Related Experiment Video
Updated: Dec 23, 2025
A Quantitative Detection Method for MicroRNAs in the Kidney of an Ischemic Kidney Injury Mouse Model
Published on: September 11, 2020
Long non‑coding RNA CASC2 ameliorates sepsis‑induced acute kidney injury by regulating the miR‑155 and NF‑κB pathway
Min Wang1, Jilou Wei1, Futai Shang1
1Department of Intensive Care Unit, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China.
Abstract:
Sepsis is a systemic inflammatory response syndrome that can cause multiple‑organ damage, including acute kidney injury (AKI). Studies have shown that the long non‑coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the CASC2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide‑stimulated human renal tubular epithelial HK‑2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro‑inflammatory microRNA (miR)‑155. In addition, the upregulation of CASC2 significantly suppressed the nuclear factor κB (NF‑κB) signaling pathway. In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis‑induced AKI by inhibiting the miR‑155 and NF‑κB pathway‑mediated inflammation.
Insights
Long non-coding RNA CASC2 is decreased in sepsis patients and protects against sepsis-induced acute kidney injury (AKI) by inhibiting inflammation and cell death.
Area of Science:
- Biomedical Science
- Molecular Biology
- Renal Medicine
Background:
- Sepsis can lead to multi-organ damage, notably acute kidney injury (AKI).
- Long non-coding RNA cancer susceptibility candidate 2 (CASC2) is implicated in various diseases, but its role in AKI is unknown.
- CASC2 expression and function in sepsis-induced AKI require investigation.
Purpose of the Study:
- To investigate the expression and role of CASC2 in sepsis-induced AKI.
- To explore the underlying molecular mechanisms of CASC2 in renal tubular epithelial cells.
- To determine if CASC2 could be a therapeutic target for sepsis-induced AKI.
Main Methods:
- Serum CASC2 levels were measured in sepsis patients and healthy controls.
- CASC2 expression was correlated with AKI severity.
- In vitro experiments using lipopolysaccharide-stimulated HK-2 cells assessed CASC2's effects on cell viability, inflammation, apoptosis, and oxidative stress.
- Interactions between CASC2, miR-155, and the NF-κB pathway were analyzed.
Main Results:
- CASC2 expression was significantly lower in sepsis patients compared to healthy subjects.
- Lower CASC2 levels correlated with increased AKI severity.
- CASC2 enhanced HK-2 cell viability while reducing inflammatory factor secretion, apoptosis, and oxidative stress.
- CASC2 negatively regulated miR-155 and suppressed the NF-κB signaling pathway.
Conclusions:
- CASC2 expression is reduced in sepsis and associated with AKI severity.
- CASC2 exerts protective effects against sepsis-induced renal injury by modulating inflammation, apoptosis, and oxidative stress.
- CASC2 may represent a novel therapeutic target for sepsis-induced AKI via inhibition of the miR-155/NF-κB pathway.
More Related Videos
Related Concept Videos
01:29Acute Kidney Injury II: Pathophysiology
01:22Acute Kidney Injury I: Introduction
02:39lncRNA - Long Non-coding RNAs
01:30Acute Kidney Injury IV: Diagnostic Studies and Prevention