LncRNA DLEU1 contributes to the progression of septic myocardial dysfunction by targeting miR-381-3p

Tian Tian; Na Zhang; Guoxin Hu; Rong Lu; Jian Liu

doi:10.5114/ceji.2024.144199

eISSN: 1644-4124
ISSN: 1426-3912

Central European Journal of Immunology

Current issue Archive Manuscripts accepted About the journal Special Issues Editorial board Abstracting and indexing Subscription Contact Instructions for authors Publication charge Ethical standards and procedures

Editorial System

Submit your Manuscript

3/2024
vol. 49

Send email

Copy url:

abstract:

Original paper

LncRNA DLEU1 contributes to the progression of septic myocardial dysfunction by targeting miR-381-3p

Tian Tian

¹

,

Na Zhang

²

,

Guoxin Hu

³

,

Rong Lu

⁴

,

Jian Liu

⁵

Department of Geratology, Shengli Oilfield Central Hospital, Dongying, China
Disease Prevention and Control Center of Dongying District, Dongying, China
Department of Emergency, Shengli Oilfield Central Hospital, Dongying, China
Department of Clinical Laboratory, Shengli Oilfield Central Hospital, Dongying, China
Department of Intensive Care Unit, Shengli Oilfield Central Hospital, Dongying, China

Cent Eur J Immunol 2024; 49 (3): 227-237

DOI: https://doi.org/10.5114/ceji.2024.144199

Online publish date: 2024/11/12

View full text Get citation

PlumX metrics:

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)-1β, 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.

keywords:

LncRNA DLEU1 contributes to the progression of septic myocardial dysfunction by targeting miR-381-3p

Tian Tian 1 , Na Zhang 2 , Guoxin Hu 3 , Rong Lu 4 , Jian Liu 5

DLEU1, miR-381-3p, sepsis, myocardial injury, inflammation

Tian Tian

¹

,

Na Zhang

²

,

Guoxin Hu

³

,

Rong Lu

⁴

,

Jian Liu

⁵