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Published on: June 15, 2018
LncRNA DLEU1 contributes to the progression of septic myocardial dysfunction by targeting miR-381-3p
Tian Tian1, Na Zhang2, Guoxin Hu3
1Department of Geratology, Shengli Oilfield Central Hospital, Dongying, China.
Insights
This study reveals that DLEU1 exacerbates sepsis-induced myocardial injury by promoting inflammation and oxidative stress. Downregulating DLEU1 or targeting the DLEU1/miR-381-3p axis may offer therapeutic strategies for sepsis-related cardiac dysfunction.
Area of Science:
- Cardiology
- Molecular Biology
- Sepsis Research
Background:
- Sepsis frequently leads to cardiac dysfunction.
- Understanding the molecular mechanisms underlying sepsis-induced myocardial injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the regulatory role of DLEU1 in sepsis-induced myocardial injury.
- To explore the potential therapeutic implications of targeting the DLEU1/miR-381-3p axis.
Main Methods:
- In vitro: HL-1 cardiomyocytes treated with lipopolysaccharide (LPS).
- In vivo: Cecum ligation and perforation (CLP) mouse model of sepsis.
- Assessed cell viability (CCK-8), apoptosis (Annexin-V), inflammatory factors (ELISA), oxidative stress (ELISA), and cardiac function (cardiac ultrasound).
Main Results:
- DLEU1 expression increased with LPS treatment, correlating with inflammation and oxidative stress.
- DLEU1 downregulation attenuated LPS-induced cardiomyocyte apoptosis, inflammation, and oxidative stress.
- In septic mice, DLEU1 knockdown improved cardiac function and reduced inflammation/oxidative stress.
- MiR-381-3p acted as a competing endogenous RNA (ceRNA) for DLEU1, reversing its effects.
Conclusions:
- The DLEU1/miR-381-3p axis is a key regulator of myocardial injury during sepsis.
- Targeting this axis presents a potential therapeutic avenue for sepsis-induced cardiac complications.
Introduction:
Cardiac dysfunction is a common complication of sepsis. This study aimed to elucidate the regulatory effect of DLEU1 on sepsis-induced myocardial injury.
Material And Methods:
HL-1 cardiomyocytes were treated with lipopolysaccharide (LPS) to mimic sepsis-induced myocardial injury in vitro, and the mouse septic model was established through cecum ligation and perforation (CLP). Cell viability was evaluated using Cell Counting Kit-8 (CCK-8), while apoptosis was assessed via Annexin-V staining. Pro-inflammatory factors including tumor necrosis factor α (TNF-α), interleukin (IL)-1 β, IL-6, and oxidative stress indicators were detected by ELISA kits. Cardiac function in mice was determined using cardiac ultrasound, and myocardial indices were detected by ELISA.
Results:
DLEU1 levels were up-regulated gradually in HL-1 cardiomyocytes after LPS treatment in a dose-dependent manner, along with the overactivation of inflammatory responses and oxidative stress. DLEU1 downregulation alleviated LPS-induced cell apoptosis, inflammatory response and oxidative stress. In vivo, DLEU1 knockdown improved the cardiac function of septic mice, and alleviated inflammation and oxidative stress. MiR-381-3p, acting as a competing endogenous RNA (ceRNA) of DLEU1, reversed the effects of DLEU1 in both septic cell and mouse models.
Conclusions:
The results indicate that the DLEU1/miR-381-3p axis is an intrinsic regulator of myocardial injury in sepsis.
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