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Published on: February 9, 2014
LncRNA PCED1B-AS1 Inhibits Sepsis-Induced Acute Kidney Injury by Promoting Transformation of Macrophages from M1 to
Peng Huang1,2, Youfu Li3, SiDan Wang1
1Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise City, Guangxi, People's Republic of China.
Purpose:
A common complication observed in septic patients under intensive care is acute kidney injury (AKI), which is characterized by acute onset and strong inflammation, resulting in poor clinical outcomes for patients. This study aims to explore the expression status of PCED1B-AS1 in sepsis-induced AKI and to preliminarily investigate the molecular mechanism by which PCED1B-AS1 affects AKI.
Patients And Methods:
This study included 105 healthy individuals and 220 patients with sepsis (110 patients with AKI and 110 non-AKI patients). The levels of PCED1B-AS1 were examined by RT-qPCR. Macrophage polarization was induced by LPS treatment of RAW264.7 cells, and an in vitro renal injury model was established using HK-2 cells. Cell proliferation ability was evaluated by CCK-8 assay, apoptosis was detected by flow cytometry, and the levels of inflammatory factors were assessed using ELISA kits. The dual-luciferase assay was used to verify the interrelationship among the PCED1B-AS1/miR-361-3p/SOCS1 axis.
Results:
PCED1B-AS1 was downregulated in sepsis patients without AKI and further reduced in AKI patients. PCED1B-AS1 could differentiate healthy individuals from non-AKI sepsis patients and identify AKI patients. Additionally, low PCED1B-AS1 expression correlated with poor AKI prognosis. Overexpression of PCED1B-AS1 promoted the polarization of M1 macrophages to M2 by regulating the miR-361-3p/SOCS1 axis, thereby inhibiting apoptosis and inflammatory responses in HK-2 cells.
Conclusion:
PCED1B-AS1 may serve as a potential diagnostic and prognostic marker and inhibit sepsis-induced AKI by promoting transformation of macrophages from M1 to M2 type via regulating the miR-361-3p/SOCS1 axis.
Insights
Long non-coding RNA PCED1B-AS1 is downregulated in sepsis-induced acute kidney injury (AKI). Upregulating PCED1B-AS1 may inhibit AKI by promoting M2 macrophage polarization via the miR-361-3p/SOCS1 axis.
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- Sepsis-induced acute kidney injury (AKI) is a critical complication in intensive care with poor outcomes.
- Understanding the molecular mechanisms underlying sepsis-AKI is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the expression of PCED1B-AS1 in sepsis-induced AKI.
- To explore the potential molecular mechanism of PCED1B-AS1 in sepsis-AKI.
Main Methods:
- RT-qPCR to quantify PCED1B-AS1 levels in patients and cell models.
- In vitro models using RAW264.7 and HK-2 cells to study macrophage polarization and renal injury.
- CCK-8, flow cytometry, and ELISA to assess cell viability, apoptosis, and inflammatory factors.
- Dual-luciferase assay to validate the PCED1B-AS1/miR-361-3p/SOCS1 axis interaction.
Main Results:
- PCED1B-AS1 expression was significantly downregulated in sepsis patients, with further reduction in AKI patients.
- PCED1B-AS1 levels could distinguish healthy individuals, non-AKI sepsis patients, and AKI patients, correlating with prognosis.
- Overexpression of PCED1B-AS1 promoted M1 to M2 macrophage polarization, inhibited HK-2 cell apoptosis, and reduced inflammation via the miR-361-3p/SOCS1 pathway.
Conclusions:
- PCED1B-AS1 may serve as a valuable diagnostic and prognostic biomarker for sepsis-induced AKI.
- PCED1B-AS1 inhibits sepsis-induced AKI by modulating macrophage polarization and inflammatory responses through the miR-361-3p/SOCS1 axis.
Related Concept Videos
Acute Kidney Injury II: Pathophysiology
Acute Kidney Injury I: Introduction
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Acute Kidney Injury III: Clinical Manifestations

