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MiR-223-3p reduces high glucose and high fat-induced endothelial cell injury in diabetic mice by regulating NLRP3 expression.

ABSTRACT: Expression levels of miR-223-3p and NLRP3 in high glucose and high fat (HGHF)-induced diabetic mice, and the mechanism on the injury of mouse cardiac microvascular endothelial cells (MCMECs) were investigated. Four-week C57BL/6J laboratory mice were selected and randomized into a control group and a model group (n=10 each). Mice in the model group were fed with HGHF diet to establish a mouse model of diabetes. Further MCMECs were purchased to construct carriers through transient transfection, and were separated into a normal group (cultured in the normal environment), a model group (not transfected), a blank carrier group (transfected with miR-NC), a miR-223-3p-mimics group, and a miR-223-3p-inhibitor group. RT-qPCR was used to detect the expression levels of miR-223-3p and NLRP3, and western blot analysis to detect the expression levels of NLRP3, apoptosis-related proteins Bax and caspase-3, and anti-apoptotic protein Bcl-2. Flow cytometry was used to observe apoptosis and TargetScan to predict the target relationship between miR-223-3p and NLRP3. Dual-luciferase reporter gene assay was used to detect the relationship between miR-223-3p and NLRP3. Compared with those in the control group, the mice in the model group had significantly lower expression of miR-223-3p. However, significantly higher mRNA and protein expression levels of NLRP3 were observed (P<0.05). After modeling, miR-223-3p overexpression downregulated the expression levels of NLRP3 mRNA, Bax and NLRP3 protein, as well as inhibited endothelial cell apoptosis (P<0.05), while the inhibition of miR-223-3p expression upregulated the expression levels and promoted apoptosis. In conclusion, miR-223-3p expression is low, however, NLRP3 is highly expressed in the heart tissue of HGHF-induced diabetic mice. miR-223-3p reduces the injury of MCMECs and inhibits endothelial cell apoptosis in mice by regulating the expression of NLRP3.

SUBMITTER: Deng B

PROVIDER: S-EPMC7388564 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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miR-223-3p reduces high glucose and high fat-induced endothelial cell injury in diabetic mice by regulating NLRP3 expression.

Deng Bo B Hu Ying Y Sheng Xia X Zeng Huijun H Huo Yanan Y

Experimental and therapeutic medicine 20200610 2

Expression levels of miR-223-3p and NLRP3 in high glucose and high fat (HGHF)-induced diabetic mice, and the mechanism on the injury of mouse cardiac microvascular endothelial cells (MCMECs) were investigated. Four-week C57BL/6J laboratory mice were selected and randomized into a control group and a model group (n=10 each). Mice in the model group were fed with HGHF diet to establish a mouse model of diabetes. Further MCMECs were purchased to construct carriers through transient transfection, an ...[more]

PMID: 32765674

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Project description:Background: Kawasaki disease (KD) is a self-limiting illness with acute systematic vascular inflammation. It causes pathological changes in mostly medium and small-sized arteries, especially the arteria coronaria, which adds the risk of developing coronary heart disease in adults. Materials and methods: We detected the miR-223-3p expression in 30 KD patients combined with 12 normal controls using miRNA microarrays and RT-PCR. A KD mouse model was constructed using Candida albicans water insoluble substance (CAWS). We also checked the miR-223-3p's expression using qRT-PCR. The Luciferase reporting system was implemented to validate the correlation between miR-223-3p and Interleukin-6 receptor subunit beta (IL-6ST). TNF-? was used to stimulate human coronary artery endothelial cells (HCAECs), and miR-223-3p activator or inhibitor and KD serum were used to treat HCAECs. A Western blotting automatic quantitative analysis protein imprinting system was used to test the expression of signal transducer and the activator of transcription 3 (STAT3), phosphorylated-signal transducer and the activator of transcription 3 (pSTAT3) and NF-?B p65. Results: Clinical trials found that miR-223-3p expressions were markedly different (more than 2-fold) between the acute KD group and the control group. E-selectin and intercellular cell adhesion molecule-1 (ICAM-1) levels were also significantly higher (about 2-fold) in KD especially with coronary artery lesions. MiR-223-3p could alleviate vascular endothelial damage in KD mice, and IL-6 (Interleukin-6), E-selectin and ICAM-1 were simultaneously negative. The values of IL-6, E-selectin, and ICAM-1 mRNA expressions decreased, while the value of IL-6ST was increased between the agonist treated mice and KD mice. The RT-qPCR consequences displayed that miR-223-3p explored the highest expression on the third day in both the KD mice as well as the agonist group. MiR-223-3p can directly combine with IL-6ST 3' untranslatable regions (UTR) and held back the IL-6's expression. Overexpression of miR-223 down regulated IL6ST expression and decreased the expression of p-STAT3 and NF-?B p65, while the miR-223 inhibitor could reverse the above process. Conclusion: MiR-223-3p is an important regulatory factor of vascular endothelial damage in KD and could possibly become a potential target of KD treatment in the future.

Dataset Information

MiR-223-3p reduces high glucose and high fat-induced endothelial cell injury in diabetic mice by regulating NLRP3 expression.

Publications

miR-223-3p reduces high glucose and high fat-induced endothelial cell injury in diabetic mice by regulating NLRP3 expression.

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