PMID- 35100096
OWN - NLM
STAT- MEDLINE
DCOM- 20220307
LR  - 20220403
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 2
DP  - 2022 Feb
TI  - High hydrostatic pressure (30 atm) enhances the apoptosis and inhibits the 
      proteoglycan synthesis and extracellular matrix level of human nucleus pulposus 
      cells via promoting the Wnt/beta-catenin pathway.
PG  - 3070-3081
LID - 10.1080/21655979.2022.2025518 [doi]
AB  - Hydrostatic pressure is known to regulate bovine nucleus pulposus cell 
      metabolism, but its mechanism in human nucleus pulposus cells (HNPCs) remains 
      obscure, which attracts our attention and becomes the focus in this study. 
      Specifically, HNPCs were treated with SKL2001 (an agonist in the Wnt/beta-catenin 
      pathway) or XAV-939 (an inhibitor of the Wnt/beta-catenin pathway), and pressurized 
      under the hydrostatic pressure of 1, 3 and 30 atm. The viability, apoptosis and 
      proteoglycan synthesis of treated HNPC were assessed by CCK-8, flow cytometry and 
      radioisotope incorporation assays. The levels of extracellular matrix, 
      Collagen-II, matrix metalloproteinase 3 (MMP3), Wnt-3a and beta-catenin were 
      measured by toluidine blue staining, immunocytochemistry and Western blot. 
      Appropriate hydrostatic stimulation (3 atm) enhanced the viability and 
      proteoglycan synthesis yet inhibited the apoptosis of HNPCs, which also 
      up-regulated extracellular matrix and Collagen-II levels, and down-regulated 
      MMP3, Wnt-3a and beta-catenin levels in treated HNPCs. Furthermore, high hydrostatic 
      pressure (30 atm) inhibited the viability and proteoglycan synthesis, and 
      promoted the morphological change and apoptosis of HNPCs, which also 
      down-regulated extracellular matrix and Collagen-II levels and up-regulated MMP3, 
      Wnt-3a and beta-catenin levels. Besides, SKL2001 reversed the effects of hydrostatic 
      pressure (3 atm) on inhibiting Wnt-3a, beta-catenin, and MMP3 levels and promoting 
      Collagen-II level in HNPC; whereas, XAV-939 reversed the effects of high 
      hydrostatic pressure (30 atm) on promoting MMP3, Wnt-3a, and beta-catenin levels and 
      inhibiting Collagen-II level and proteoglycan synthesis of HNPCs. Collectively, 
      high hydrostatic pressure promoted the apoptosis and inhibited the viability of 
      HNPCs via activating the Wnt/beta-catenin pathway.
FAU - Shi, Zongting
AU  - Shi Z
AD  - Department of Spine, Beijing University of Chinese Medicine Third Affiliated 
      Hospital, Beijing, China.
FAU - He, Jun
AU  - He J
AD  - Department of Orthopedics, Zhejiang Hospital, Hangzhou City, Zhejiang Province, 
      China.
FAU - He, Jian
AU  - He J
AD  - Department of Orthopedics, Zhejiang Hospital, Hangzhou City, Zhejiang Province, 
      China.
FAU - Xu, Yuan
AU  - Xu Y
AUID- ORCID: 0000-0001-5207-1730
AD  - Department of Orthopedics, Zhejiang Hospital, Hangzhou City, Zhejiang Province, 
      China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Proteoglycans)
RN  - 0 (beta Catenin)
SB  - IM
MH  - Apoptosis/physiology
MH  - Cells, Cultured
MH  - Extracellular Matrix/*metabolism
MH  - Humans
MH  - Hydrostatic Pressure/adverse effects
MH  - Intervertebral Disc Degeneration/etiology/metabolism/pathology
MH  - Nucleus Pulposus/cytology/metabolism/*physiology
MH  - Protein Biosynthesis/physiology
MH  - Proteoglycans/*biosynthesis
MH  - Wnt Signaling Pathway/physiology
MH  - beta Catenin/metabolism
PMC - PMC8974124
OTO - NOTNLM
OT  - Hydrostatic pressure
OT  - Wnt/beta-catenin pathway
OT  - apoptosis
OT  - human nucleus pulposus cells
OT  - viability
COIS- No potential conflict of interest was reported by the authors.
EDAT- 2022/02/01 06:00
MHDA- 2022/03/08 06:00
PMCR- 2022/01/31
CRDT- 2022/01/31 17:14
PHST- 2022/01/31 17:14 [entrez]
PHST- 2022/02/01 06:00 [pubmed]
PHST- 2022/03/08 06:00 [medline]
PHST- 2022/01/31 00:00 [pmc-release]
AID - 2025518 [pii]
AID - 10.1080/21655979.2022.2025518 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Feb;13(2):3070-3081. doi: 10.1080/21655979.2022.2025518.