TP508 Promotes Bone Regeneration on Distraction Osteogenesis via the Activation of Wnt/β-catenin Signaling Pathway

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INTRODUCTION: TP508 is a thrombin peptide that participates in the inflammatory response and wound healing. Its role in the molecular mechanism of distraction osteogenesis remains unclear. This study established a tibia distraction osteogenesis (DO) model in rats and investigated the role and mechanism of TP508 in bone regeneration during DO.

METHOD: Micro-computed tomography (Micro-CT) and hematoxylin-eosin (HE) staining were used to track osteogenesis. Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to measure the expression of osteoblast-related factors, Wnt/β- catenin signaling-related proteins and genes. Immunohistochemistry was used to measure the expression of β-catenin in the cytoplasm and nucleus. TP508 accelerated bone regeneration increased the expression of the osteoblast-related factors Alkaline phosphatase (ALP), runt-related transcription factor 2 (RUNX2), and osteocalcin (OCN).

RESULTS: After the Wnt signaling was inhibited by LGK974, the expression of osteoblast-related factors was downregulated, leading to a decrease in bone regeneration ability. More importantly, TP508 upregulated β-catenin and its target CYCLIN-D1 and could reverse the decreased osteogenic ability caused by LGK974.

CONCLUSION: In conclusion, TP508 promotes bone regeneration in DO by activating the Wnt/β- catenin signaling pathway.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - year:2024

Enthalten in:

Current pharmaceutical biotechnology - (2024) vom: 11. März

Sprache:

Englisch

Beteiligte Personen:

Li, Kehan [VerfasserIn]
Liu, Linan [VerfasserIn]
Zhang, Jingyi [VerfasserIn]
Liao, Chenyu [VerfasserIn]
Hu, Jian [VerfasserIn]
Song, Jian [VerfasserIn]

Links:

Volltext

Themen:

Distraction osteogenesis
Journal Article
Molecular mechanism
TP508
Thrombin peptide
Tissue engineering
Wnt signalling

Anmerkungen:

Date Revised 12.03.2024

published: Print-Electronic

Citation Status Publisher

doi:

10.2174/0113892010289575240306033011

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM369582527