MiR-150 predicts survival in patients with sepsis and inhibits LPS-induced inflammatory factors and apoptosis by targeting NF-κB1 in human umbilical vein endothelial cells

Ma, Yuezhen; Liu, Yanni; Hou, Haoqing; Yao, Yanfen; Meng, Hua

doi:10.1016/j.bbrc.2018.04.168

Cited by 40 publications

(37 citation statements)

References 17 publications

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“…Furthermore, our data indicated that miR-150-5p alleviated LPS-induced inflammatory response and apoptosis of RAW264.7 cells. Consistent with our findings, Ma et al [15] manifested that miR-150 inhibited inflammatory response and apoptosis in LPStreated human umbilical vein endothelial cells by targeting NF-κB1.…”

Section: Discussionsupporting

confidence: 93%

“…Moreover, miR-150 was reported to be involved in the pathogenesis of sepsis [13,14]. A recent document demonstrated that miR-150 repressed LPS-induced inflammatory factors and apoptosis by regulating NF-κB1 in human umbilical vein endothelial cells [15]. Additionally, LPS infusion into healthy humans led to decreased miR-150 expression in peripheral blood leukocytes [16].…”

Section: Introductionmentioning

confidence: 99%

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Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1

et al. 2020

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Circulating miR-150-5p has been identified as a prognostic marker in patients with critical illness and sepsis. Herein, we aimed to further explore the role and underlying mechanism of miR-150-5p in sepsis. Quantitative real-time-PCR assay was performed to detect the expression of miR-150-5p upon stimulation with lipopolysaccharide (LPS) in RAW264.7 cells. The levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β were measured by ELISA assay. Cell apoptosis was determined using flow cytometry. Western blot was used to assess notch receptor 1 (Notch1) expression in LPS-induced RAW264.7 cells. Dual-luciferase reporter assay was employed to validate the target of miR-150-5p. Our data showed that miR-150-5p was downregulated and Notch1 was upregulated in LPS-stimulated RAW264.7 cells. miR-150-5p overexpression or Notch1 silencing alleviated LPS-induced inflammatory response and apoptosis in RAW264.7 cells. Moreover, Notch1 was a direct target of miR-150-5p. Notch1 abated miR-150-5p-mediated anti-inflammation and anti-apoptosis in LPS-induced RAW264.7 cells. miR-150-5p alleviated LPS-induced inflammatory response and apoptosis at least partly by targeting Notch1 in RAW264.7 cells, highlighting miR-150-5p as a target in the development of anti-inflammation and anti-apoptosis drugs for sepsis treatment.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1

et al. 2020

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“…Numerous studies have indicated the pivotal roles of miRNAs in the initiation and development of various human diseases, including malignancies (22), metabolic diseases (23) and cardiovascular diseases (24). In sepsis, there are also functional miRNAs that are linked to the progression of the disease by the regulation of inflammatory response, such as miR-150 (25) and miR-27a (26), e.g. miR-375 (25) and miR-25 (26).…”

Section: Discussionmentioning

confidence: 99%

“…In sepsis, there are also functional miRNAs that are linked to the progression of the disease by the regulation of inflammatory response, such as miR-150 (25) and miR-27a (26), e.g. miR-375 (25) and miR-25 (26). In addition, certain miRNAs with ectopic expression patterns have critical roles in the pathogenesis of NS by regulating the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Clinical significance of miR‑181a in patients with neonatal sepsis and its regulatory role in the lipopolysaccharide‑induced inflammatory response

Guo

2020

Exp Ther Med

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Neonatal sepsis (NS) poses a serious threat to the health of neonates worldwide. The present study aimed to investigate the diagnostic value of microRNA (miR)-181a in patients with NS and the regulatory role of miR-181a in lipopolysaccharide (LPS)-induced inflammation. A total of 102 neonates with NS and 50 neonates without sepsis were enrolled in the present study. The serum levels of miR-181a were estimated using reverse transcription-quantitative PCR. Receiver operating characteristic (ROC) analysis was performed to evaluate the diagnostic value of miR-181a for NS. The effect of miR-181a on the expression of Toll-like receptor (TLR)4 was assessed after modification of the expression of miR-181a in monocytes isolated from the blood of neonates in vitro. An ELISA was used to measure the concentration of inflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-8 in the supernatant of monocytes. The serum levels of miR-181a were decreased in patients with NS compared with those in the controls. The area under the ROC curve of miR-181a was 0.893 with a sensitivity of 83.3% and a specificity of 84.0%. LPS stimulation in monocytes also led to a decrease in the expression of miR-181a. TLR4 was proven to be a direct target gene of miR-181a, according to the results of a luciferase reporter assay, and overexpression of miR-181a suppressed TLR4 expression in monocytes. Regarding LPS-induced inflammation, it was revealed that the upregulated levels of TNF-α and IL-8 induced by LPS were reduced by overexpression of miR-181a in monocytes. In conclusion, decreased serum levels of miR-181a may serve as a diagnostic biomarker in patients with NS and overexpression of miR-181a inhibits the LPS-induced inflammatory response at least partially by targeting TLR4. Aberrant miR-181a may be a non-invasive biomarker for NS patients, and provide a novel insight into the pathologic mechanisms of action behind the development of NS.

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“…Remarkably, miRNAs have been shown to affect endothelial function and the vascular barrier [ 16 , 18 , 19 , 20 ]. The cytokine-mediated activation of endothelial cells is based on the initiation of signaling cascades whose mediators are known to be influenced by miRNAs [ 16 , 17 , 21 , 22 , 23 ]. Numerous studies also prove the modulating effect of miRNAs on the expression of the adhesion molecules e-selectin, ICAM-1, and VCAM-1, which are essential for the extravasation of leukocytes [ 17 , 18 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Polyunsaturated Fatty Acids of Both the Omega-3 and the Omega-6 Family Abrogate the Cytokine-Induced Upregulation of miR-29a-3p by Endothelial Cells

et al. 2020

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Cellular processes fundamentally depend on protein expression control. At this, protein expression is regulated on the transcriptional and the post-transcriptional level. PUFAs are already known to affect gene transcription. The present study was conducted to answer the question whether PUFAs are also able to impact on the miRNA-mediated post-transcriptional fine-tuning of mRNA copy numbers. To this end, cellular miRNA profiles were screened by means of next-generation sequencing and NanoString analysis to compare PUFA-enriched to unsupplemented endothelial cells exposed to an inflammatory milieu. Validation took place by droplet digital PCR, allowing for an absolute quantification of RNA copy numbers. The analyses revealed that the stimulation-induced upregulation of miR-29a-3p is blocked by PUFA enrichment of endothelial cells. What is more, mRNA copy numbers of miR-29a-3p targets, namely the coagulation factors PAI-1, TF, and vWF, as well as the proinflammatory cytokines IL-1β, IL-6, and IL-8, were reduced in PUFA-enriched endothelial cells compared to unsupplemented cells, counteracting the stimulatory effect of an inflammatory environment. These data hint toward a new mechanism of action by which PUFAs modulate the functionality of endothelial cells. Apparently, the inflammation-modulating properties of PUFAs are also mediated at the post-transcriptional level.

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MiR-150 predicts survival in patients with sepsis and inhibits LPS-induced inflammatory factors and apoptosis by targeting NF-κB1 in human umbilical vein endothelial cells

Cited by 40 publications

References 17 publications

Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1

Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1

Clinical significance of miR‑181a in patients with neonatal sepsis and its regulatory role in the lipopolysaccharide‑induced inflammatory response

Polyunsaturated Fatty Acids of Both the Omega-3 and the Omega-6 Family Abrogate the Cytokine-Induced Upregulation of miR-29a-3p by Endothelial Cells

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