hsa-miR-885-5p As Post Transcription Regulator of Matrix metalloproteinase 9 in Tuberculous Meningitis
Apoorva Aggarwal1, Neeraj Singla2, Monidipa Konar1
1Department of Biochemistry, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012 India.
Abstract:
Matrix metalloproteinase 9 (MMP9) has a potent role in neuroinflammation in tuberculous meningitis (TBM). Recent researches have highlighted the regulation of MMP9 levels by microRNAs, thereby altering their level and affecting critical functions, such as blood-brain barrier integrity. In this study, the activity of MMP9 was assessed by gelatin zymography, and the expression of hsa-miR-885-5p was evaluated by qRT-PCR in the cerebrospinal fluid (CSF) of TBM patients and healthy controls (HC). MMP9 expression was observed in the CSF of TBM patients only and none in HC. Additionally, hsa-miR-885-5p expression was significantly downregulated in TBM patients compared to healthy controls. These findings suggest that the dysregulation of hsa-miR-885-5p may lead to altered MMP9 levels in TBM patients, contributing to neuroinflammation. Therefore, targeting these microRNAs could serve as a new treatment modality to combat neuroinflammation in TBM patients.
Insights
Matrix metalloproteinase 9 (MMP9) drives neuroinflammation in tuberculous meningitis (TBM). Downregulated hsa-miR-885-5p in TBM patients correlates with increased MMP9, suggesting a new therapeutic target for TBM neuroinflammation.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Matrix metalloproteinase 9 (MMP9) plays a significant role in neuroinflammation associated with tuberculous meningitis (TBM).
- MicroRNAs are known regulators of MMP9, impacting critical functions like blood-brain barrier integrity.
Purpose of the Study:
- To investigate the relationship between MMP9 activity and hsa-miR-885-5p expression in the cerebrospinal fluid (CSF) of TBM patients.
- To explore the potential role of hsa-miR-885-5p dysregulation in TBM-associated neuroinflammation.
Main Methods:
- MMP9 activity was measured using gelatin zymography.
- hsa-miR-885-5p expression levels were quantified via qRT-PCR in CSF samples from TBM patients and healthy controls (HC).
Main Results:
- MMP9 was detected in the CSF of TBM patients but not in HC.
- hsa-miR-885-5p expression was significantly lower in TBM patients compared to HC.
Conclusions:
- The findings suggest that decreased hsa-miR-885-5p levels contribute to elevated MMP9, exacerbating neuroinflammation in TBM.
- Targeting hsa-miR-885-5p presents a potential therapeutic strategy for managing neuroinflammation in TBM.
