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Updated: Nov 2, 2025
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
The Expression of Semaphorin 7A in Human Periapical Lesions
Yao Song1, Liu Wang1, Jiatong Li1
1State Key Laboratory of Oral Diseases and National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Introduction:
Semaphorin 7A (SEMA7A) is a membrane-bound or secretory protein exerting multiple functions in the regulation of inflammation, neural degradation, and cancer progression. Human periapical lesions are chronic and infectious diseases mainly caused by bacteria. However, the involvement of SEMA7A in human periapical lesions is still unclear. This study aimed to explore the expression of SEMA7A in human periapical lesions accompanied by the potential association of SEMA7A with matrix metalloproteinase (MMP)-1 and MMP-3 during the progression of apical periodontitis.
Methods:
Samples of periapical lesions and healthy controls were collected. Total RNA and protein were extracted respectively for quantitative real-time polymerase chain reaction and Western blot analysis. Additionally, 6 healthy samples and 27 periapical lesion samples were fixed, dehydrated, and embedded for further histologic and immunochemical analysis. The expression of SEMA7A was quantified by average integrated optical density. Immunofluorescence analysis was conducted to explore the colocalization of SEMA7A/MMP-1 and SEMA7A/MMP-3.
Results:
Compared with healthy controls, the messenger RNA and protein expression of SEMA7A was markedly up-regulated in periapical lesions. A stronger expression of MMP-1, MMP-3, and inflammatory cytokines was exhibited in periapical lesions than in healthy groups. An increasing expression of SEMA7A can be observed in both the periapical granuloma group and the radicular cyst group compared with the normal group (P < .01). Immunofluorescence results showed the colocalization of SEMA7A with both MMP-1 and MMP-3 in vascular vessels and extracellular matrix.
Conclusions:
SEMA7A was up-regulated in periapical periodontitis and might be involved in the tissue destruction and infiltration of immune cells in periapical lesions.
Insights
Semaphorin 7A (SEMA7A) is elevated in periapical lesions, suggesting its role in tissue destruction and immune cell infiltration during apical periodontitis.
Area of Science:
- Oral Biology
- Immunology
- Pathology
Background:
- Semaphorin 7A (SEMA7A) is implicated in inflammation, neural degradation, and cancer.
- Human periapical lesions are chronic bacterial infections with unclear SEMA7A involvement.
- Apical periodontitis involves tissue destruction and immune cell infiltration.
Purpose of the Study:
- To investigate SEMA7A expression in human periapical lesions.
- To explore the association between SEMA7A and matrix metalloproteinases (MMP)-1 and MMP-3 in apical periodontitis.
Main Methods:
- Quantitative real-time PCR and Western blot for SEMA7A expression.
- Histologic and immunochemical analysis of periapical lesion and healthy samples.
- Immunofluorescence to assess SEMA7A colocalization with MMP-1 and MMP-3.
Main Results:
- SEMA7A mRNA and protein levels were significantly higher in periapical lesions than in healthy controls.
- MMP-1, MMP-3, and inflammatory cytokines showed increased expression in periapical lesions.
- SEMA7A colocalized with MMP-1 and MMP-3 in vascular vessels and extracellular matrix.
Conclusions:
- SEMA7A is upregulated in periapical periodontitis.
- SEMA7A may contribute to tissue destruction and immune cell infiltration in periapical lesions.
