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Updated: Sep 20, 2026

Non-invasive In Vivo Fluorescence Optical Imaging of Inflammatory MMP Activity Using an Activatable Fluorescent Imaging Agent
Published on: May 8, 2017
[Expression of MMP-2, MMP-9 and TIMP-1 and the effects of methylprednisolone in EAM]
1Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China.
Objective:
To study the function of MMP-2 (matrix metalloproteinase-2), MMP-9 (matrix metalloproteinase-9) and TIMP-1 (tissue inhibitor of metalloproteinase-1) in the pathogenesis of EAM (experimented autoimmune myositis) rats, and to evaluate the effect of methylprednisolone on the mRNA and protein expression of MMP-2, MMP-9 and TIMP-1.
Methods:
The expression levels of MMP-2, MMP-9 and TIMP-1 in the peripheral blood, spleen lymphocytes and muscles were examined among the EAM group, EAMM group and control group by RT-PCR and immunohistochemical techniques.
Results:
1. The degree of episode in the EAMM group was lower than that in the EAM group. Also, the infiltration of the inflammatory cells and the necrosis of the muscles were milder in the EAMM group than those in the EAM group. 2. The mRNA expression of MMP-2 and MMP-9 in the lymphocytes of the peripheral blood and spleen and the protein expression of MMP-2 and MMP-9 in the muscle tissues all increased significantly in the EAM group compared with those of the control group. However, the mRNA and protein expression of MMP-2 and MM-9 was suppressed significantly in contrast with that in the EAM group. 3. The mRNA and protein expression of TIMP-1 in the EAMM group increased with statistical significance compared with that in the EAM group.
Conclusion:
The upregulation of the expression of MMP-2 and MMP-9 may be related with the onset of EAM. TIMP-1 may be involved in the suppression of immunoreaction. Methylprednisolone may reduce the pathological damages of EAM, and this protective mechanism may be due to the inhibited expression of MMP-2 and MMP-9 and promoted expression of TIMP-1.
Insights
Matrix metalloproteinase-2 (MMP-2) and MMP-9 upregulation correlates with experimental autoimmune myositis (EAM) onset. Methylprednisolone treatment reduces EAM pathology by inhibiting MMP-2/MMP-9 and promoting TIMP-1.
Area of Science:
- Immunology
- Molecular Biology
- Pathology
Context:
- Experimented autoimmune myositis (EAM) is an inflammatory muscle disease.
- Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) play roles in tissue remodeling and inflammation.
- Understanding MMP-2, MMP-9, and TIMP-1 roles in EAM is crucial for therapeutic development.
Purpose:
- To investigate the roles of MMP-2, MMP-9, and TIMP-1 in the pathogenesis of EAM in rats.
- To evaluate the therapeutic effects of methylprednisolone on MMP-2, MMP-9, and TIMP-1 expression in EAM.
Summary:
- Increased MMP-2 and MMP-9 mRNA and protein expression were observed in EAM rats compared to controls.
- Methylprednisolone treatment significantly reduced EAM symptoms, inflammatory cell infiltration, and muscle necrosis.
- Methylprednisolone therapy inhibited MMP-2 and MMP-9 expression while promoting TIMP-1 expression in EAM rats.
Impact:
- The findings suggest MMP-2 and MMP-9 are involved in EAM pathogenesis.
- TIMP-1 may play a role in suppressing the immunoreaction in EAM.
- Methylprednisolone demonstrates protective effects against EAM, potentially via modulation of MMPs and TIMP-1.
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