The role of TGF ‐β1/Smad2/3 pathway in platelet‐rich plasma in retarding intervertebral disc degeneration

Autor: Qing Shi, Chunshen Wu, Chenxi Yuan, Xue-Feng Li, Xuesong Zhu, Huilin Yang, Jun Zou, Jiale Qian
Rok vydání: 2016
Předmět:
0301 basic medicine
Pathology
medicine.medical_specialty
Nucleus Pulposus
nucleus pulpous
Blotting
Western

rabbit
Enzyme-Linked Immunosorbent Assay
Smad2 Protein
Real-Time Polymerase Chain Reaction
Transforming Growth Factor beta1
Extracellular matrix
03 medical and health sciences
0302 clinical medicine
medicine
Animals
Platelet
Smad3 Protein
Platelet activation
Collagen Type II
Aggrecan
Cell Proliferation
intervertebral disc degeneration
Platelet Count
Platelet-Rich Plasma
Chemistry
Intervertebral disc
Original Articles
Cell Biology
TGF‐β1/Smad2/3
Immunohistochemistry
Magnetic Resonance Imaging
Cell biology
030104 developmental biology
medicine.anatomical_structure
Gene Expression Regulation
030220 oncology & carcinogenesis
Platelet-rich plasma
Molecular Medicine
Original Article
Rabbits
Signal transduction
platelet‐rich plasma
Signal Transduction
Transforming growth factor
Zdroj: Journal of Cellular and Molecular Medicine
ISSN: 1582-4934
1582-1838
DOI: 10.1111/jcmm.12847
Popis: Recent studies have suggested that platelet‐rich plasma (PRP) injections are an effective way to retard intervertebral disc degeneration, but the mechanism of action is unclear. Activated platelets release some growth factors, such as transforming growth factor‐β1 (TGF‐β1), which positively modulate the extracellular matrix of nucleus pulposus cells. The purpose of this study was to explore the mechanism underlying the PRP‐mediated inhibition of intervertebral disc degeneration. In an in vitro study, we found that the proliferation of nucleus pulposus cells was greatly enhanced with 2.5% PRP treatment. The TGF‐β1 concentration was much higher after PRP treatment. PRP administration effectively increased the collagen II, aggrecan and sox‐9 mRNA levels and decreased collagen X levels. However, Western blotting demonstrated that specifically inhibiting TGF‐β1 signalling could significantly prevent nucleus pulpous cellular expression of Smad2/3 and matrix protein. In a rabbit study, magnetic resonance imaging revealed significant recovery signal intensity in the intervertebral discs of the PRP injection group compared with the very low signal intensity in the control groups. Histologically, the PRP plus inhibitor injection group had significantly lower expression levels of Smad2/3 and collagen II than the PRP group. These results demonstrated that a high TGF‐β1 content in the platelets retarded disc degeneration in vitro and in vivo. Inhibiting the TGF‐β1/Smad2/3 pathway could prevent this recovery by inactivating Smad2/3 and down‐regulating the extracellular matrix. Therefore, the TGF‐β1/Smad2/3 pathway might play a critical role in the ability of PRP to retard intervertebral disc degeneration.
Databáze: OpenAIRE