The intestinal injury caused by ischemia‐reperfusion is attenuated by amniotic fluid stem cells via the release of tumor necrosis factor‐stimulated gene 6 protein

Koike, Yuhki; Li, Bo; Lee, Carol; Alganabi, Mashriq; Zhu, Haitao; Chusilp, Sinobol; Lee, Dorothy; Cheng, Siwei; Li, Qi; Pierro, Agostino

doi:10.1096/fj.201902892rr

Cited by 12 publications

(9 citation statements)

References 50 publications

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“…Serum levels of TSG‐6 are elevated in many inflammatory diseases. 5 , 21 , 22 , 23 , 24 , 25 , 26 Szántó S 10 et al revealed that in the collagen antibody‐induced arthritis model, the joints of mice with TSG‐6 gene defects are more severely damaged. Interestingly, in an inflammatory environment, the TSG‐6 concentrations in FLS were markedly increased.…”

Section: Discussionmentioning

confidence: 99%

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Tumor necrosis factor‐alpha stimulated gene‐6: A biomarker reflecting disease activity in rheumatoid arthritis

Liu

et al. 2022

Clinical Laboratory Analysis

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Background To explore the serum tumor necrosis factor‐alpha stimulated gene‐6 (TSG‐6) level and its association with disease activity in rheumatoid arthritis (RA) patients. Methods We recruited 176 RA patients, 178 non‐RA patients (lupus erythematosus, osteoarthritis, ulcerative colitis, ankylosing spondylitis and psoriasis) and 71 healthy subjects. Serum TSG‐6 levels were detected by enzyme‐linked immunosorbent assay (ELISA). RA patients were divided into inactive RA and active RA groups by disease activity score of 28 joints based on C‐reactive protein (DAS28‐CRP). The receiver operating characteristic (ROC) curve and Spearman's rank correlation test analyzed the correlation between TSG‐6 concentration and RA disease activity. Results Tumor necrosis factor‐alpha stimulated gene‐6 levels in the RA group were increased (p < 0.01). TSG‐6 concentrations indicated an upward tendency with increased disease activity; The area under the curve (AUC) of TSG‐6 for diagnosing RA and assessing the severity of RA were 0.78 and 0.80, respectively; The combination of TSG‐6 and anti‐mutated citrullinated vimentin antibodies (anti‐MCV) (sensitivity:98.4%)improved the diagnostic accuracy of RA. Binary logistic regression analysis showed that TSG‐6 was an independent risk factor related to the severity of RA, and OR (95% CI) was 1.2 (1.003–1.453). Conclusion The TSG‐6 levels in RA patients were elevated and related to disease activity. Therefore, TSG‐6 may serve as a new potential biomarker for evaluating RA disease activity.

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Section: Discussionmentioning

confidence: 99%

“…Possible explanations for this positive correlation will be complex. Serum levels of TSG‐6 are elevated in many inflammatory diseases 5,21–26 . Szántó S 10 et al revealed that in the collagen antibody‐induced arthritis model, the joints of mice with TSG‐6 gene defects are more severely damaged.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor‐alpha stimulated gene‐6: A biomarker reflecting disease activity in rheumatoid arthritis

Liu

et al. 2022

Clinical Laboratory Analysis

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“…Intestinal I/R injuries can arise following shock, trauma, intestinal infarction, and other serious conditions [ 24 ]. These injuries can, in turn, result in a breakdown of the intestinal barrier, thereby facilitating bacterial translocation, septicemia, and multi-organ failure leading to death [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-26b-5p Targets DAPK1 to Reduce Intestinal Ischemia/Reperfusion Injury via Inhibition of Intestinal Mucosal Cell Apoptosis

et al. 2021

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Background Emerging evidence has suggested that miRNAs are important regulators of intestinal I/R injury, but their function in this context remains elusive. Aims To evaluate the role of miR-26b-5p in intestinal I/R injury. Methods We utilized in vivo murine models of intestinal I/R and in vitro Mode-K cell-based models of oxygen and glucose deprivation/reperfusion (OGD/R) to examine the function of miR-26b-5p in intestinal I/R injury. The expression of miR-26b-5p in intestinal mucosa and Mode-K cell was detected by RT-PCR. HE staining and Chiu's score were used to evaluate intestinal mucosa injury severity. Apoptosis was detected by TUNEL stain, flow cytometry, and western blot. TargetScan and StarBase prediction algorithms were applied to predict putative target genes of miR-26b-5p and validated by luciferase reporter analyses. Results We found that the expression of miR-26b-5p in intestinal mucosa was markedly decreased during I/R injury. We additionally found miR-26b-5p overexpression to markedly disrupt intestinal I/R-or OGD/R-induced injury in vivo and in vitro, whereas inhibiting this miRNA had an adverse impact and resulted in increased intestinal tissue injury and Mode-K cell damage. From a mechanistic perspective, miR-26b-5p was predicted to target DAPK1, which was related to cellular apoptosis. Luciferase reporter assay results confirmed that miR-26b-5p directly targets DAPK1 in Mode-K cells, thereby suppressing OGD/R-induced cell apoptosis. Conclusion Our findings show that miR-26b-5p may prevent intestinal I/R injury via targeting DAPK1 and inhibiting intestinal mucosal cell apoptosis, suggesting that this miRNA may be a viable target for the treatment of intestinal I/R injury.

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“… 22 Several severe conditions, including shock, thrombus and others, are the predisposing factors for this disease. 23 Because of the damage to the intestinal barrier, patients are more prone to the translation of bacterial, septicemia, and multi-organ failure. 24 Previously, there were several studies related to the role of miRNA in intestinal ischemia-reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Potentially Functional microRNA-mRNA Regulatory Networks in Intestinal Ischemia-Reperfusion Injury: A Bioinformatics Analysis

Jiang¹,

Chen²,

Zhang³

et al. 2021

JIR

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Background: Intestinal ischemia-reperfusion (II/R) injury is a common clinical complication associated with high mortality, for which microRNA (miRNA) drives potentially its pathophysiological progression. MiRNAs regulate different messenger RNAs (mRNAs). However, the regulatory network between miRNAs and mRNAs in intestinal ischemiareperfusion injury is elusive. Methods: We analyzed the different expression of mRNAs and miRNAs in intestinal tissues from patients from three groups (arterial group (group A), venous group (group V), control group (group C)). Common differentially expressed (Co-DE) miRNAs and differentially expressed mRNAs were acquired via concerned analyses among the three groups. Co-DE mRNAs were shared parts of target mRNAs and differentially expression mRNAs. Cytoscape was employed to construct the regulatory network between miRNAs and mRNAs. Gene Ontology (GO) analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway depicted the functions and potential pathway associated with Co-DE mRNAs. Using the STRING and Cytoscape, we found critical mRNAs in the protein-protein interaction (PPI) network. Results: The miRNA-mRNA network comprised 8 Co-DE miRNAs and 140 Co-DE mRNAs. Of note, 140 Co-DE mRNAs were targets of these 8 miRNAs, and their roles were established through the functional exploration via GO analysis and KEGG analysis. PPI network and Cytoscape revealed COL1A2, THY1, IL10, MMP2, SERPINH1, COL3A1, COL14A1, and P4HA1 as the top 8 key mRNAs. Conclusion:This study has demonstrated a miRNA-mRNA regulatory network in intestinal ischemia-reperfusion injury, and explored the key mRNAs and their potential functions. These findings could provide new insight into prognostic markers and therapeutic targets for patients with intestinal ischemia-reperfusion injury in clinical practice.

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The intestinal injury caused by ischemia‐reperfusion is attenuated by amniotic fluid stem cells via the release of tumor necrosis factor‐stimulated gene 6 protein

Cited by 12 publications

References 50 publications

Tumor necrosis factor‐alpha stimulated gene‐6: A biomarker reflecting disease activity in rheumatoid arthritis

Tumor necrosis factor‐alpha stimulated gene‐6: A biomarker reflecting disease activity in rheumatoid arthritis

MicroRNA-26b-5p Targets DAPK1 to Reduce Intestinal Ischemia/Reperfusion Injury via Inhibition of Intestinal Mucosal Cell Apoptosis

Potentially Functional microRNA-mRNA Regulatory Networks in Intestinal Ischemia-Reperfusion Injury: A Bioinformatics Analysis

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