Exogenous parathyroid hormone alleviates intervertebral disc degeneration through the sonic hedgehog signalling pathway mediated by creb

Abstract: As an important hormone that regulates the balance of calcium and phosphorus, parathyroid hormone (PTH) has also been found to have an important function in intervertebral disc degeneration (IVDD). Our aim was to investigate the mechanism by which PTH alleviates IVDD. In this study, the PTH 1 receptor was found to be highly expressed in severely degenerated human nucleus pulposus (NP) cells. We found in the mouse model of IVDD that supplementation with exogenous PTH alleviated the narrowing of the intervertebral space and the degradation of the extracellular matrix (ECM) caused by tail suspension (TS). In addition, inflammation, oxidative stress, and apoptosis levels were significantly increased in the intervertebral disc tissues of TS-induced mice, and the activity of NP cells was decreased. TS also led to the downregulation of Sonic hedgehog (SHH) signalling pathway-related signal molecules in NP cells such as SHH, Smoothened, and GLI1. However, supplementation with exogenous PTH can reverse these changes. In vitro, PTH also promotes the activity of NP cells and the secretion of ECM. However, the antagonist of the SHH signalling pathway can inhibit the therapeutic effect of PTH on NP cells. In addition, a cAMP-response element-binding protein, as an important transcription factor, was found to mediate the promotion of PTH on the SHH signalling pathway. Our results revealed that PTH can alleviate IVDD by inhibiting inflammation, oxidative stress, and apoptosis and improving the activity of NP cells via activating the SHH signalling pathway

Location
Deutsche Nationalbibliothek Frankfurt am Main
Extent
Online-Ressource
Language
Englisch
Notes
ISSN: 1942-0994

Event
Veröffentlichung
(where)
Freiburg
(who)
Universität
(when)
2024
Creator
Li, You
Wei, Yifan
Li, He
Che, Hui
Miao, Dengshun
Ma, Cheng
Ren, Yongxin

DOI
10.1155/2022/9955677
URN
urn:nbn:de:bsz:25-freidok-2456359
Rights
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Last update
14.08.2025, 10:48 AM CEST

Data provider

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Associated

  • Li, You
  • Wei, Yifan
  • Li, He
  • Che, Hui
  • Miao, Dengshun
  • Ma, Cheng
  • Ren, Yongxin
  • Universität

Time of origin

  • 2024

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