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Published on: March 30, 2018
NPY and CGRP Inhibitor Influence on ERK Pathway and Macrophage Aggregation during Fracture Healing
Peng Tang1, Chunguang Duan1, Zheng Wang1
1Department of Trauma and Orthopaedics, Xijing Hospital, the Fourth Military Medical University, Xi'an, China.
Aim:
The aims of this study are to investigate the effects of neurotransmitters NPY and CGRP on ERK signaling in fracture healing, and to identify the correlation between macrophage aggregation and fracture healing.
Methods:
Male Sprague-Dawley rats were used to build a fracture model. The neurotransmitter receptor inhibitors were injected intraperitoneally into the rats. Immunofluorescence staining and ELISA were employed to determine the expression of NPY and CGRP in fracture area and the peripheral blood, respectively. Micro-CT together with histological staining were utilized to assess the fracture healing conditions. Relative protein expression was determined using western blot. Immunofluorescence staining was used to detect the aggregation of macrophages in the injury area.
Results:
During fracture healing, the serum NPY and CGRP significantly increased. The levels of NPY and CGRP reached a peak in the 8th week and reduced significantly thereafter. NPY and CGRP inhibitors could inhibit fracture healing and down-regulate the phosphorylated ERK. Macrophages (NPY+ and CGRP+) aggregated in the injury area.
Conclusion:
NPY and CGRP participated in fracture healing, in which they were also shown to influence phosphorylated ERK expression. In addition, macrophages are involved in the fracture healing process.
Insights
Neuropeptide Y (NPY) and Calcitonin Gene-Related Peptide (CGRP) influence fracture healing by affecting ERK signaling and macrophage aggregation. Their levels peak around 8 weeks post-injury.
Area of Science:
- Biomedical research
- Molecular biology
- Regenerative medicine
Background:
- Fracture healing is a complex biological process.
- The roles of specific neurotransmitters in bone repair are not fully understood.
- ERK signaling pathway is crucial for cellular processes, including bone regeneration.
Purpose of the Study:
- To investigate the effects of Neuropeptide Y (NPY) and Calcitonin Gene-Related Peptide (CGRP) on ERK signaling in fracture healing.
- To determine the correlation between macrophage aggregation and the efficiency of fracture healing.
Main Methods:
- A rat fracture model was established.
- Neurotransmitter receptor inhibitors were administered.
- Immunofluorescence, ELISA, Micro-CT, and Western blot were used to assess molecular and histological changes.
- Macrophage aggregation was quantified in the injury area.
Main Results:
- Serum levels of NPY and CGRP increased significantly during fracture healing, peaking at 8 weeks.
- Inhibitors of NPY and CGRP impaired fracture healing and reduced phosphorylated ERK levels.
- Macrophages expressing NPY and CGRP were observed to aggregate at the fracture site.
Conclusions:
- NPY and CGRP play a role in fracture healing.
- These neurotransmitters modulate phosphorylated ERK expression during bone repair.
- Macrophage aggregation is associated with the fracture healing process.
