Protective effects of microRNA‐22‐3p against retinal pigment epithelial inflammatory damage by targeting NLRP3 inflammasome

Hu, Zizhong; Lv, Xuemei; Chen, Lu; Gu, Xunyi; Qian, Huiming; Fransisca, Silvia; Zhang, Zhengyu; Liu, Qing-Huai

doi:10.1002/jcp.28523

Cited by 44 publications

(19 citation statements)

References 37 publications

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“…The expression of miR‐22‐3p is closely correlated to the NLRP3 inflammasome. Some studies reported that miR‐22‐3p plays an essential protective role in the inflammatory injury and cell apoptosis by inhibiting the mRNA and protein expression of NLRP3, Caspase‐1, and IL‐1β through targeting NLRP3 22‐24 . However, one study revealed that miR‐22‐3p could inhibit Sirtuin 1 protein expression and promote the high expression of inflammatory cytokines tumor necrosis factor‐α, IL‐1β, and IL‐8, which are vital for the development of inflammation 25 .…”

Section: Discussionmentioning

confidence: 99%

MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3

et al. 2021

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Background MicroRNAs (miRNAs) have been shown to play a crucial role in inflammation regulation; however, their relationship with inflammation in acute gouty arthritis has not been fully elucidated. Herein, we conducted a study to explore the regulatory roles of miR‐223‐3p and miR‐22‐3p in gouty‐associated inflammation. Methods In vitro and in vivo experiments were conducted to examine the molecular mechanisms of miRNA regulation in gouty inflammation. Dual‐luciferase reporter assay was used to verify the direct target of miR‐223‐3p and miR‐22‐3p. Results We found that miR‐223‐3p and miR‐22‐3p interacted with the 3′ untranslated region segment of NLRP3 (nucleotide‐binding domain leucine‐rich repeat [NLR] and pyrin domain containing receptor 3) and inhibited its expression. A decreased expression of miR‐223‐3p and miR‐22‐3p was observed in both mice air pouch synovium and phorbol myristrate acetate‐treated THP‐1 cells stimulated with monosodium urate (P < .05). Compared with the negative control group, NLRP3 expression at the transcript and protein level in miR‐223‐3p and miR‐22‐3p overexpression group significantly decreased after 6 hours of monosodium urate treatment in vivo and in vitro (P < .05). The results of the dual‐luciferase reporter assay demonstrated that miR‐223‐3p and miR‐22‐3p directly targeted NLRP3. Conclusion The findings of the present study show that miR‐223‐3p and miR‐22‐3p can reduce the inflammatory effects of gout by inhibiting the expression of NLRP3.

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Section: Discussionmentioning

confidence: 99%

MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3

et al. 2021

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“…The correlation between miR-22-3p and MMP-3, MMP-7 was observed, suggesting that miR-22-3p can regulate metastasis, and its regulation of MMPs is one of the mechanisms. MMP-3 and MMP-7 are the most associated factors with miR-22-3p and the most important downstream genes of miR-22-3p (Hu et al, 2019;Lv et al, 2018). MMP-7 has the strongest effect on the degradation of extracellular matrix, and when MMP-7 is activated, which can regulate interstitial angiogenesis, epithelial-mesenchymal transformation and cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

MiR-22-3p Expression is down-regulated in lung adenocarcinoma

Zhou

Qin

et al. 2021

Acta Biochim Pol

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Background: Our current study was performed with an attempt to detect the expression of microRNA-22-3p (miR-22-3p) in lung adenocarcinoma, as well as to analyze its role in clinical practice. In addition, its relationship with vascular endothelial growth factor (VEGF) and metastasis related indexes was focused. Material and Method: The trials in which 62 cases of lung adenocarcinoma were received to collect tumor tissue (study group) and normal lung tissue (control group) were eligible for this study. The expression of miR-22-3p in the two groups was detected through RT-PCR. Immunohistochemical method was used to detect the expression of VEGF and leukocyte differentiation antigen 31 (CD31) marked microvessel density (MVD) in lung adenocarcinoma. The expressions of matrix metalloproteinase-3 (MMP-3) and matrix metalloproteinase-7 (MMP-7) in lung adenocarcinoma were also detected through the use of Western Blot. Results: The present study revealed significant difference in the expression of miR-22-3p between the two groups. No significant difference in the expression of gender, age, neural invasion and the number of lesions were observed between groups. There was significant difference in the expression of miR-22-3p in the maximum diameter of tumor, pleural recidivism, vascular recidivism, lymph node metastasis and different TNM stages. Based on survival analysis, miR-22-3p was linked to survival time. Correlation analysis indicated that there was negative correlation between miR-22-3p and VEGF, miR-22-3p and MVD, miR-22-3p and MMP-3, and miR-22-3p and MMP-7 in lung adenocarcinoma. Conclusion: Our findings provide evidence that miR-22-3p is low expressed in lung adenocarcinoma tissues and the low expression of miR-22-3p is closely associated with clinicopathological characteristics and the prognosis. MiR-22-3p may be involved in the tumor progression of lung adenocarcinoma and may serve as a biomarker for the diagnosis and prognosis of lung adenocarcinoma.

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“…MicroRNA (miRNA), a sort of single-stranded noncoding small RNA, is known to negatively regulate gene expression posttranscriptionally, either by inhibiting translation or destabilizing its target transcripts. [14][15][16] Recent studies have identified that NLRP3 can be regulated by several miRNAs in various diseases, including miR-22-3p, 17 miR-21, 18 miR-132, 19 miR-181a, 20 and so on. However, few studies have investigated which miRNAs might target and regulate NLRP3 in macrophages during liver injury.…”

Section: Introductionmentioning

confidence: 99%

Cannabinoid Receptor 1/miR-30b-5p Axis Governs Macrophage NLRP3 Expression and Inflammasome Activation in Liver Inflammatory Disease

Yang

Tian

Zhang

et al. 2020

Molecular Therapy - Nucleic Acids

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Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) has been regarded as an important initiator or promoter in multiple inflammatory diseases. However, the relationship between cannabinoid receptor 1 (CB1) and macrophage NLRP3 inflammasome and the corresponding molecular mechanism in liver inflammation remain unclear. Mouse liver injury models were induced by carbon tetrachloride (CCl 4 ) or methionine-choline-deficient and high fat (MCDHF) diet. Human liver tissues were obtained from patients with different chronic liver diseases. CB1 expression was increased in liver tissue and macrophages of CCl 4 -and MCDHF-treated mice, positively correlated with NLRP3. CB1 agonist ACEA (Arachiodonyl-2'-Chloroethylamide) promoted NLRP3 expression and NLRP3 inflammasome activation in macrophages. CB1 blockade with its antagonist AM281 reduced NLRP3 expression, inflammasome activation, and liver inflammation in CCl 4 -and MCDHF-treated mice. MicroRNA-30b-5p (miR-30b-5p), screened by the intersection of bioinformatics databases and downregulated miRNAs in injured liver, negatively correlated with NLRP3 in mouse and human liver. miR-30b-5p was involved in CB1-mediated activation of NLRP3 inflammasome in macrophages by directly targeting NLRP3. Importantly, administration of miR-30b-5p agomir targeted NLRP3 and attenuated liver inflammation in the injured liver. Altogether, CB1/miR-30b-5p axis modulates NLRP3 expression and NLPR3 inflammasome activation in macrophages during liver inflammation, which provides a potential target for liver disease.

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Protective effects of microRNA‐22‐3p against retinal pigment epithelial inflammatory damage by targeting NLRP3 inflammasome

Cited by 44 publications

References 37 publications

MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3

MiR‐223‐3p and miR‐22‐3p inhibit monosodium urate‐induced gouty inflammation by targeting NLRP3

MiR-22-3p Expression is down-regulated in lung adenocarcinoma

Cannabinoid Receptor 1/miR-30b-5p Axis Governs Macrophage NLRP3 Expression and Inflammasome Activation in Liver Inflammatory Disease

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