 
      proliferation and regulates premature senescence of cells. The aim of this study 
      was to confirm whether HBP1 deficiency could protect stress-induced NP cells 
      premature senescence. PATIENTS AND METHODS: Firstly, HBP1 protein level in human 
      degenerated intervertebral disc tissues was detected. Then, NP cells were 
      isolated from disc samples and transfected with plasmid to upregulate 
      HBP1expression. H2O2 and interleukin-1b (IL-1b) were used to induce NP cells 
      premature senescence in a different manner. Thereafter, cell viability, 
      proliferation, and apoptosis were measured, and the protein expressions of 
      collagen II, HBP1, and p16, were determined by Western blot or 
      immunofluorescence. Finally, the mRNA levels of aggrecan, collagen I, IL-6, 
      Transforming Growth Factor-alpha (TNF-alpha), and matrix metalloproteinase-3 (MMP-3) were 
      determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). 
      RESULTS: The data indicated that HBP1 was upregulated in degenerated NP tissues. 
      HBP1 gene overexpression increased p16 expression, affected NP cell 
      proliferation, and caused cell apoptosis. In addition, HBP1 also decreased the 
      collagen II and aggrecan expressions but increased collagen I, IL-6, TNF-alpha, and 
      MMP-3 levels. Moreover, the silencing of HBP1 markedly reversed the H2O2 and 
      IL-1b induced NP cell senescence by reducing p16 expression, apoptotic cell 
      population, and inflammatory response and by promoting cell proliferation. 
      CONCLUSIONS: In summary, HBP1 accumulation contributes to the senescence of NP 
      cells, and HBP1 deficiency protects stress-induced NP cells premature senescence.
FAU - Liu, W
AU  - Liu W
AD  - Department of Spine Surgery, The First Hospital of Jilin University, Changchun, 
      China. 5296827@qq.com.
FAU - Li, W-C
AU  - Li WC
FAU - Pan, X-F
AU  - Pan XF
FAU - Sha, H
AU  - Sha H
FAU - Gong, W-Q
AU  - Gong WQ
FAU - Yan, M
AU  - Yan M
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Aggrecans)
RN  - 0 (CDKN2A protein, human)
RN  - 0 (Collagen Type I)
RN  - 0 (Collagen Type II)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p16)
RN  - 0 (Cytokines)
RN  - 0 (HBP1 protein, human)
RN  - 0 (High Mobility Group Proteins)
RN  - 0 (Repressor Proteins)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 3.4.24.17 (MMP3 protein, human)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Adult
MH  - Aggrecans/genetics
MH  - Cell Survival
MH  - Cellular Senescence/*genetics
MH  - Collagen Type I/genetics
MH  - Collagen Type II/genetics/metabolism
MH  - Cyclin-Dependent Kinase Inhibitor p16/metabolism
MH  - Cytokines/metabolism
MH  - Female
MH  - Gene Expression
MH  - High Mobility Group Proteins/genetics/*metabolism
MH  - Humans
MH  - Hydrogen Peroxide
MH  - Intervertebral Disc Degeneration/genetics/*metabolism
MH  - Male
MH  - Matrix Metalloproteinase 3/genetics
MH  - Middle Aged
MH  - Nucleus Pulposus/*cytology
MH  - Repressor Proteins/genetics/*metabolism
MH  - Stress, Physiological/genetics
MH  - Up-Regulation
EDAT- 2020/09/24 06:00
MHDA- 2021/05/11 06:00
CRDT- 2020/09/23 09:03
PHST- 2020/09/23 09:03 [entrez]
PHST- 2020/09/24 06:00 [pubmed]
PHST- 2021/05/11 06:00 [medline]
AID - 22805 [pii]
AID - 10.26355/eurrev_202009_22805 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):8685-8693. doi: 
      10.26355/eurrev_202009_22805.