Role of miR‐106‐mediated mitogen‐activated protein kinase signaling pathway in oxidative stress injury and inflammatory infiltration in the liver of the mouse with gestational hypertension

Wang, Zhihui; Bao, Xiufang; Song, Longfei; Tian, Yuying; Sun, Ping

doi:10.1002/jcb.29552

Cited by 12 publications

(6 citation statements)

References 32 publications

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“…Similarly, increased levels of reactive oxygen species (ROS) resulted to the decreased expression of miR-106a ( Wang et al, 2010 ). On the other hand, elevated levels of miR-106a prevented oxidative stress injury and inflammation in hepatic mouse with gestational hypertension ( Wang Z. et al, 2019 ), resulting to repression of the expressions of HIF1-α and VEGF in diabetic retina ( Ling et al, 2013 ). In addition, miR-106a has been associated with macrophage activation, suggesting its involvement in inflammation ( Zhu et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Differential Expression of Serum TUG1, LINC00657, miR-9, and miR-106a in Diabetic Patients With and Without Ischemic Stroke

Abdelaleem

Shaker

Mohamed

et al. 2022

Front. Mol. Biosci.

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Background: Ischemic stroke is one of the serious complications of diabetes. Non-coding RNAs are established as promising biomarkers for diabetes and its complications. The present research investigated the expression profiles of serum TUG1, LINC00657, miR-9, and miR-106a in diabetic patients with and without stroke.Methods: A total of 75 diabetic patients without stroke, 77 patients with stroke, and 71 healthy controls were recruited in the current study. The serum expression levels of TUG1, LINC00657, miR-9, and miR-106a were assessed using quantitative real-time polymerase chain reaction assays.Results: We observed significant high expression levels of LINC00657 and miR-9 in the serum of diabetic patients without stroke compared to control participants. At the same time, we found marked increases of serum TUG1, LINC00657, and miR-9 and a marked decrease of serum miR-106a in diabetic patients who had stroke relative to those without stroke. Also, we revealed positive correlations between each of TUG1, LINC00657, and miR-9 and the National Institutes of Health Stroke Scale (NIHSS). However, there was a negative correlation between miR-106a and NIHSS. Finally, we demonstrated a negative correlation between LINC00657 and miR-106a in diabetic patients with stroke.Conclusion: Serum non-coding RNAs, TUG1, LINC00657, miR-9, and miR-106a displayed potential as novel molecular biomarkers for diabetes complicated with stroke, suggesting that they might be new therapeutic targets for the treatment of diabetic patients with stroke.

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Section: Discussionmentioning

confidence: 99%

Differential Expression of Serum TUG1, LINC00657, miR-9, and miR-106a in Diabetic Patients With and Without Ischemic Stroke

Abdelaleem

Shaker

Mohamed

et al. 2022

Front. Mol. Biosci.

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“…29,30 Studies have found that miR-106a inhibited oxidative stress injury and inflammatory infiltration in the liver of the mouse with gestational hypertension by inhibiting the mitogen-activated protein kinase signaling pathway. 31 MiR-106b expression was significantly inhibited in activated bone marrow derived dendritic cells (BMDCs) stimulated by OVA. And miR-106b negatively regulated the allergic properties of BMDCs and subsequent Th2 polarization by targeting early growth response (Egr)-2.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA SNHG16, binding with miR-106b-5p, promoted cell apoptosis and inflammation in allergic rhinitis by up-regulating leukemia inhibitory factor to activate the JAK1/STAT3 signaling pathway

Fang

Zhang

et al. 2021

Hum Exp Toxicol

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Allergic rhinitis (AR) is a type I hypersensitive disease. Long non-coding RNA (lncRNA) SNHG16 acts as an oncogene in a variety of tumors and promotes the occurrence of inflammation in many inflammatory diseases. The study aims to investigate the expression of SNHG16 and its potential biological functions in AR. RT-qPCR results showed that the expression of SNHG16 in AR was up-regulated. The AR cell model was constructed by stimulating primary nasal mucosal epithelial cells from AR patients with IL-13. After knocking down the expression of lncRNA SNHG16, cell apoptosis was detected by flow cytometry, and the expression of inflammatory factors was detected by ELISA. The results showed that SNHG16 promoted cell apoptosis and inflammation. Then, bioinformatics analysis was used to screen miRNAs bound with SNHG16. Luciferase reporter gene assay and RNA pull-down experiment were used to verify the relationship. We found that the expression of miR-106b-5p was down-regulated and leukemia inhibitory factor (LIF) expression was up-regulated in the AR cell model. The expression of phospho-Janus kinase 1 and p-signal transducer and activator of transcription 3 (STAT3) were detected by Western blotting. Silencing the expression of LIF could inhibit the activity of JAK1/STAT3 pathway and further inhibit cell apoptosis and the occurrence of inflammation. Then transfected SNHG16 shRNA alone or together with miR-106b-5p antagomir into the AR cell model, we found that silencing the expression of SNHG16 down-regulated the expression of LIF and inhibited the activity of the JAK1/STAT3 pathway, cell apoptosis, and inflammation. However, miR-106b-5p antagomir weakened its inhibitory effects. The role of SNHG16 in AR was further verified by the ovalbumin-induced AR mouse model in vivo. In conclusion, SNHG16 up-regulates LIF expression by binding with miR-106b-5p, thus promoting the activity of JAK1/STAT3 pathway, and promoting the development of AR. These results provide new targets for the treatment of AR and may help reduce the damage caused by AR.

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“…Other miRNAs differentiating the SWR/J control from the WT control group of mice, such as miR-20 and miR-106, are associated with the regulation of glucose metabolism [33], whilst miR-93 and miR-106 might affect liver diseases [34]. Additionally, miR-106 has been linked with regulation of the MAPK signaling pathway during oxidative stress [35]. The differences in expression of these miRNAs in the serum of NET-KO, SWR/J and WT mice under control conditions may affect the subsequent genotype dependent stress response.…”

Section: Discussionmentioning

confidence: 99%

Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice

Solich

Kuśmider

Faron-Górecka

et al. 2020

Cells

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In the present study, we used three strains of mice with various susceptibility to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype, as well as two strains of mice displaying two different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and SWR/J. The procedure of restraint stress (RS, 4 h) was applied, and the following behavioral experiments (the forced swim test and sucrose preference test) indicated that NET-KO and SWR/J mice were less sensitive to RS than WT mice. Then, we aimed to find the miRNAs which changed in similar ways in the serum of NET-KO and SWR/J mice subjected to RS, being at the same time different from the miRNAs found in the serum of WT mice. Using Custom TaqMan Array MicroRNA Cards, with primers for majority of miRNAs expressed in the serum (based on a preliminary experiment using the TaqMan Array Rodent MicroRNA A + B Cards Set v3.0, Thermo Fisher Scientific, Waltham, MA, USA) allowed the identification of 21 such miRNAs. Our further analysis focused on miR-1 and miR-155 and their targets-these two miRNAs are involved in the regulation of BDNF expression and can be regarded as biomarkers of stress-resilience.Cells 2020, 9, 917 2 of 17 are regarded as endogenous "hubs" (as Issler and Chen have put it) for the fine tuning of target gene expression or an "expression switch", and can provide deeper insight into complex biological processes underlying stress response.In the present study, we used three strains of mice differentially reacting to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype [7-9], as well as two other strains of mice displaying different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and swiss SWR/J, described extensively by Szklarczyk and co-workers [10]. The different reaction to stress of these strains of mice has been confirmed by measuring corticosterone level. The NET-KO mice display a slower increase in corticosterone level after stress compared with WT animals, while corticosterone level was not changed at 2 h after restraint stress in the blood of SWR/J mice [8,10]. We applied the procedure of restraint stress (RS), which has been shown to induce an uncontrollable aversive situation that produces both physical and psychological consequences leading to neuronal and behavioral alterations [11]. The aim of following molecular studies was to find biomarkers for different behavioral responses to RS among miRNAs expressed in the serum of three genotypes under study. This goal was achieved, as we were able to identify a group of miRNAs differentiating the stress response of NET-KO and SWR/J mice from WT animals. The most interesting were the alterations in the miR-1 and miR-155 levels, which are involved in regulation of BDNF expression, which in turn affects important biochemical processes. Materials and Methods AnimalsH...

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Role of miR‐106‐mediated mitogen‐activated protein kinase signaling pathway in oxidative stress injury and inflammatory infiltration in the liver of the mouse with gestational hypertension

Cited by 12 publications

References 32 publications

Differential Expression of Serum TUG1, LINC00657, miR-9, and miR-106a in Diabetic Patients With and Without Ischemic Stroke

Differential Expression of Serum TUG1, LINC00657, miR-9, and miR-106a in Diabetic Patients With and Without Ischemic Stroke

Long non-coding RNA SNHG16, binding with miR-106b-5p, promoted cell apoptosis and inflammation in allergic rhinitis by up-regulating leukemia inhibitory factor to activate the JAK1/STAT3 signaling pathway

Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice

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