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Published on: May 21, 2018
LncRNA NORAD Enhances Inflammatory Injury in Sepsis-Associated Acute Lung Damage Through miR-150-5p/STAT1-Dependent
Han Liu1, Xi-Xi Chen2, Gui-Hua Wei1
1Intensive Care Unit, Jiujiang City Key Laboratory of Cell Therapy, Jiujiang No. 1 People's Hospital, Jiujiang, Jiangxi, China.
The Kaohsiung Journal of Medical Sciences
|March 4, 2026
Summary
Long non-coding RNA NORAD worsens sepsis-induced acute lung injury (ALI) by activating the miR-150-5p/STAT1 pathway. Inhibiting NORAD shows therapeutic potential for treating sepsis-related lung damage.
Area of Science:
- Molecular Biology
- Immunology
- Pathology
Background:
- Sepsis frequently leads to acute lung injury (ALI), a critical condition.
- The specific role of the long non-coding RNA NORAD in sepsis-induced ALI pathogenesis is not well understood.
Purpose of the Study:
- To investigate the role of lncRNA NORAD in sepsis-induced ALI.
- To elucidate the underlying molecular mechanisms involving NORAD, miR-150-5p, and STAT1.
Main Methods:
- Utilized lipopolysaccharide (LPS)-stimulated cell models (BEAS-2B, HBEC3-KT) and a cecal ligation and puncture (CLP)-induced ALI mouse model.
- Employed dual-luciferase and RIP assays to explore molecular interactions.
- Assessed cell viability, apoptosis, cytokine levels, bronchoalveolar lavage fluid (BALF) protein, wet/dry (W/D) ratio, caspase-3 levels, and histological scores.
Main Results:
- NORAD expression was significantly upregulated in ALI models, promoting cell injury and lung damage.
- NORAD directly targeted miR-150-5p, leading to STAT1 upregulation and activation of JAK/STAT and NF-κB signaling pathways.
- Silencing NORAD ameliorated ALI in vitro and in vivo, while manipulating miR-150-5p or STAT1 confirmed the regulatory axis.
Conclusions:
- NORAD exacerbates sepsis-induced ALI through the miR-150-5p/STAT1 signaling pathway.
- Targeting NORAD presents a potential therapeutic strategy for sepsis-related lung injury.
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