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Identification of Matrix Metalloproteinase 3 as a Potential Biomarker for Dry Eye Disease
Xichen Wan1,2,3, Mingrui Cheng1,2,3, Changchang Xin1,2,3
1Department of Ophthalmology, Eye & ENT Hospital, State Key Laboratory of Brain Function and Disorders, Fudan University, Shanghai, China.
Purpose:
This study aimed to investigate matrix metalloproteinase 3 (MMP-3) levels in tears from patients with dry eye disease (DED) and a DED model and analyze the correlations between tear MMP-3 levels and clinical parameters in patients.
Methods:
A hyperosmotic-induced DED model was used to assess the expression levels of MMPs. For this, 59 patients with DED (59 eyes) and 21 healthy volunteers (21 eyes) were enrolled in a cross-sectional study. Clinical parameters related to dry eye and tear MMP-3 levels were collected and analyzed. After blocking MMP-3, the DED-related phenotype was measured to evaluate the role of MMP-3 in the DED model.
Results:
MMP-3 mRNA expression was significantly increased in the DED model in vitro (P = 0.003), and tear MMP-3 levels were significantly elevated in patients with DED (P < 0.001). Moreover, tear MMP-3 levels were positively correlated with the corneal fluorescence staining (CFS) score (P < 0.001) and disease duration (P < 0.001) in patients with DED. A receiver operating characteristic curve analysis revealed a cutoff value of 41.014 ng/mL for the diagnosis of DED, with a sensitivity of 79.7%, a specificity of 85.7%, and an area under the curve of 0.848 (P < 0.001). In the DED model, MMP-3 inhibition significantly alleviated cell apoptosis and inflammation, as well as increased cell viability.
Conclusions:
MMP-3 levels were significantly elevated in both the DED model and in the tears of patients with DED. Tear MMP-3 levels correlated with the CFS score and may likely serve as a biomarker for DED. The inhibition of MMP-3 expression attenuated DED-induced cell apoptosis, increased cell viability, and reduced inflammation in vitro.
Translational Relevance:
Tear MMP-3 levels were closely associated with the CFS score of patients with DED, and the inhibition of MMP-3 alleviated the DED-related phenotype in vitro, thereby suggesting that MMP-3 is a potential biomarker for DED diagnosis and could aid in the development of therapeutic targets.
Insights
Matrix metalloproteinase 3 (MMP-3) is elevated in dry eye disease (DED) tears and models. Targeting MMP-3 shows therapeutic potential for DED, suggesting it as a diagnostic biomarker.
Area of Science:
- Ophthalmology
- Biochemistry
- Molecular Biology
Background:
- Dry eye disease (DED) is a prevalent ocular surface condition with complex etiologies.
- Matrix metalloproteinases (MMPs), particularly MMP-3, are implicated in inflammatory processes.
- Understanding the role of MMP-3 in DED pathogenesis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate matrix metalloproteinase 3 (MMP-3) levels in tears of patients with DED.
- To analyze the correlation between tear MMP-3 levels and clinical parameters in DED patients.
- To evaluate the therapeutic potential of MMP-3 inhibition in a DED model.
Main Methods:
- A cross-sectional study involving 59 DED patients and 21 healthy controls.
- Utilized a hyperosmotic-induced DED model in vitro.
- Measured tear MMP-3 levels and clinical parameters including corneal fluorescence staining (CFS) score and disease duration.
- Assessed the effect of MMP-3 inhibition on DED-related phenotypes in the in vitro model.
Main Results:
- Significantly elevated MMP-3 mRNA expression in the DED model (P = 0.003).
- Tear MMP-3 levels were significantly higher in DED patients (P < 0.001).
- Tear MMP-3 levels positively correlated with CFS score and disease duration (P < 0.001).
- MMP-3 inhibition reduced DED-induced cell apoptosis and inflammation, while increasing cell viability.
Conclusions:
- Matrix metalloproteinase 3 (MMP-3) is significantly elevated in dry eye disease (DED) and its animal models.
- Tear MMP-3 levels correlate with clinical signs of DED, suggesting its potential as a diagnostic biomarker.
- Inhibition of MMP-3 demonstrates therapeutic promise by alleviating DED-related cellular damage and inflammation.
