Long noncoding RNA ANRIL alleviates hypoxia-induced pulmonary microvascular endothelial cell damage
Yijin Qi1, Mingyue Chen1, Tianyi Zhang1
1School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China.
European Journal of Clinical Investigation
|March 30, 2024
Summary
Long noncoding RNA ANRIL protects against high-altitude pulmonary edema by inhibiting miR-181c-5p in lung cells. This finding offers a potential therapeutic target for hypoxic injury.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Cell Biology
Background:
- High-altitude pulmonary edema (HAPE) is a critical condition.
- Long noncoding RNAs (lncRNAs) are implicated in HAPE pathogenesis.
- The specific role of ANRIL in HAPE remains unclear.
Purpose of the Study:
- To investigate the mechanism of ANRIL in hypoxic injury of pulmonary microvascular endothelial cells (PMVECs).
- To explore the effect of ANRIL on PMVEC function under hypoxic conditions.
Main Methods:
- Established a hypoxic model of PMVECs.
- Manipulated ANRIL expression (overexpression) and miR-181c-5p levels (knockdown).
- Assessed cell proliferation, apoptosis, migration, and levels of key proteins and factors.
Main Results:
- Hypoxia suppressed PMVEC proliferation and migration, increasing apoptosis, decreasing ANRIL, and increasing miR-181c-5p.
- ANRIL overexpression protected PMVECs from hypoxic injury, reducing inflammatory and apoptosis markers.
- ANRIL and miR-181c-5p knockdown exhibited similar protective effects against hypoxia.
Conclusions:
- ANRIL protects against hypoxia-induced injury in PMVECs.
- This protection is mediated through the negative regulation of miR-181c-5p.
- ANRIL represents a potential therapeutic target for HAPE.
Keywords:
antisense noncoding RNA in the INK4 locushigh‐altitude pulmonary oedemamiR‐181c‐5ppulmonary microvascular endothelial cellsMore Related Videos
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