IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway

Hong, Ting; Li, Saiqi; Guo, Xiaoyu; Wei, Yazhong; Zhang, Jingjing; Su, Xiaohui; Zhou, Miao; Jin, Haizhen; Miao, Qing; Shen, Lei; Zhu, Minfang; He, Binglin

doi:10.3389/fcell.2021.742662

Cited by 6 publications

(2 citation statements)

References 31 publications

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“…The cellular model of SIC was established by lipopolysaccharide (LPS, Sigma-Aldrich, United States) incubation based on reported protocol ( 12 , 24 ). Briefly, H9C2 cells were cultured in DMEM containing 10 μg/ml LPS for 12 h. Morphology of cardiomyocytes was observed.…”

Section: Methodsmentioning

confidence: 99%

Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction

Liu

Guo

Jin

et al. 2022

Front. Cardiovasc. Med.

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BackgroundSepsis-induced cardiomyopathy (SIC) is one major cause of death for sepsis but lacks timely diagnosis and specific treatment due to unclear mechanisms. Lipocalin-2 (LCN-2) is a key regulator of lipid metabolism which has been recently proved closely related to sepsis, however, the relationship between LCN-2 and septic myocardial injury remains unknown. We aim to explore the role of LCN-2 in the pathological progress of SIC based on clinical and laboratory evidence.MethodsConsecutive patients admitted to the intensive care unit (ICU) from August 2021 to April 2022 fulfilling the criteria of severe sepsis were included. The level of LCN-2 in plasma was assayed and analyzed with clinical characteristics. Biostatistical analysis was performed for further identification and pathway enrichment. Mouse model for SIC was thereafter established, in which plasma and tissue LCN-2 levels were tested. RNA sequencing was used for verification and to reveal the possible mechanism. Mitochondrial function and intracellular lipid levels were assayed to further assess the biological effects of targeting LCN-2 in cardiomyocytes with small interference RNAs (siRNAs).ResultsThe level of LCN-2 in plasma was markedly higher in patients with severe sepsis and was associated with higher cardiac biomarkers and lower LVEF. In the in vivo experiment, circulating LCN-2 from plasma was found to increase in SIC mice. A higher level of LCN-2 transcription in myocardial tissue was also found in SIC and showed a clear time relationship. RNA sequencing analysis showed the level of LCN-2 was associated with several gene-sets relevant to mitochondrial function and lipid metabolism-associated pathways. The suppression of LCN-2 protected mitochondrial morphology and limited the production of ROS, as well as restored the mitochondrial membrane potential damaged by LPS. Neutral lipid staining showed prominent lipid accumulation in LPS group, which was alleviated by the treatment of siLCN2.ConclusionThe level of LCN-2 is significantly increased in SIC at both circulating and tissue levels, which is correlated with the severity of myocardial injury indicators, and may work as an early and great predictor of SIC. LCN-2 probably participates in the process of septic myocardial injury through mediating lipid accumulation and affecting mitochondrial function.

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Section: Methodsmentioning

confidence: 99%

Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction

Liu

Guo

Jin

et al. 2022

Front. Cardiovasc. Med.

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“…Cardiomyocyte apoptosis is a key component of SIC ( Cai et al, 2020 ; Qi et al, 2020 ), and inhibiting cardiomyocyte apoptosis can effectively improve myocardial injury in sepsis ( Hong et al, 2021 ). Mitochondrial damage activates cardiomyocyte apoptosis, and pro-apoptotic proteins Bax and Bad translocate to the mitochondrial outer membrane and interact with it, causing the opening of the mitochondrial permeability transition pore (MPTP).…”

Section: Discussionmentioning

confidence: 99%

Rutin Inhibits Cardiac Apoptosis and Prevents Sepsis-Induced Cardiomyopathy

Meng

Liu

et al. 2022

Front. Physiol.

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Rutin is a flavanol-type polyphenol that consists of flavanol quercetin and the disaccharide rutinose, which has been reported to exert various biological effects such as antioxidant and anti-inflammatory activities. It is not clear whether rutin has a protective effect on sepsis-induced cardiomyopathy (SIC). In this study, we used male C57BL/6 mice and cecal ligation and puncture (CLP) surgery to establish the model of SIC. Rutin was precautionarily treated (50, 100, 200 mg/kg per day, 7 days) before CLP. The results showed that rutin pretreatment (100, 200 mg/kg per day, 7 days) reduced the mortality of murine sepsis. We chose the 100 mg/kg dose for further studies. Mice were pretreatment with rutin (100 mg/kg per day, 7 days) before subjected to CLP, and myocardial tissue and blood samples were collected 24 h after CLP. Serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and cTNT decreased, while interleukin-10 (IL-10) increased with rutin pretreatment. The cardiomyocytes apoptosis and mitochondrial dysfunction were also alleviated with rutin pretreatment. In conclusion, this study confirmed the efficacy of rutin-enriched diet in the prophylaxis of cardiac apoptosis and cardiac injury induced by CLP in mouse model. It provides a potential new approach on SIC prophylaxis in sepsis.

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IL-13 alleviates acute kidney injury and promotes regeneration via activating the JAK-STAT signaling pathway in a rat kidney transplantation model

Yu,

Zhang,

Pei

et al. 2024

Life Sciences

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IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway

Cited by 6 publications

References 31 publications

Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction

Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction

Rutin Inhibits Cardiac Apoptosis and Prevents Sepsis-Induced Cardiomyopathy

IL-13 alleviates acute kidney injury and promotes regeneration via activating the JAK-STAT signaling pathway in a rat kidney transplantation model

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