MiR-940 Serves as a Diagnostic Biomarker in Patients with Sepsis and Regulates Sepsis-Induced Inflammation and Myocardial Dysfunction

Zhang, Shijuan; Wei, Yuhong; Liu, Jinxia; Zhuang, Yu-tian

doi:10.2147/jir.s316169

Cited by 6 publications

(5 citation statements)

References 32 publications

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“…In both preclinical and clinical research, CK-MB and cTnI are the preferred cardiac markers to detect myocardial injury. 43 The present results are consistent with the prior studies demonstrating that sepsis-related myocardial dysfunction occurs within 8-24 h of sepsis and is associated with elevated cardiac enzyme levels. [44][45][46] CLP is one of the widely employed surgical models in experimental research to induce myocardial sepsis 47,48 as it mimics the development of severe sepsis conditions in humans.…”

Section: Discussionsupporting

confidence: 93%

“…In the present study, the CLP procedure significantly increased the myocardial injury in mice accessed via elevated serum CK‐MB and cTnI levels following 24 h of ligation and puncture. In both preclinical and clinical research, CK‐MB and cTnI are the preferred cardiac markers to detect myocardial injury 43 . The present results are consistent with the prior studies demonstrating that sepsis‐related myocardial dysfunction occurs within 8–24 h of sepsis and is associated with elevated cardiac enzyme levels 44–46 .…”

Section: Discussionsupporting

confidence: 89%

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Exogenous fetuin‐A protects against sepsis‐induced myocardial injury by inhibiting oxidative stress and inflammation in mice

Hassan

Hanifa

Navik

et al. 2023

Fundamemntal Clinical Pharma

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Sepsis‐induced myocardial injury is a consequence of septicemia and is one of the major causes of death in intensive care units. A serum glycoprotein called fetuin‐A is secreted largely by the liver, tongue, placenta, and adipose tissue. Fetuin‐A has a variety of biological and pharmacological properties. The anti‐inflammatory and antioxidant glycoprotein fetuin‐A has shown its efficacy in a number of inflammatory disorders including sepsis. However, its protective role against sepsis‐induced myocardial injury remains elusive. The purpose of this work is to explore the role of fetuin‐A in mouse models of myocardial injury brought on by cecal ligation and puncture (CLP). CLP significantly induced the myocardial injury assessed in terms of elevated myocardial markers (serum CK‐MB, cTnI levels), inflammatory markers (IL‐6, TNF‐α) in the serum, and oxidative stress markers (increased MDA levels and decreased reduced glutathione) in heart tissue homogenate following 24 h of ligation and puncture. Further, hematoxylin and eosin (H&E) staining showed considerable histological alterations in the myocardial tissue of sepsis‐developed mice. Interestingly, fetuin‐A pretreatment (50 and 100 mg/kg) for 4 days before the CLP procedure significantly improved the myocardial injury and was evaluated in perspective of a reduction in the CK‐MB, cTnI levels, IL‐6, and TNF‐α in sepsis‐developed animals. Fetuin‐A pretreatment significantly attenuated the oxidative stress and improved the myocardial morphology in a dose‐dependent manner. The present study provides preliminary evidence that fetuin‐A exerts protection against sepsis‐induced cardiac dysfunction in vivo via suppression of inflammation and oxidative damage.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 89%

Exogenous fetuin‐A protects against sepsis‐induced myocardial injury by inhibiting oxidative stress and inflammation in mice

Hassan

Hanifa

Navik

et al. 2023

Fundamemntal Clinical Pharma

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“…Meanwhile, circRNAs have been manifested to mediate SA-ALI progression by binding miRNAs (24). The abundance of miR-940 was identified to be declined in sepsis patients and cecal ligation-perforation-stimulated sepsis animal models, and overexpression of miR-940 alleviated injury and inflammatory processes in sepsis models (25). Here, through circinteractome software prediction and using targeted validation experiment, miR-940 was manifested to be a miRNA target of circ_0001226, and miR-940 level was apparently reduced in SA-ALI patients and LPS-triggered BEAS-2B cells.…”

Section: Discussionmentioning

confidence: 99%

Interfering Hsa_circ_0001226 Mitigates LPS-Induced Beas-2b Cell Injury by Regulating Mir-940/Tgfbr2 Pathway

Mo,

Yi,

Bei

et al. 2023

Shock

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Background: Sepsis-associated acute lung injury (SA-ALI) is a serious threat to human health. A growing body of evidence suggested that circular RNAs may be involved in ALI progression. The aim of this study was to investigate the effect and mechanism of circ_0001226 on lipopolysaccharide (LPS)–induced BEAS-2B cells. Methods: BEAS-2B cells were stimulated with LPS to establish a SA-ALI cell model. The expression of circ_0001226, miR-940, and transforming growth factor beta receptor II (TGFBR2) were monitored by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were evaluated by the Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine assay, and flow cytometry. The levels of interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α were calculated by enzyme-linked immunosorbent assay. Western blot was implemented to test the protein levels of PCNA, Bax, and TGFBR2. Dual-luciferase reporter assay and RNA pull-down assay were adopted to investigate the interaction between circ_0001226 and miR-940, as well as TGFBR2 and miR-940. Results: The levels of circ_0001226 and TGFBR2 were elevated, and miR-940 was decreased in SA-ALI serum specimens and LPS-evoked BEAS-2B cells. Besides that, circ_0001226 interference contributed to cell proliferation and restrained apoptosis and inflammation in LPS-induced BEAS-2B cells. Mechanically, circ_0001226 worked as a molecular sponge of miR-940 to regulate TGFBR2 expression. Conclusion: Circ_0001226 deficiency weakened LPS-mediated proliferation inhibition and inflammatory processes in BEAS-2B cells by binding miR-940 and regulating TGFBR2.

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“…In other words, hsa_circ_0038382, miR-940 and TBX5 formed the regulatory network to regulate keloid formation. The role of miR-940 has been reported in multiple diseases, such as sepsis, 34 spinal cord injury 35 and cancer. 36 The overexpression of miR-940 has been shown to induce the progression of cervical cancer.…”

Section: Discussionmentioning

confidence: 99%

hsa_circ_0038382 upregulates T-box transcription factor 5 to inhibit keloid formation by interacting with miR-940

Cai¹,

Hu²,

Liu³

et al. 2022

Adv Clin Exp Med

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Background.A keloid is a benign fibroproliferative skin tumor whose formation is regulated by circular RNAs (circRNAs). However, the effect and regulatory mechanism of hsa_circ_0038382 on keloid formation have not been investigated.Objectives. This study aimed to identify the function and mechanism of hsa_circ_0038382 in keloid formation. Materials and methods.The expression levels of hsa_circ_0038382, microRNA-940 (miR-940) and T-box transcription factor 5 (TBX5) were measured using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). After cell transfection of keloid fibroblasts, the effect of the hsa_circ_0038382/ miR-940/TBX5 axis on keloid formation was assessed using cell function tools such as the cell counting kit-8 (CCK-8) assay, transwell migration assay and transwell invasion assay. The binding sites among hsa_circ_0038382, miR-940 and TBX5 were predicted with CircInteractome and TargetScan, and further identified using luciferase assays.Results. The levels of hsa_circ_0038382 and TBX5 were reduced, whereas the level of miR-940 was elevated in keloid samples. Cell function experiments confirmed that hsa_circ_0038382 can inhibit keloid formation by suppressing proliferation, migration and invasion of keloid fibroblasts. Luciferase assays proved that hsa_circ_0038382 can absorb miR-940 to regulate TBX5 expression in keloids. Additionally, the overexpression of TBX5 restored the effect of hsa_circ_0038382 knockdown on keloid fibroblasts.Conclusions. This study suggests that hsa_circ_0038382 attenuates keloid formation by regulating the miR-940/TBX5 axis, which might provide a potential therapeutic target in the treatment of keloid formation.

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MiR-940 Serves as a Diagnostic Biomarker in Patients with Sepsis and Regulates Sepsis-Induced Inflammation and Myocardial Dysfunction

Cited by 6 publications

References 32 publications

Exogenous fetuin‐A protects against sepsis‐induced myocardial injury by inhibiting oxidative stress and inflammation in mice

Exogenous fetuin‐A protects against sepsis‐induced myocardial injury by inhibiting oxidative stress and inflammation in mice

Interfering Hsa_circ_0001226 Mitigates LPS-Induced Beas-2b Cell Injury by Regulating Mir-940/Tgfbr2 Pathway

hsa_circ_0038382 upregulates T-box transcription factor 5 to inhibit keloid formation by interacting with miR-940

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