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Published on: May 21, 2018
Methylprednisolone alleviates lung injury in sepsis by regulating miR-151-5p/USP38 pathway
Zhize Yuan1, Qiuyun Wang2, Yongchang Tan2
1Department of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai 200433, China.
Background:
Acute lung injury (ALI) is manifested by increased blood vessel permeability within the lungs and subsequent impairment of alveolar gas exchange. Methylprednisolone (MP) is commonly used as a treatment for ALI to reduce inflammation, yet its molecular mechanism remains unclear. This study aims to explore the underlying mechanisms of MP on ALI in a model induced by lipopolysaccharide (LPS).
Material And Methods:
The proliferation, viability, apoptosis, and miR-151-5p expression of alveolar type II epithelial cells (AECII) were detected using the cell EdU assay, Annexin V/PI Apoptosis Kit, counting kit-8 (CCK-8) assay, and RT-qPCR. Western blot analysis was used to detect the Usp38 protein level. IL-6 and TNF-α were measured by ELISA. The combination of miR-151-5p and USP38 was determined by chromatin immunoprecipitation (ChIP)-PCR and dual-luciferase reporter assay.
Results:
MP greatly improved pulmonary function in vivo, reduced inflammation, and promoted the proliferation of the alveolar type II epithelial cells (AECII) in vitro. By comparing the alterations of microRNAs in lung tissues between MP treatment and control groups, we found that miR-151-5p exhibited a significant increase after LPS-treated AECII, but decreased after MP treatment. Confirmed by a luciferase reporter assay, USP38, identified as a downstream target of miR-151-5p, was found to increase after MP administration. Inhibition of miR-151-5p or overexpression of USP38 in AECII significantly improved the anti-inflammatory, anti-apoptotic, and proliferation-promotive effects of MP.
Conclusion:
In summary, our data demonstrated that MP alleviates the inflammation and apoptosis of AECII induced by LPS, and promotes the proliferation of AECII partially via miR-151-5p suppression and subsequent USP38 activation.
Insights
Methylprednisolone (MP) treats acute lung injury (ALI) by reducing inflammation and apoptosis. It works by suppressing miR-151-5p, which activates USP38, promoting alveolar cell proliferation.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Cell Biology
Background:
- Acute lung injury (ALI) involves lung blood vessel permeability and impaired gas exchange.
- Methylprednisolone (MP) is used for ALI to reduce inflammation, but its mechanism is unclear.
- Lipopolysaccharide (LPS) is a common inducer of ALI models.
Purpose of the Study:
- To investigate the molecular mechanisms of Methylprednisolone (MP) in treating acute lung injury (ALI) induced by lipopolysaccharide (LPS).
- To explore the role of miR-151-5p and USP38 in MP's therapeutic effects on ALI.
Main Methods:
- Assessed alveolar type II epithelial cell (AECII) proliferation, viability, and apoptosis using EdU, CCK-8, and Annexin V/PI assays.
- Quantified miR-151-5p expression via RT-qPCR and USP38 protein levels via Western blot.
- Utilized ELISA for cytokine measurement and ChIP-PCR/dual-luciferase assays to confirm miR-151-5p and USP38 interaction.
Main Results:
- MP improved pulmonary function, reduced inflammation, and enhanced AECII proliferation in ALI models.
- LPS increased miR-151-5p in AECII, while MP treatment decreased it.
- MP increased USP38 levels, a downstream target of miR-151-5p. Inhibiting miR-151-5p or overexpressing USP38 mimicked MP's protective effects.
Conclusions:
- MP alleviates LPS-induced inflammation and apoptosis in AECII.
- MP promotes AECII proliferation by suppressing miR-151-5p and activating USP38.
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