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Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells
Published on: May 2, 2017
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Long non-coding RNA H19 down-regulates miR-181a to facilitate endothelial angiogenic function
Aidong Zhu1,2, Lifen Chu1, Qiuju Ma1
1a Department of Vascular Surgery, Jining No.1 People's Hospital , Jining , China.
Artificial Cells, Nanomedicine, and Biotechnology
|July 4, 2019
Summary
The long non-coding RNA H19 enhances vascular endothelial cell functions like migration and tube formation. H19 promotes angiogenesis by down-regulating miR-181a, activating JNK and AMPK signaling pathways.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- H19 is a well-studied long non-coding RNA (lncRNA) with known roles in various diseases.
- Its specific function in vascular endothelial cells requires further elucidation.
Purpose of the Study:
- To investigate the functional role of H19 in human microvascular endothelial cells (HMEC-1).
- To explore the molecular mechanisms underlying H19's effects on endothelial cell behavior.
Main Methods:
- Overexpression and silencing of H19 and miR-181a in HMEC-1 cells.
- Assays for cell viability, migration, and tube formation.
- Western blotting for protein levels (MMP-2, MMP-9, VEGF, eNOS) and signaling pathways (JNK, AMPK).
- Quantitative real-time PCR for RNA levels (miR-181a).
Main Results:
- H19 overexpression significantly enhanced HMEC-1 cell viability, migration, and tube-formation capacity.
- H19 up-regulated MMP-2, MMP-9, VEGF, and eNOS protein levels, while down-regulating miR-181a.
- These effects were reversed by miR-181a overexpression and amplified by miR-181a silencing.
- H19 activated JNK and AMPK signaling pathways, an effect modulated by miR-181a levels.
Conclusions:
- Overexpression of H19 improves HMEC-1 cell viability, migration, and tube-formation capacity.
- H19 exerts pro-angiogenic effects, potentially by down-regulating miR-181a.
- This mechanism involves the subsequent activation of JNK and AMPK signaling pathways.
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