STIM1 mediates IAV-induced inflammation of lung epithelial cells by regulating NLRP3 and inflammasome activation via targeting miR-223

Liu, Cuicui; Miao, Yi; Chen, Ruilin; Zhang, Yongqing; Wu, Hua; Yang, Sheng; Shang, Liqun

doi:10.1016/j.lfs.2020.118845

Cited by 25 publications

(20 citation statements)

References 32 publications

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“…The therapeutic value of CY-09 has been mainly reported in inflammatory diseases, including inflammation after spinal cord injuries Fan et al (2020) and cerebral ischemia/reperfusion injuries ( Sun et al, 2020 ). Recently, researchers also focused on contributing chronic inflammation created by NLRP3 activation to carcinogenesis, including proliferation, angiogenesis, immunosuppression, and metastasis Liu et al (2021) , Huang et al (2017) , and Chen et al (2018) showed that blockage of the NLRP3 inflammasome could enhance the antitumor immune responses in head and neck squamous cell carcinoma, suggesting that the NLRP3 inflammasome pathway may be regarded as a novel approach for the treatment of head and neck squamous cell carcinoma. Inhibition of the NLRP3 inflammasome through an NLRP3-specific antagonist could also reduce the cell viability in pancreatic adenocarcinoma ( Yaw et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

NLRP3 Overexpression Associated With Poor Prognosis and Presented as an Effective Therapeutic Target in Osteosarcoma

et al. 2021

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Despite the development of diagnostic and treatment strategies, the survival outcome of patients with osteosarcoma remains poor. Nod-like receptor protein 3 (NLRP3) plays a crucial role in the inflammasome pathway, which is related to the progression of various tumors. However, the effect of NLRP3 on osteosarcoma has not yet been well explored. Our study aimed to investigate the role of NLRP3 in the malignant biological behavior of osteosarcoma as well as its therapeutic value. Immunohistochemistry was applied to investigate the NLRP3 expression in osteosarcoma and osteochondroma specimens. Cell Counting Kit-8, colony formation, wound healing, transwell, and flow cytometry assays were used to explore the contribution of NLRP3 to the proliferation, migration, invasion, apoptosis and cell cycle distribution of osteosarcoma cells in vitro. Western blot was performed to evaluate the expression of NLRP3 and the related proteins in osteosarcoma cell lines after the blockade of NLRP3 using CY-09 and lentivirus intervention. Furthermore, tumor formation assay was used to analyze the effect of NLRP3 on the growth of osteosarcoma in vivo. The results showed that the NLRP3 protein was overexpressed in osteosarcoma, which was independently correlated with the poor prognosis of patients. Moreover, NLRP3 suppression by the inhibitor of CY-09 or lentivirus-induced gene knockdown inhibited the cell proliferation, migration, invasion and promoted the cell apoptosis and G1 cell cycle arrest in osteosarcoma via targeting the inflammasome pathway. Our in vivo results confirmed that the inhibition of NLRP3 suppressed the tumor formation of osteosarcoma. In conclusion, NLRP3 may be regarded as an independent prognostic biomarker and a potential therapeutic target for osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

NLRP3 Overexpression Associated With Poor Prognosis and Presented as an Effective Therapeutic Target in Osteosarcoma

et al. 2021

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“… 75 Another study showed that the miR-223/NLRP3 axis was involved in stromal interaction molecule 1-mediated lung epithelial injury in influenza A virus-induced infection. 76 Furthermore, the expression of miR-155 was up-regulated in Porphyromonas gingivalis -induced macrophages and the knockdown of miR-155 could reduce NLRP3 inflammasome-mediated pyroptosis. 77 These studies showed that miRNAs mainly participated in microbial infection by regulating NLRP3 inflammasome pathways.…”

Section: The Roles Of Ncrnas In Inflammasomes Activation In Inflammatory Diseasesmentioning

confidence: 98%

Non-Coding RNAs: Master Regulators of Inflammasomes in Inflammatory Diseases

Wang¹,

Yang²,

Yang³

et al. 2021

JIR

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Emerging data indicates that non-coding RNAs (ncRNAs) represent more than just “junk sequences” of the genome and have been found to be involved in multiple diseases by regulating various biological process, including the activation of inflammasomes. As an important aspect of innate immunity, inflammasomes are large immune multiprotein complexes that tightly regulate the production of pro-inflammatory cytokines and mediate pyroptosis; the activation of the inflammasomes is a vital biological process in inflammatory diseases. Recent studies have emphasized the function of ncRNAs in the fine control of inflammasomes activation either by directly targeting components of the inflammasomes or by controlling the activity of various factors that control the activation of inflammasomes; consequently, ncRNAs may represent potential therapeutic targets for inflammatory diseases. Understanding the precise role of ncRNAs in controlling the activation of inflammasomes will help us to design targeted therapies for multiple inflammatory diseases. In this review, we summarize the regulatory role and therapeutic potential of ncRNAs in the activation of inflammasomes by focusing on a range of inflammatory diseases, including microbial infection, sterile inflammatory diseases, and fibrosis-related diseases. Our goal is to provide new ideas and perspectives for future research.

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“…Attenuates epithelial cell injury [30,39,40] Role of miR-223 in macrophage polarization miRNAs are key regulators of various biological processes and have regulated macrophage (Mø) polarization and promoted inflammatory activities. miR-223 is significantly down-regulated during human monocyte-macrophage differentiation [25].…”

Section: Role Of Mir-223 In Granulocyte Differentiationmentioning

confidence: 99%

“…Therefore, miR-223 restricts NLRP3 activation and acts as a protective factor during inflammatory responses 65 . Liu et al 40 illustrated that the stromal interaction molecule 1 (STIM1) regulated NLRP3 expression by binding the AACUGA motif in miR-223. On the other hand, silencing STIM1 alleviates influenza A virus (IAV)-induced inflammation in lung epithelial cells by inactivating the NLRP3 and inflammasome by promoting the miR-223 expression 40 .…”

Section: Molecular Mechanism Of Action Of Mir-223 At the Cellular Levelmentioning

confidence: 99%

miR-223: An Effective Regulator of Immune Cell Differentiation and Inflammation

Jiao¹,

Wang²,

Luoreng³

et al. 2021

Int. J. Biol. Sci.

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MicroRNAs (miRNAs) play a critical role in regulating various biological processes, such as cell differentiation and immune modulation by binding to their target genes. miR-223 is a miRNA with important functions and has been widely investigated in recent years. Under certain physiological conditions, miR-223 is regulated by different transcription factors, including sirtuin1 (Sirt1), PU.1 and Mef2c, and its biological functions are mediated through changes in its cellular or tissue expression. This review paper summarizes miR-223 biosynthesis and its regulatory role in the differentiation of granulocytes, dendritic cells (DCs) and lymphocytes, macrophage polarization, and endothelial and epithelial inflammation. In addition, it describes the molecular mechanisms of miR-223 in regulating lung inflammation, rheumatoid arthritis, enteritis, neuroinflammation and mastitis to provide insights into the existing molecular regulatory networks and therapies for inflammatory diseases in humans and animals.

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STIM1 mediates IAV-induced inflammation of lung epithelial cells by regulating NLRP3 and inflammasome activation via targeting miR-223

Cited by 25 publications

References 32 publications

NLRP3 Overexpression Associated With Poor Prognosis and Presented as an Effective Therapeutic Target in Osteosarcoma

NLRP3 Overexpression Associated With Poor Prognosis and Presented as an Effective Therapeutic Target in Osteosarcoma

Non-Coding RNAs: Master Regulators of Inflammasomes in Inflammatory Diseases

miR-223: An Effective Regulator of Immune Cell Differentiation and Inflammation

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