MicroRNA‐351‐5p aggravates intestinal ischaemia/reperfusion injury through the targeting of MAPK13 and Sirtuin‐6

Hu, Yu‐Peng; Tao, Xufeng; Han, Xu; Xu, Lina; Yin, Lianhong; Sun, Huijun; Qi, Yan; Xu, Youwei; Peng, Jinyong

doi:10.1111/bph.14428

Cited by 31 publications

(29 citation statements)

References 48 publications

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“…Previous studies have shown that miRNAs can control the pathological process of II/R injury (Y. Hu et al, ; Z. Li et al, ; Y. Li, Wen, et al, ; Y. Li, Xu, et al, ). In addition, some miRNAs including miR‐375 and miR‐371 have been confirmed as the markers for clinical diagnosis and treatment of diseases (Piano et al, ; Salvatori et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are important endogenous regulators leading to RNA degradation and/or inhibition of protein synthesis (He et al, ; Y. Hu et al, ; Z. Liu et al, ). Recent studies have shown that some miRNAs including miR‐378, miR‐351‐5P, and miR‐665‐3p play important roles in regulating II/R injury (Y. Hu et al, ; Z. Li et al, ; Y. Li, Wen, et al, ; Y. Li, Xu, et al, ). MiR‐378 can protect against II/R injury via inhibiting intestinal mucosal cell apoptosis (Y. Li, Wen, et al, ; Y. Li, Xu, et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…MiR‐378 can protect against II/R injury via inhibiting intestinal mucosal cell apoptosis (Y. Li, Wen, et al, ; Y. Li, Xu, et al, ). Inhibition of miR‐351‐5p can alleviate II/R‐induced intestinal oxidative stress, inflammation, and apoptosis via targeting MAPK13 and sirtuin‐6 (Y. Hu et al, ). Inhibition of miR‐665‐3p can inhibit inflammation and apoptosis in II/R via targeting the autophagy‐related gene 4B (Z. Li et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are important endogenous regulators leading to RNA degradation and/or inhibition of protein synthesis (He et al, 2018;Y. Hu et al, 2018;Z.…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have shown that some miRNAs including miR-378, miR-351-5P, and miR-665-3p play important roles in regulating II/R injury (Y. Hu et al, 2018;Y. Li, Wen, et al, 2017 ;Y.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐29b‐3p reduces intestinal ischaemia/reperfusion injury via targeting of TNF receptor‐associated factor 3

Dai

Zhang

Han

et al. 2019

British J Pharmacology

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Background and Purpose The microRNA miR‐29b‐3p shows important roles in regulating apoptosis and inflammation. However, its effects on intestinal ischaemia/reperfusion (II/R) injury have not been reported. Here we have investigated the functions of miR‐29b‐3p on II/R injury on order to find drug targets to treat the injury. Experimental Approach Two models ‐ in vitro hypoxia/reoxygenation (H/R) of IEC‐6 cells; in vivo, II/R injury in C57BL/6 mice were used. Western blotting and dual‐luciferase reporter assays were used and mimic and siRNA transfection tests were applied to assess the effects of miR‐29b‐3p on II/R injury via targeting TNF receptor‐associated factor 3 (TRAF3). Key Results The H/R procedure decreased cell viability and promoted inflammation and apoptosis in IEC‐6 cells, and the II/R procedure also promoted intestinal inflammation and apoptosis in mice. Expression levels of miR‐29b‐3p were decreased in H/R‐induced cells and II/R‐induced intestinal tissues of mice compared with control group or sham group, which directly targeted TRAF3. Decreased miR‐29b‐3p level markedly increased TRAF3 expression via activating TGF‐α‐activated kinase 1 phosphorylation, increasing NF‐κB (p65) levels to promote inflammation, up‐regulating Bcl2‐associated X expression, and down‐regulating Bcl‐2 expression to trigger apoptosis. In addition, the miR‐29b‐3p mimetic and TRAF3 siRNA in IEC‐6 cells markedly suppressed apoptosis and inflammation to alleviate II/R injury via inhibiting TRAF3 signallimg. Conclusions and Implications The miR‐29b‐3p played a critical role in II/R injury, via targeting TRAF3, which should be considered as a significant drug target to treat the disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are important endogenous regulators leading to RNA degradation and/or inhibition of protein synthesis (He et al, 2018;Y. Hu et al, 2018;Z.…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have shown that some miRNAs including miR-378, miR-351-5P, and miR-665-3p play important roles in regulating II/R injury (Y. Hu et al, 2018;Y. Li, Wen, et al, 2017 ;Y.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐29b‐3p reduces intestinal ischaemia/reperfusion injury via targeting of TNF receptor‐associated factor 3

Dai

Zhang

Han

et al. 2019

British J Pharmacology

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miR‐182‐5p contributes to intestinal injury in a murine model of Staphylococcus aureus pneumonia‐induced sepsis via targeting surfactant protein D

Wei

Tian

et al. 2019

Journal Cellular Physiology

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Sepsis is a severe clinical disease, which is resulted from the excessive host inflammation response to the infection. Growing evidence indicates that Staphylococcus aureus pneumonia is a significant cause of sepsis, which can lead to intestinal injury, inflammation, and apoptosis. Studies have shown that miR-182-5p can serve as a tumor oncogene or a tumor suppressive microRNA in various cancers, however, its biological role in sepsis is still uninvestigated. Here, we reported that miR-182-5p was obviously increased in S. aureus pneumonia mice models. Loss of miR-182-5p inhibited intestinal damage and intestinal apoptosis as indicated by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. In addition, we observed the lack of miR-182-5p altered the local inflammatory response to pneumonia in the intestine. Elevated tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were observed in intestinal tissue of pneumonia groups compared with the shams. Furthermore, miR-182-5p knockout (KO) pneumonia group demonstrated decreased levels of intestinal TNF-α and IL-6. Primary murine intestinal epithelial cells were isolated and cultured in our investigation. We exhibited downregulation of miR-182-5p repressed intestinal epithelial cells apoptosis and rescued the cell viability. Meanwhile, miR-182-5p caused elevated cell apoptosis and reduced cell proliferation. Moreover, the surfactant protein D (SP-D) binds with the bacterial pathogens and remove the pathogens and apoptotic bodies, which exhibits important roles in modulating immune responses. It was displayed in our study that SP-D was greatly decreased in pneumonia mice models. SP-D was predicted as a downstream target of miR-182-5p. These data concluded that miR-182-5p promoted intestinal injury in S. aureus pneumonia-induced sepsis via targeting SP-D. K E Y W O R D S miR-182, pneumonia, sepsis, surfactant protein D

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Unveiling the molecular complexity of intestinal ischemia–reperfusion injury through omics technologies

Alicehajic,

Duivenvoorden,

Lenaerts

2024

Proteomics

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Intestinal ischemia–reperfusion injury (IR) is implicated in various clinical conditions and causes damage to the intestinal epithelium resulting in intestinal barrier loss. This presents a substantial clinical challenge, emphasizing the importance of gaining a comprehensive understanding of molecular events to aid in the identification of novel therapeutic targets. This review systematically explores the extent to which omics technologies—transcriptomics, proteomics, metabolomics, and metagenomics—have already contributed to deciphering the molecular mechanisms contributing to intestinal IR injury, in in vivo and in vitro animal and human models, and in clinical samples. Recent breakthroughs involve applying omics methodologies on exosomes, organoids, and single cells, shedding light on promising avenues and valuable targets to reduce intestinal IR injury. Future directions aimed at expediting clinical translation are discussed as well and include multi‐omics data integration to facilitate the identification of key regulatory nodes driving intestinal IR injury and advancing human organoid models based on the novel insights by single‐cell omics technologies, offering hope for clinical application of therapeutic strategies in the years to come.

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MicroRNA‐351‐5p aggravates intestinal ischaemia/reperfusion injury through the targeting of MAPK13 and Sirtuin‐6

Cited by 31 publications

References 48 publications

MicroRNA‐29b‐3p reduces intestinal ischaemia/reperfusion injury via targeting of TNF receptor‐associated factor 3

MicroRNA‐29b‐3p reduces intestinal ischaemia/reperfusion injury via targeting of TNF receptor‐associated factor 3

miR‐182‐5p contributes to intestinal injury in a murine model of Staphylococcus aureus pneumonia‐induced sepsis via targeting surfactant protein D

Unveiling the molecular complexity of intestinal ischemia–reperfusion injury through omics technologies

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