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Published on: May 21, 2018
Serum Exosomal miR-216a Contributes to Acute Pancreatitis-Associated Acute Lung Injury by Enhancing Endothelial Cell
Huiyun Zhu1, Xianzhu Zhou1, Xingcheng Sun2
1Departments of Gastroenterology.
Background:
Acute pancreatitis (AP) is an internal medical emergency disease, with fatal complications including acute lung injury (ALI). Recent studies have highlighted the critical roles of exosomal microRNAs (miRNAs) in AP-ALI. In the present study, we aim to investigate the role of serum exosomal miR-216a in AP-ALI and its underlying mechanisms.
Methods:
The levels of miR-216a in patients and rat models with AP and AP-ALI were assessed through real-time quantitative PCR (qRT-PCR) analysis. Patient and rat blood exosomes were isolated and cocultured with HUVECs. The permeability of HUVECs was evaluated through transendothelial electrical resistance (TEER) assay. Bioinformatics predicting and luciferase reporter assays were used to identified potential targets of miR-216a. In addition, miR-216a mimic and LAMC1 overexpressed plasmid were constructed to identify the effects of miR-216a/LAMC1 axis on endothelial cell permeability in vitro. Anti-miR-216a and exosomes were used to identify the critical role of exosomal miR-216a in AP-ALI in vivo.
Results:
The findings indicated that there was a significant upregulation of miR-216a in AP-ALI patients and rat models. The occurrence of ALI during AP progression promoted the expression of serum exosomal miR-216a. Exosomal could promote HUVECs permeability by releasing miR-216a. For target studies, miR-216a was found to bind to LAMC1 to regulate its transcription level. MiR-216a-mediated downregulation of LAMC1 lead to increased permeability of HUVECs. Exosome-derived miR-216a has also been proved to promote lung damage in AP-ALI rats.
Conclusions:
In summary, serum exosomal miR-216a can promote the onset and progression of AP-ALI by augmenting endothelial cell vascular permeability. This finding presents a theoretical basis for exploring new therapeutic approaches targeting AP-ALI.
Insights
Serum exosomal miR-216a promotes acute lung injury (ALI) in acute pancreatitis (AP) by increasing vascular permeability. Targeting this microRNA offers a potential therapeutic strategy for AP-ALI.
Area of Science:
- Biochemistry
- Molecular Biology
- Pathology
Background:
- Acute pancreatitis (AP) is a critical condition with severe complications like acute lung injury (ALI).
- Exosomal microRNAs (miRNAs) play a significant role in the pathogenesis of AP-ALI.
- The specific role of serum exosomal miR-216a in AP-ALI requires further investigation.
Purpose of the Study:
- To investigate the role of serum exosomal miR-216a in AP-ALI.
- To elucidate the underlying molecular mechanisms of miR-216a in AP-ALI.
- To explore exosomal miR-216a as a potential therapeutic target for AP-ALI.
Main Methods:
- Real-time quantitative PCR (qRT-PCR) to assess miR-216a levels in patients and rat models.
- Isolation of exosomes from blood and co-culture with HUVECs to evaluate endothelial permeability (TEER assay).
- Bioinformatics, luciferase reporter assays, and in vitro/in vivo experiments to identify miR-216a targets and assess its role in AP-ALI.
Main Results:
- miR-216a was significantly upregulated in AP-ALI patients and rat models.
- Exosomal miR-216a increased HUVEC permeability by downregulating LAMC1.
- Exosome-derived miR-216a exacerbated lung damage in AP-ALI rats.
Conclusions:
- Serum exosomal miR-216a promotes AP-ALI by increasing endothelial cell vascular permeability.
- The miR-216a/LAMC1 axis is a key pathway in AP-ALI pathogenesis.
- This study provides a theoretical basis for novel therapeutic strategies targeting exosomal miR-216a in AP-ALI.
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