A novel long noncoding RNA-lncRNA-AABR07066529.3 alleviates inflammation, apoptosis, and pyroptosis by inhibiting MyD88 in lipopolysaccharide-induced myocardial depression

被引：5

作者：

Wen, Ri ^{[1
]}

Zhang, Tie-Ning ^{[1
]}

Zhang, Tao ^{[1
]}

Tong, Yu-Jing ^{[1
]}

Song, Wen-Liang ^{[1
]}

Liu, Yong-Ping ^{[1
]}

Yang, Ni ^{[1
]}

Liu, Chun-Feng ^{[1
]}

机构：

[1] China Med Univ, Dept Pediat, PICU, Shengjing Hosp, 36 SanHao St, Shenyang 110004, Liaoning, Peoples R China

来源：

FASEB JOURNAL | 2023年 / 37卷 / 08期

基金：

中国国家自然科学基金;

关键词：

apoptosis; endotoxemia; inflammation; long noncoding RNAs; MyD88; myocardial depression; pyroptosis; sepsis; SEPSIS; EPIDEMIOLOGY; CONTRIBUTES; RECEPTOR;

D O I：

10.1096/fj.202201680R

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Sepsis-induced myocardial depression (SIMD) is common in pediatric intensive care units and seriously threatens children's health. Recently, long noncoding RNAs (lncRNAs) have been showed to play important roles in various diseases; however, its role in SIMD is unclear. In this study, we used lipopolysaccharide (LPS)-treated rats and H9c2 cardiomyocytes to mimic SIMD in vivo and in vitro. We found that the expression of a novel lncRNA, we named lncRNA-AABR07066529.3, was elevated in LPS-induced rat heart tissue and H9c2 cardiomyocytes. In addition, LPS-induced inflammation, apoptosis, and pyroptosis were significantly exacerbated after lncRNA-AABR07066529.3 knockdown. Moreover, we found that myeloid differentiation factor 88 (MyD88) was upregulated in LPS-treated groups and was inhibited by lncRNA-AABR07066529.3. Besides, MyD88 knockdown abolished lncRNA-AABR07066529.3 silencing effects on inflammation, apoptosis, and pyroptosis induced by LPS in H9c2 cardiomyocytes. In our study, we found lncRNA-AABR07066529.3 exerted protective effects on LPS-induced cardiomyocytes by regulating MyD88 and might serve as a potential treatment target for SIMD.

引用

页数：15

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