Journal articles: 'MicroRNA-223'

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Vickers, Kasey C., Stuart R. Landstreet, Michael G. Levin, Bassem M. Shoucri, Cynthia L. Toth, Robert C. Taylor, Brian T. Palmisano, et al. "MicroRNA-223 coordinates cholesterol homeostasis." Proceedings of the National Academy of Sciences 111, no. 40 (September 22, 2014): 14518–23. http://dx.doi.org/10.1073/pnas.1215767111.

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Pulikkan, John A., Viola Dengler, Philomina S. Peramangalam, Abdul A. Peer Zada, Carsten Müller-Tidow, Stefan K. Bohlander, Daniel G. Tenen, and Gerhard Behre. "Cell-cycle regulator E2F1 and microRNA-223 comprise an autoregulatory negative feedback loop in acute myeloid leukemia." Blood 115, no. 9 (March 4, 2010): 1768–78. http://dx.doi.org/10.1182/blood-2009-08-240101.

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Abstract Transcription factor CCAAT enhancer binding protein α (C/EBPα) is essential for granulopoiesis and its function is deregulated in leukemia. Inhibition of E2F1, the master regulator of cell-cycle progression, by C/EBPα is pivotal for granulopoiesis. Recent studies show microRNA-223 (miR-223), a transcriptional target of C/EBPα, as a critical player during granulopoiesis. In this report, we demonstrate that during granulopoiesis microRNA-223 targets E2F1. E2F1 protein was up-regulated in miR-223 null mice. We show that miR-223 blocks cell-cycle progression in myeloid cells. miR-223 is down-regulated in different subtypes of acute myeloid leukemia (AML). We further show that E2F1 binds to the miR-223 promoter in AML blast cells and inhibits miR-223 transcription, suggesting that E2F1 is a transcriptional repressor of the miR-223 gene in AML. Our study supports a molecular network involving miR-223, C/EBPα, and E2F1 as major components of the granulocyte differentiation program, which is deregulated in AML.

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Olisova, Olga Yu, Vladimir V. Demkin, Natalia G. Chernova, Jessika R. Amshinskaya, and Andrey A. Kazakov. "MicroRNA as a diagnostic marker in cutaneous T-cell lymphomas." Russian Journal of Skin and Venereal Diseases 25, no. 1 (August 3, 2022): 5–16. http://dx.doi.org/10.17816/dv106327.

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BACKGROUND: In recent years, thanks to the development of methods of molecular genetic analysis, microRNA has become one of the promising markers for the diagnosis of many human diseases. AIMS: to study microRNA as a new method for the diagnosis of fungal mycosis. MATERIALS AND METHODS: The study included 30 patients with histologically confirmed diagnosis of T-cell lymphomas of the skin, 25 were diagnosed with fungal mycosis, 5 ― Cesari syndrome. The control group consisted of 10 patients with benign lymphoproliferative dermatoses. The patients underwent the determination of microRNA 223, 16, 326, 663, 423, 711 in blood plasma. MicroRNA was also detected in plasma in patients with T-cell lymphomas of the skin at early and late stages. RESULTS: Statistically significant difference of 223, 16, 326, 711 microRNAs in blood plasma was revealed in patients with fungal mycosis, compared with patients with benign lymphoproliferative dermatoses. Statistically significant difference of 663 microRNA in blood plasma was revealed in patients with T-cell lymphomas of the skin at early and late stages. A statistically significant difference of 223, 711 microRNAs in blood plasma was revealed in patients with fungal mycosis at an early stage compared with patients with benign lymphoproliferative dermatoses. CONCLUSION: The determination of microRNA 223, 16, 326, 711 in blood plasma can be used for early diagnosis of T-cell lymphomas of the skin.

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Kilic, Ismail Dogu, Yavuz Dodurga, Burcu Uludag, Yusuf I. Alihanoglu, Bekir Serhat Yildiz, Yasar Enli, Mucahit Secme, and H. Eren Bostancı. "microRNA -143 and -223 in obesity." Gene 560, no. 2 (April 2015): 140–42. http://dx.doi.org/10.1016/j.gene.2015.01.048.

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Camargo, Fernando D., Jonathan J. Johnnidis, Marian H. Harris, Sandra Stehling-Sun, Robert T. Wheeler, Michael Lam, Oktay Kirak, and Mark D. Fleming. "Regulation of Progenitor Cell Proliferation and Granulocyte Function by microRNA-223." Blood 110, no. 11 (November 16, 2007): 507. http://dx.doi.org/10.1182/blood.v110.11.507.507.

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Abstract MicroRNAs are abundant in animal genomes and have been predicted to have important roles in a broad range of gene expression programs. Despite this prominence, there is a dearth of functional knowledge regarding individual mammalian microRNAs. Using a loss-of-function allele in mice, we report here that the myeloid-specific microRNA-223 (miR-223) negatively regulates progenitor proliferation and granulocyte differentiation and activation. miR-223 mutant mice have an expanded granulocytic compartment resulting from a specific and cell-autonomous increase in the number of granulocyte-monocyte progenitors (GMPs). We show that Mef2c, a transcription factor that promotes GMP renewal, is a target of miR-223 and that genetic ablation of Mef2c suppresses progenitor expansion and corrects the neutrophilic phenotype in miR-223 null mice. In addition, granulocytes lacking miR-223 are hypermature, hypersensitive to activating stimuli and display increased fungicidal activity. Consequent to this neutrophil hyperactivity, miR-223 mutant mice spontaneously develop inflammatory lung pathology and exhibit exaggerated tissue destruction following endotoxin challenge. Our results present a new paradigm in miRNA-mediated gene regulation, in which a microRNA can negatively modulate the proliferation and differentiation program of the lineage to which it is most strongly associated.

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Pulikkan, John Anto, Viola Dengler, Abdul Peerzada, Stefan Bohlander, Daniel G. Tenen, and Gerhard Behre. "A Molecular Network Comprising MicroRNA-223, E2F1 and C/Ebpα in Granulopoiesis and in Acute Myeloid Leukemia." Blood 112, no. 11 (November 16, 2008): 1803. http://dx.doi.org/10.1182/blood.v112.11.1803.1803.

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Abstract MicroRNAs play crucial roles in gene expression programmes and have been demonstrated to have major influence in various biological processes. Recent findings suggest aberrant regulation of microRNAs is a hall mark of many cancers including leukemia. MicroRNA-223 (miR-223) is regulated by the transcription factor CCAAT enhancer binding protein α (C/EBPα) and is upregulated during granulopoiesis. miR-223 mutant mice display defects in granulopoiesis pointing out the importance of miR-223 during granulopoiesis. Recent studies suggest that loss of function or expression of C/ EBPα is a major step in the development of acute myeloid leukemia (AML). Using an inducible cell line model, we show that C/EBPα upregulates microRNA-223 expression during granulopoiesis. Based on these findings, we hypothesized that miR-223 could be downregulated in human AML. Here we report that miR-223 is downregulated in different subtypes of AML as analysed by quantitative Real-Time RT-PCR. We investigated what are the critical targets of miR-223 during granulopoiesis. Computational analysis suggests that E2F1, the transcription factor that promotes cell cycle progression which is inhibited by C/EBPα during granulopoiesis, could be a putative target of miR-223. By luciferase assay using 3’UTR of E2F1, we show that E2F1 is a potential target of miR-223. miR-223 downregulates E2F1 by translational repression as revealed by reduction in E2F1 protein level. Silencing of miR-223 leads to upregulation of E2F1 protein level as analyzed by Western blot analysis. Proliferation assays as well as cell cycle analysis demonstrate that miR-223 blocks cell cycle progression in myeloid cells. Interestingly, sequence analysis of miR-223 promoter revealed putative E2F1 binding sites. We demonstrate that E2F1 inhibits the microRNA-223 promoter activity through its transactivation domain as shown by promoter assay. Furthermore, overexpression of E2F1 down regulates the expression of miR-223, suggesting E2F1 acting as a transcriptional repressor of the miR-223 gene. Meanwhile, C/EBPα transactivates miR-223 promoter activity. We also report that E2F1 is able to block granulocytic differentiation. Recent studies demonstrate that disruption of E2F1 inhibition by C/EBPα leads to leukemia, pointing out the significance of E2F1 inhibition in the development of AML. Our data support a circuitry comprising miR-223, C/EBPα and E2F1 as major components of the granulocyte differentiation programme, which is deregulated in AML. Manipulation of miR-223 could be therapeutically relevant in AML subtypes in which E2F1 inhibition is deregulated.

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Zhang, Xiutian, Peng Tan, Yuan Zhuang, and Lei Du. "hsa_circRNA_001587 upregulates SLC4A4 expression to inhibit migration, invasion, and angiogenesis of pancreatic cancer cells via binding to microRNA-223." American Journal of Physiology-Gastrointestinal and Liver Physiology 319, no. 6 (December 1, 2020): G703—G717. http://dx.doi.org/10.1152/ajpgi.00118.2020.

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Human circular (hsa_circ)RNA_001587 and solute carrier family 4 member 4 (SLC4A4) are poorly expressed, but microRNA (miR)-223 is overexpressed in pancreatic cancer (PC) cells. hsa_circRNA_001587 binds to miR-223. Overexpression of hsa_circRNA_001587 inhibits PC progression. Overexpression of miR-223 downregulates the expression of SLC4A4 and promotes PC cell growth. hsa_circRNA_001587 may be a potential target for PC treatment.

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Laffont, Benoit, Aurélie Corduan, Hélène Plé, Anne-Claire Duchez, Nathalie Cloutier, Eric Boilard, and Patrick Provost. "Activated platelets can deliver mRNA regulatory Ago2•microRNA complexes to endothelial cells via microparticles." Blood 122, no. 2 (July 11, 2013): 253–61. http://dx.doi.org/10.1182/blood-2013-03-492801.

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Key Points Activated platelets release microRNA miR-223 preferentially through MPs that can be internalized by endothelial cells. Platelet MP-derived Ago2•microRNA complexes are functional and can regulate endogenous gene expression in recipient endothelial cells.

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M’baya-Moutoula, Eleonore, Alexandre Marchand, Isabelle Six, Noura Bahrar, Tanja Celic, Nathalie Mougenot, Pierre Maitrias, et al. "Inhibition of miR-223 Expression Using a Sponge Strategy Decreases Restenosis in Rat Injured Carotids." Current Vascular Pharmacology 18, no. 5 (August 10, 2020): 507–16. http://dx.doi.org/10.2174/1570161117666190705141152.

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Objective: Restenosis is a frequent complication of angioplasty. It consists of a neointimal hyperplasia resulting from progression and migration of vascular smooth muscle cells (VSMC) into the vessel lumen. microRNA miR-223 has recently been shown to be involved in cardiovascular diseases including atherosclerosis, vascular calcification and arterial thrombosis. In this study, our aim was to assess the impact of miR-223 modulation on restenosis in a rat model of carotid artery after balloon injury. Methods: The over and down-expression of miR-223 was induced by adenoviral vectors, containing either a pre-miR-223 sequence allowing artificial miR-223 expression or a sponge sequence, trapping the native microRNA, respectively. Restenosis was quantified on stained rat carotid sections. Results: In vitro, three mRNA (Myocyte Enhancer Factor 2C (MEF2C), Ras homolog gene family, member B (RhoB) and Nuclear factor 1 A-type (NFIA)) reported as miR-223 direct targets and known to be implicated in VSMC differentiation and contractility were studied by RT-qPCR. Our findings showed that down-expression of miR-223 significantly reduced neointimal hyperplasia by 44% in carotids, and was associated with a 2-3-fold overexpression of MEF2C, RhoB and NFIA in a murine monocyte macrophage cell line, RAW 264.7 cells. Conclusions: Down-regulating miR-223 could be a potential therapeutic approach to prevent restenosis after angioplasty.

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Gu, Yuan Yuan, Guan Nan Zhou, Yao Li, Hong Yu He, Jing Xin Ding, and Ke Qin Hua. "HDAC10 Inhibits Cervical Cancer Progression through Downregulating the HDAC10-microRNA-223-EPB41L3 Axis." Journal of Oncology 2022 (January 19, 2022): 1–12. http://dx.doi.org/10.1155/2022/8092751.

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Background. Although the tumorigenesis of cervical cancer (CC) has been widely investigated and recognized, the study of the systematic impact of histone deacetylase 10 (HDAC10), microRNA, and downstream molecular mechanisms in CC is still limited. Herein, cervical cancer, precancer lesions, and normal cervical tissues were collected to test the expression level of HDAC10, miR-223, and EPB41L3. The mechanism of HDAC10, miR-223, and EPB41L3 was interpreted in cervical cancer cells after HDAC10, miR-223, or EPB41L3 expression was altered. Results. HDAC10 was poorly expressed in cervical cancer and precancer lesions, while miR-223 was highly expressed in cervical cancer. HDAC10 bound to miR-223, and miR-223 targeted EPB41L3. HDAC10 depressed the invasion property and tumorigenesis of cervical cancer via downregulating miR-223 and subsequently targeting EPB41L3. Conclusion. The study clarifies that HDAC10 inhibits cervical cancer by downregulating miR-223 and subsequently targeting EPB41L3 expression, which might provide a new insight for management upon cervical cancer and precancer lesions.

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Youssef, Amany Ragab, Samah Bastawy, Karim Montasser, Sally Abed, Muhammad Diasty, Mohamed Elegezy, Elshahat A. Yousef, Ahmed Bahy-eldeen Ibrahem, and Mostafa Anees Mahmoud. "MicroRNA-30e and MicroRNA-223 Expression for Early Diagnosis of Hepatocellular Carcinoma Associated with Hepatitis C Virus." Advances in Medicine and Medical Research 3, no. 1 (January 25, 2020): 97–104. http://dx.doi.org/10.31377/ammr.v3i1.647.

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Background. The goals of this study were to elucidate the use of the expression of microRNA-30e (miR-30e) and microRNA-223 (miR-223) as diagnostic biomarkers for early diagnosis of hepatocellular carcinoma (HCC) associated with hepatitis C virus (HCV) infection. Methods. The study included three groups, the first group included thirty patients with HCC associated with HCV, the second group included thirty patients with cirrhosis with HCV and the third group included thirty healthy control subjects. Blood samples were obtained for determination of serum expression of miR-30e and miR-223 by real time polymerase chain reaction. Results. There was significant decrease of miR-30e of expression in patients with HCC (0.16 ± 0.1) compared to both patients with cirrhosis (0.4 ± 0.2, P<0.01) and healthy control subjects (1.2 ± 0.4, P<0.001). There was also significant reduction of miR-223 expression levels in patients with HCC (0.2 ± 0.1) compared to patients with cirrhosis (0.5 ± 0.2, P<0.01) and healthy control subjects (1.0 ± 0.1, P<0.001). There was also significant decrease of miR-30e expression in late stage versus early stage of HCC (0.1 ± 0.0 vs. 0.22 ± 0.1, P<0.001), while there was no significant difference of alpha-fetoprotein (AFP) between patients with late and early HCC. Also, values of miR-223 had significantly reduced levels in late HCC compared to its expression values in early HCC (0.1± 0.0 vs. 0.23 ± 0.2, P<001). Conclusion. There was significant reduction of expression of miR-30e and miR-223 in serum of HCC patients compared to either patients with cirrhosis or healthy subjects. These results show that the combined use of both biomarkers had better sensitivity in the diagnosis of HCC compared to AFP.

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Zhang, Shijie, Yi Liu, Zhong Zheng, Xuemin Zeng, Dongxu Liu, Chunling Wang, and Kang Ting. "MicroRNA-223 Suppresses Osteoblast Differentiation by Inhibiting DHRS3." Cellular Physiology and Biochemistry 47, no. 2 (2018): 667–79. http://dx.doi.org/10.1159/000490021.

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Background/Aims: In this study, we aimed to use bioinformatics tools to identify the specific miRNAs and mRNAs involved in osteogenic differentiation and to further explore the way in which miRNA regulates osteogenic differentiation. Methods: The microarray GSE80614, which includes data from 3 human mesenchymal stromal cells (hMSCs) and 3 hMSCs after 72 hours (hr) of osteogenic differentiation, was used to screen for differentially expressed mRNAs. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of these mRNAs were conducted using Gene Set Enrichment Analysis (GSEA). Then, the miRanda website was employed to detect the binding sites of DHRS3. In vitro experiments, including RT-PCR and western blotting, were used to detect miR-233 and DHRS3 expression levels 7 and 14 days (d) after the induction of osteogenic differentiation using human bone marrow-derived mesenchymal stem cells (hBMSCs). The target relationship between miR-223 and DHRS3 was confirmed by a dual luciferase assay. ALP (alkaline phosphatase) staining, ARS (Alizarin Red S) staining and western blotting (Runx2, OPN, OCN) were used to detect the level of osteogenic differentiation after transfection with miR-223 mimics and DHRS3 cDNA. Results: In this study, 127 mRNAs differentially expressed during osteogenic differentiation were identified in GSE80614. GO term and KEGG pathway enrichment analyses found that the retinol metabolism pathway was activated during osteogenic differentiation and that DHRS3, which is involved in the pathway, was upregulated. During osteogenic differentiation in hBMSCs, miR-223 was gradually downregulated, while DHRS3 was upregulated. After 14 days of osteogenic differentiation, ALP and ARS staining assay results showed strong ALP activity and extracellular matrix calcification with the inhibition of miR-223 or the overexpression of DHRS3. Furthermore, the expression levels of Runx2, OPN, and OCN were upregulated with the knockdown of miR-223 or the overexpression of DHRS3, while the simultaneous transfection of a miR-223 agomir and DHRS3 cDNA resulted in no significant difference from the negative control (NC) group. Conclusion: The inhibition of miR-223 promotes the osteogenic differentiation of hBMSCs via the upregulation of DHRS3.

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Xu, Yanfei, Tanushri Sengupta, and Alexander C. Minella. "A Screen In Primary Erythroblasts Reveals a MicroRNA-Centered Homeostatic Mechanism for Regulating Cyclin E Activity." Blood 116, no. 21 (November 19, 2010): 1543. http://dx.doi.org/10.1182/blood.v116.21.1543.1543.

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Abstract Abstract 1543 A growing body of evidence highlights the importance of microRNAs in regulating the expression of mediators of cell cycle progression. A theme emerging from these studies is that microRNAs participate in feedback or feed-forward circuits to provide bistability for key transition points in the cell cycle. We previously have shown that proper regulation of cyclin E activity is required for normal erythroid cell maturation in vivo, using cyclin ET74AüT393A knock-in mice, which have markedly dysregulated cyclin E due to its failure to interact with the Fbw7 ubiquitin ligase complex. We hypothesized that we could identify novel, microRNA-based molecular circuitry for maintaining appropriate levels of cyclin E activity by screening cyclin E knock-in erythroblasts for alterations in microRNA expression. We analyzed data we obtained from multiplex real-time PCR arrays comparing the expression of over 500 microRNAs in cyclin ET74A T393A knock-in versus wild-type erythroblasts (Ter119+/CD71+) and found down-regulated expression of a number of microRNAs targeting CDK inhibitors. We also identified down-regulated expression of potential microRNA regulators of Fbw7 expression. We found that overexpression of miR-223, in particular, significantly reduces Fbw7 mRNA levels, increases endogenous cyclin E protein and activity levels, and increases genomic instability. We next confirmed that miR-223 targets the Fbw7 3’ untranslated region. We then found that reduced miR-223 expression leads to increased Fbw7 expression and decreased cyclin E activity. Finally, we found that miR-223 expression in K562 cells is responsive to acute alterations in cyclin E regulation by the Fbw7 pathway and that dysregulated Fbw7 expression alters the erythroid differentiation capacity of these cells. Mir-223 plays an important role in myeloid and erythroid differentiation by regulating multiple substrates involved in these maturation programs. Here, we identify Fbw7 as a novel target of miR-223. Our data also indicate that miR-223 modulates Fbw7 expression as part of a homeostatic mechanism to regulate cyclin E activity and provide the first evidence that activity of the SCFFbw7 ubiquitin ligase can be controlled by the microRNA pathway. Disclosures: No relevant conflicts of interest to declare.

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Yang, Yanfang, Zhansheng Jiang, Ning Ma, Bin Wang, Jun Liu, Lina Zhang, and Lin Gu. "MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer." Cellular Physiology and Biochemistry 45, no. 2 (2018): 856–66. http://dx.doi.org/10.1159/000487180.

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Background/Aims: To investigate the cellular effects and clinical significance of microRNA-223 (miR-223) in breast cancer by targeting stromal interaction molecule1 (STIM1). Methods: Breast cancer cell lines (T47D, MCF-7, SKB-R3, MDA-MB-231 and MDA-MB-435) and a normal breast epithelial cell line (MCF-10A) were prepared for this study. MiR-223 mimics, anti-miR-223 and pcDNA 3.1-STIM1 were transiently transfected into cancer cells independently or together, and then RT-qPCR was performed to detect the expressions of miR-223 and STIM1 mRNA, dual-luciferase reporter assay was conducted to examine the effects of miR-223 on STIM1, Western blotting was used to measure the expressions of the STIM1 proteins, MTT and Trans-well assays were performed to detect cell proliferation and invasion. Finally, the correlation of miR-223 and STIM1 was investigated by detecting with ISH and IHC in breast cancer specimens or the corresponding adjacent normal tissues. Results: Compared with normal cells and tissues, breast cancer tissues and cells exhibited significantly lower expression of miR-223, but higher expression of STIM1. MiR-223 could inhibit the proliferation and invasiveness of breast cancer cells by negatively regulating the expressions of STIM1. Reimplantation with STIM1 partially rescued the miRNA-223-induced inhibition of breast cancer cells. Clinical data revealed that high expression of STIM1 and miR-223 was respectively detrimental and beneficial factor impacting patient’s disease-free survival (DFS) rather than overall survival (OS). Moreover, Pearson correlation analysis also confirmed that STIM1 was inversely correlated with miR-223. Conclusion: MiR-223 inhibits the proliferation and invasion of breast cancer by targeting STIM1. The miR-223/STIM1 axis could possibly be a potential therapeutic target for treating breast cancer patients.

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Aziz, Faisal, Abhijit Chakraborty, Imran Khan, and Josh Monts. "Relevance of miR-223 as Potential Diagnostic and Prognostic Markers in Cancer." Biology 11, no. 2 (February 6, 2022): 249. http://dx.doi.org/10.3390/biology11020249.

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In 1993, the discovery of microRNAs in Caenorhabditis elegans (C. elegans) altered the paradigmatic view of RNA biology and post-transcriptional gene regulation. Further study revealed the role of microRNAs in disease development and progression. In particular, this review highlights microRNA-223 (miR-223 or miRNA-223) expression in malignant neoplastic disorders. miR-223 expression controls aspects of hematopoiesis and apoptosis, and cell proliferation, migration, and invasion. miR-223 regulates a number of gene targets, including cytoplasmic activation/proliferation-associated protein-1 (Caprin-1), insulin-like growth factor-1 receptor (IGF-1R), and other cell proliferation- and cell cycle-associated genes. Several studies have proposed miR-223 as a novel biomarker for early cancer diagnosis. Here, we emphasize miR-223′s role in the development and progression of cancer.

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Thum, Thomas. "MicroRNA-223 Made Its Way Into Vascular Research." Circulation Research 113, no. 12 (December 6, 2013): 1270–71. http://dx.doi.org/10.1161/circresaha.113.302747.

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Wu, Lihui, Huihui Li, Cheng You Jia, Wei Cheng, Mei Yu, Min Peng, Yuanqing Zhu, et al. "MicroRNA-223 regulates FOXO1 expression and cell proliferation." FEBS Letters 586, no. 7 (March 8, 2012): 1038–43. http://dx.doi.org/10.1016/j.febslet.2012.02.050.

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Harraz, M. M., S. M. Eacker, X. Wang, T. M. Dawson, and V. L. Dawson. "MicroRNA-223 is neuroprotective by targeting glutamate receptors." Proceedings of the National Academy of Sciences 109, no. 46 (October 29, 2012): 18962–67. http://dx.doi.org/10.1073/pnas.1121288109.

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Yuan, Xiaoyi, Nathaniel Berg, Jae Woong Lee, Thanh-Thuy Le, Viola Neudecker, Na Jing, and Holger Eltzschig. "MicroRNA miR-223 as regulator of innate immunity." Journal of Leukocyte Biology 104, no. 3 (July 3, 2018): 515–24. http://dx.doi.org/10.1002/jlb.3mr0218-079r.

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Chen, Shih-Yao, Ting-Chien Tsai, Yuan-Tsung Li, Yun-Chiao Ding, Chung-Teng Wang, Jeng-Long Hsieh, Chao-Liang Wu, Po-Ting Wu, and Ai-Li Shiau. "Interleukin-23 Mediates Osteoclastogenesis in Collagen-Induced Arthritis by Modulating MicroRNA-223." International Journal of Molecular Sciences 23, no. 17 (August 26, 2022): 9718. http://dx.doi.org/10.3390/ijms23179718.

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Interleukin-23 (IL-23) plays a pivotal role in rheumatoid arthritis (RA). IL-23 and microRNA-223 (miR-223) are both up-regulated and mediate osteoclastogenesis in mice with collagen-induced arthritis (CIA). The aim of this study was to examine the association between IL-23 and miR-223 in contributing to osteoclastogenesis and arthritis. Levels of IL-23p19 in joints of mice with CIA were determined. Lentiviral vectors expressing short hairpin RNA (shRNA) targeting IL-23p19 and lisofylline (LSF) were injected intraperitoneally into arthritic mice. Bone marrow-derived macrophages (BMMs) were treated with signal transducers and activators of transcription 4 (STAT4) specific shRNA and miR-223 sponge carried by lentiviral vectors in response to IL-23 stimulation. Treatment responses were determined by evaluating arthritis scores and histopathology in vivo, and detecting osteoclast differentiation and miR-223 levels in vitro. The binding of STAT4 to the promoter region of primary miR-223 (pri-miR-223) was determined in the Raw264.7 cell line. IL-23p19 expression was increased in the synovium of mice with CIA. Silencing IL-23p19 and inhibiting STAT4 activity ameliorates arthritis by reducing miR-223 expression. BMMs from mice in which STAT4 and miR-223 were silenced showed decreased osteoclast differentiation in response to IL-23 stimulation. IL-23 treatment increased the expression of miR-223 and enhanced the binding of STAT4 to the promoter of pri-miR-223. This study is the first to demonstrate that IL-23 promotes osteoclastogenesis by transcriptional regulation of miR-223 in murine macrophages and mice with CIA. Furthermore, our data indicate that LSF, a selective inhibitor of STAT4, should be an ideal therapeutic agent for treating RA through down-regulating miR-223-associated osteoclastogenesis.

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Guo, Ju, Runfu Cao, Xingwei Yu, Zewen Xiao, and Zhiwen Chen. "MicroRNA-223-3p inhibits human bladder cancer cell migration and invasion." Tumor Biology 39, no. 2 (February 2017): 101042831769167. http://dx.doi.org/10.1177/1010428317691678.

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The regulation of initiation and progression during carcinogenesis of bladder carcinoma is not completely elucidated. Dysregulation of microRNAs has been detected to play critical roles in the development of various cancers, including bladder carcinoma, whereas the involvement of miR-223-3p in the tumorigenesis of bladder carcinoma has not been studied. Here, we show that significantly higher levels of nuclear receptor coactivator 1 and significantly lower levels of miR-223-3p were detected in bladder carcinoma tissue, compared to the adjacent non-tumor tissue. In addition, the levels of nuclear receptor coactivator 1 and miR-223-3p were inversely correlated. Moreover, low miR-223-3p levels in bladder carcinoma specimens were associated with poor prognosis. In vitro, depletion of miR-223-3p increased bladder carcinoma cell invasion, which was abolished by overexpression of nuclear receptor coactivator 1. Bioinformatics studies demonstrate that miR-223-3p may bind to the 3′-UTR of nuclear receptor coactivator 1 messenger RNA to inhibit its protein translation in bladder carcinoma cells. Together, our study highlights miR-223-3p as a previously unrecognized microRNA that inhibits bladder carcinoma invasiveness via nuclear receptor coactivator 1, and this finding may be important for developing innovative therapeutic targets in treating bladder carcinoma.

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Colbert, James F., Joshay A. Ford, Sarah M. Haeger, Yimu Yang, Kyrie L. Dailey, Kristen C. Allison, Viola Neudecker, et al. "A model-specific role of microRNA-223 as a mediator of kidney injury during experimental sepsis." American Journal of Physiology-Renal Physiology 313, no. 2 (August 1, 2017): F553—F559. http://dx.doi.org/10.1152/ajprenal.00493.2016.

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Sepsis outcomes are heavily dependent on the development of septic organ injury, but no interventions exist to interrupt or reverse this process. microRNA-223 (miR-223) is known to be involved in both inflammatory gene regulation and host-pathogen interactions key to the pathogenesis of sepsis. The goal of this study was to determine the role of miR-223 as a mediator of septic kidney injury. Using miR-223 knockout mice and multiple models of experimental sepsis, we found that miR-223 differentially influences acute kidney injury (AKI) based on the model used. In the absence of miR-223, mice demonstrated exaggerated AKI in sterile models of sepsis (LPS injection) and attenuated AKI in a live-infection model of sepsis (cecal ligation and puncture). We demonstrated that miR-223 expression is induced in kidney homogenate after cecal ligation and puncture, but not after LPS or fecal slurry injection. We investigated additional potential mechanistic explanations including differences in peritoneal bacterial clearance and host stool virulence. Our findings highlight the complex role of miR-223 in the pathogenesis of septic kidney injury, as well as the importance of differences in experimental sepsis models and their consequent translational applicability.

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Liu, Xiaoxiao, Yifeng Xu, Yunfei Deng, and Hongli Li. "MicroRNA-223 Regulates Cardiac Fibrosis After Myocardial Infarction by Targeting RASA1." Cellular Physiology and Biochemistry 46, no. 4 (2018): 1439–54. http://dx.doi.org/10.1159/000489185.

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Background/Aims: Percutaneous coronary intervention reduces acute myocardial infarction (MI)-induced mortality to a great extent, but effective treatments for MI-induced cardiac fibrosis and heart failure are still lacking. MicroRNAs (miRNAs) play a variety of roles in cells and have thus been investigated extensively. MicroRNA-223 (miR-223) expression has been reported to be altered in post-MI heart failure in humans; however, the roles of miR-223 in MI remain unknown. Our study aimed to elucidate the roles of miR-223 in cardiac fibrosis. Methods: Cultured cardiac fibroblasts (CFs) were activated by TGF-β1 stimulation. Gain and loss of miR-223 and RAS p21 protein activator 1 (RASA1) knockdown in CFs were achieved by transfecting the cells with miR-223 mimics and inhibitors, as well as small interfering RNA-RASA1 (siRASA1), respectively. Quantitative real-time reverse transcriptase-polymerase chain reactions (qRT-PCR) was used to determine miR-223-3p and RASA1 expression levels, and Cell Counting Kit-8 (CCK-8), transwell migration and scratch assays were performed to assess CFs viability and migration, respectively. Western blotting was used to detect collagen I, collagen III, alpha-smooth muscle actin (a-SMA), RASA1, p-Akt/t-Akt, p-MEK1/2/t-MEK1/2, and p-ERK1/2/t-ERK1/2 protein expressions, and immunofluorescence assays were used to detect the expression of α-actin, vimentin and α-SMA. Luciferase assays were carried out to determine whether miR-223 binds to RASA1. Rat models of MI were established by the ligation of the left anterior descending (LAD) coronary artery. MiR-223 inhibition in vivo was achieved via intramyocardial injections of the miR-223 sponge carried by adeno-associated virus 9 (AAV9). The cardiac function was detected by echocardiography, and cardiac fibrosis was shown by Masson’s trichrome staining. Results: miR-223 was increased in CFs compared to cardiomypcytes, and TGF-β1 treatment increased miR-223 expression in CFs. The miR-223 mimics enhanced cell proliferation and migration and collagen I, collagen III, and α-SMA protein expression in CFs, while the miR-223 inhibitors had contrasting effects and partially prevented the promoting effects of TGF-β1. qRT-PCR and western blotting revealed that miR-223 negatively regulated RASA1 expression, and the luciferase assays showed that miR-223 suppressed the luciferase activity of the RASA1 3’ untranslated region (3'UTR), indicating that miR-223 binds directly to RASA1. Similar to transfection with the miR-223 mimics, RASA1 knockdown enhanced cell proliferation and migration and collagen I, collagen III, and α-SMA protein expression in CFs. Moreover, RASA1 knockdown partially reversed the inhibitory effects of the miR-223 inhibitor on cell proliferation and migration and collagen I, collagen III, and α-SMA protein expression, indicating that the effects of miR-223 in CFs are partially mediated by the regulation of RASA1 expression. Further exploration showed that miR-223 mimics and siRASA1 promoted MEK1/2, ERK1/2 and AKT phosphorylation, while the miR-223 inhibitors had contrasting effects. The in vivo experiments confirmed the results of the in vitro experiments and showed that miR-223 inhibition prevented cardiac functional deterioration and cardiac fibrosis. Conclusions: miR-223 enhanced cell proliferation, migration, and differentiation in CFs, thus mediated cardiac fibrosis after MI partially via the involvement of RASA1.

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Habib, Alaa, Ayman Minisi, Mahmoud Awad, Abdallah Essa, Amany Khalifa, and Somaia Shehab-Eldeen. "Serum microRNA 106 and microRNA 223 as novel biomarkers in inflammatory bowel disease." Medical Journal of Viral Hepatitis 5.1, no. 1 (November 1, 2020): 19–24. http://dx.doi.org/10.21608/mjvh.2020.125615.

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Fukao, Taro, Yoko Fukuda, Kotaro Kiga, Jafar Sharif, Kimihiro Hino, Yutaka Enomoto, Aya Kawamura, Kaito Nakamura, Tsutomu Takeuchi, and Masanobu Tanabe. "An Evolutionarily Conserved Mechanism for MicroRNA-223 Expression Revealed by MicroRNA Gene Profiling." Cell 129, no. 3 (May 2007): 617–31. http://dx.doi.org/10.1016/j.cell.2007.02.048.

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Chuang, Tung-Yueh, Hsiao-Li Wu, Chen-Chun Chen, Gloria Mabel Gamboa, Lawrence C. Layman, Michael P. Diamond, Ricardo Azziz, and Yen-Hao Chen. "MicroRNA-223 Expression Is Upregulated in Insulin Resistant Human Adipose Tissue." Journal of Diabetes Research 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/943659.

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MicroRNAs (miRNAs) are short noncoding RNAs involved in posttranscriptional regulation of gene expression and influence many cellular functions including glucose and lipid metabolism. We previously reported that adipose tissue (AT) from women with polycystic ovary syndrome (PCOS) or controls with insulin resistance (IR) revealed a differentially expressed microRNA (miRNA) profile, including upregulated miR-93 in PCOS patients and in non-PCOS women with IR. Overexpressed miR-93 directly inhibited glucose transporter isoform 4 (GLUT4) expression, thereby influencing glucose metabolism. We have now studied the role of miR-223, which is also abnormally expressed in the AT of IR subjects. Our data indicates that miR-223 is significantly overexpressed in the AT of IR women, regardless of whether they had PCOS or not. miR-223 expression in AT was positively correlated with HOMA-IR. Unlike what is reported in cardiomyocytes, overexpression of miR-223 in human differentiated adipocytes was associated with a reduction in GLUT4 protein content and insulin-stimulated glucose uptake. In addition, our data suggests miR-223 regulates GLUT4 expression by direct binding to its 3′ untranslated region (3′UTR). In conclusion, in AT miR-223 is an IR-related miRNA that may serve as a potential therapeutic target for the treatment of IR-related disorders.

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Kasper, Dionna M., Jared Hintzen, Yinyu Wu, Joey J. Ghersi, Hanna K. Mandl, Kevin E. Salinas, William Armero, et al. "The N-glycome regulates the endothelial-to-hematopoietic transition." Science 370, no. 6521 (December 3, 2020): 1186–91. http://dx.doi.org/10.1126/science.aaz2121.

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Definitive hematopoietic stem and progenitor cells (HSPCs) arise from the transdifferentiation of hemogenic endothelial cells (hemECs). The mechanisms of this endothelial-to-hematopoietic transition (EHT) are poorly understood. We show that microRNA-223 (miR-223)–mediated regulation of N-glycan biosynthesis in endothelial cells (ECs) regulates EHT. miR-223 is enriched in hemECs and in oligopotent nascent HSPCs. miR-223 restricts the EHT of lymphoid-myeloid lineages by suppressing the mannosyltransferase alg2 and sialyltransferase st3gal2, two enzymes involved in protein N-glycosylation. ECs that lack miR-223 showed a decrease of high mannose versus sialylated sugars on N-glycoproteins such as the metalloprotease Adam10. EC-specific expression of an N-glycan Adam10 mutant or of the N-glycoenzymes phenocopied miR-223 mutant defects. Thus, the N-glycome is an intrinsic regulator of EHT, serving as a key determinant of the hematopoietic fate.

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Zardo, Giuseppe, Alberto Ciolfi, Laura Vian, Linda M. Starnes, Monia Billi, Serena Racanicchi, Carmen Maresca, et al. "Polycombs and microRNA-223 regulate human granulopoiesis by transcriptional control of target gene expression." Blood 119, no. 17 (April 26, 2012): 4034–46. http://dx.doi.org/10.1182/blood-2011-08-371344.

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Abstract Epigenetic modifications regulate developmental genes involved in stem cell identity and lineage choice. NFI-A is a posttranscriptional microRNA-223 (miR-223) target directing human hematopoietic progenitor lineage decision: NFI-A induction or silencing boosts erythropoiesis or granulopoiesis, respectively. Here we show that NFI-A promoter silencing, which allows granulopoiesis, is guaranteed by epigenetic events, including the resolution of opposing chromatin “bivalent domains,” hypermethylation, recruitment of polycomb (PcG)–RNAi complexes, and miR-223 promoter targeting activity. During granulopoiesis, miR-223 localizes inside the nucleus and targets the NFI-A promoter region containing PcGs binding sites and miR-223 complementary DNA sequences, evolutionarily conserved in mammalians. Remarkably, both the integrity of the PcGs-RNAi complex and DNA sequences matching the seed region of miR-223 are required to induce NFI-A transcriptional silencing. Moreover, ectopic miR-223 expression in human myeloid progenitors causes heterochromatic repression of NFI-A gene and channels granulopoiesis, whereas its stable knockdown produces the opposite effects. Our findings indicate that, besides the regulation of translation of mRNA targets, endogenous miRs can affect gene expression at the transcriptional level, functioning in a critical interface between chromatin remodeling complexes and the genome to direct fate lineage determination of hematopoietic progenitors.

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Ismail, Noura, Clay B. Marsh, and Melissa Hunter. "MicroRNA Expression in Macrophages-Derived Microvesicles May Contribute to Cellular Survival and Differentiation." Blood 112, no. 11 (November 16, 2008): 3557. http://dx.doi.org/10.1182/blood.v112.11.3557.3557.

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Abstract Microvesicles (MV) (also know as exosomes) are small membrane-bound vesicles released by numerous cell types that contain proteins, mRNA and microRNA. We found that MV from activated monocytes drove survival and differentiation in naïve cells. We therefore were interested in understanding the content of MV produced by activated mononuclear phagocytes. Purified peripheral blood monocytes were treated in vitro for 24 h with or without the monocyte survival factors, GM-CSF or M-CSF, respectively. Examination of monocytes and macrophages by electron microscopy or culture supernatants by flow cytometry demonstrated that monocytes produced MV, which quantitatively increased upon differentiation. Treatment with GM-CSF resulted in more MV production than M-CSF-treated monocytes. To examine whether MV from differentiated cells induced myeloid maturation, the MV were collected and added to fresh monocytes; only MV derived from GM-CSF treated cells induced differentiation of naïve monocytes into macrophages. We next hypothesized that expression of microRNA contained in the MV modulated differentiation of monocytes. Profiling of MV from GM-CSF and M-CSF derived macrophages revealed only two significantly expressed microRNAs. We found that mir-155 was significantly elevated by two-fold in MV from GM-CSF-treated cells, while mir-340 was significantly increased seven-fold in M-CSF-derived MV. Notably, mir- 223 was the highest expressed microRNA in MV from both GM-CSF and M-CSF-treated cells. Recent data suggest that expression of mir-223 regulates myeloid, granulocytic and osteoclasts differentiation, and has a role in hematopoietic stem cell proliferation. While mir-223 is present in MV from both GM-CSF and M-CSF treated cells, it is possible that the low abundance of MV produce from M-CSF-treated cells resulted in less effective concentration to induce differentiation. In this model, it is also possible that regulation of proteins targeted by the increase in mir-155 and decrease mir-340 in the GM-CSF-derived MV are responsible for myeloid differentiation. Since changes in microRNA expression including mir-223 has been reported in AML, our data suggest that myeloid-derived MV in the peripheral blood containing mir-223 may be altered contributing to leukemogenesis.

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Zhi, Yi, Jinhong Pan, Wenhao Shen, Peng He, Ji Zheng, Xiaozhou Zhou, Gensheng Lu, Zhiwen Chen, and Zhansong Zhou. "Ginkgolide B Inhibits Human Bladder Cancer Cell Migration and Invasion Through MicroRNA-223-3p." Cellular Physiology and Biochemistry 39, no. 5 (2016): 1787–94. http://dx.doi.org/10.1159/000447878.

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Background/Aims: Ginkgolide B (GB) is currently used as an anticancer drug for treatment of some malignant cancers. However, whether it may have therapeutic effects on bladder cancer remains unknown. Here, we studied the effects of GB on bladder cancer cells. Methods: Bladder cells were treated with different doses of GB, and the effects on ZEB1 and microRNA-223-3p (miR-223-3p) were analyzed by RT-qPCR and/or Western blot. Prediction of a regulatory relationship between miR-93 and 3'-UTR of Beclin-1 mRNA was performed by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. Results: We found that GB dose-dependently decreased ZEB1 protein, but not mRNA, in bladder cancer cells, resulting in suppression of cell invasion. Moreover, in bladder cancer cells, GB dose-dependently decreased the levels of miR-223-3p, which suppressed the protein translation of ZEB1 through binding to 3'-UTR of ZEB1 mRNA. Overexpression of miR-223-3p decreased ZEB1 protein, while depletion of miR-223-3p increased ZEB1 protein in bladder cancer cells. Conclusion: GB inhibits bladder cancer cell invasiveness through suppressing ZEB1 protein translation via upregulating miR-223-3p.

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Neudecker, Viola, Moritz Haneklaus, Owen Jensen, Ludmila Khailova, Joanne C. Masterson, Hazel Tye, Kathryn Biette, et al. "Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome." Journal of Experimental Medicine 214, no. 6 (May 9, 2017): 1737–52. http://dx.doi.org/10.1084/jem.20160462.

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MicroRNA (miRNA)-mediated RNA interference regulates many immune processes, but how miRNA circuits orchestrate aberrant intestinal inflammation during inflammatory bowel disease (IBD) is poorly defined. Here, we report that miR-223 limits intestinal inflammation by constraining the nlrp3 inflammasome. miR-223 was increased in intestinal biopsies from patients with active IBD and in preclinical models of intestinal inflammation. miR-223-/y mice presented with exacerbated myeloid-driven experimental colitis with heightened clinical, histopathological, and cytokine readouts. Mechanistically, enhanced NLRP3 inflammasome expression with elevated IL-1β was a predominant feature during the initiation of colitis with miR-223 deficiency. Depletion of CCR2+ inflammatory monocytes and pharmacologic blockade of IL-1β or NLRP3 abrogated this phenotype. Generation of a novel mouse line, with deletion of the miR-223 binding site in the NLRP3 3′ untranslated region, phenocopied the characteristics of miR-223-/y mice. Finally, nanoparticle-mediated overexpression of miR-223 attenuated experimental colitis, NLRP3 levels, and IL-1β release. Collectively, our data reveal a previously unappreciated role for miR-223 in regulating the innate immune response during intestinal inflammation.

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Wang, Yao-Sheng, Jing Zhou, Kui Hong, Xiao-Shu Cheng, and Yi-Gang Li. "MicroRNA-223 Displays a Protective Role Against Cardiomyocyte Hypertrophy by Targeting Cardiac Troponin I-Interacting Kinase." Cellular Physiology and Biochemistry 35, no. 4 (2015): 1546–56. http://dx.doi.org/10.1159/000373970.

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Background/Aims: MicroRNAs play regulatory role in cardiovascular disease. MicroRNA-223 (miR-223) was found to be expressed abundantly in myocardium. TNNI3K, a novel cardiac troponin I (cTnI)-interacting and cardiac hypertrophy related kinase, is computationally predicted as a potential target of miR-223. This study was designed to investigate the cellular and molecular effects of miR-223 on cardiomyoctye hypertrophy, focusing on the role of TNNI3K. Methods: Neonatal rat cardiomyocytes (CMs) were cultured, and CMs hypertrophy was induced by endothelin-1 (ET-1). In vivo cardiac hypertrophy was induced by transverse aorta constriction (TAC) in rats. Expression of miR-223 in CMs and myocardium was detected by real-time PCR (RT-PCR). MiR-223 and TNNI3K were overexpressed in CMs via chemically modifed sense RNA (miR-223 mimic) transfection or recombinant adenovirus infection, respectively. Cell size was measured by surface area calculation using fluorescence microscopy after anti-α-actinin staining. Expression of hypertrophy-related genes was detected by RT-PCR. The protein expression of TNNI3K and cTnI was determined by Western blots. Luciferase assay was employed to confirm the direct binding of miR-223 to the 3'UTR of TNNI3K mRNA. Intracellular calcium was measured by sensitive fluorescent indicator (Furo-2). Video-based edge detection system was employed to measure cardiomyocyte contractility. Results: MiR-223 was downregulated in ET-1 induced hypertrophic CMs and in hypertrophic myocardium compared with respective controls. MiR-223 overexpression in CMs alleviated ET-1 induced hypertrophy, evidenced by smaller cell surface area and downregulated ANP, α-actinin, Myh6 and Myh7 expression. Luciferase reporter gene assay showed that TNNI3K serves as a direct target gene of miR-223. In miR-223-overexpressed CMs, the protein expression of TNNI3K was significantly downregulated. MiR-223 overexpression also rescued the upregulated TNNI3K expression in hypertrophic CMs. Furthermore, cTnI phosphorylation was downregulated post miR-223 overexpression. Ad.rTNNI3K increased intracellular Ca2+ concentrations and cell shortening in CMs, while miR-223 overexpression significantly rescued these hypertrophic effects. Conclusion: By direct targeting TNNI3K, miR-223 could suppress CMs hypertrophy via downregulating cTnI phosphorylation, reducing intracellular Ca2+ and contractility of CMs. miR-223 / TNNI3K axis may thus be major players of CMs hypertrophy.

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Felli, N., F. Pedini, P. Romania, M. Biffoni, O. Morsilli, G. Castelli, S. Santoro, et al. "MicroRNA 223-dependent expression of LMO2 regulates normal erythropoiesis." Haematologica 94, no. 4 (April 1, 2009): 479–86. http://dx.doi.org/10.3324/haematol.2008.002345.

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Lu, Han, Rachel J. Buchan, and Stuart A. Cook. "MicroRNA-223 regulates Glut4 expression and cardiomyocyte glucose metabolism." Cardiovascular Research 86, no. 3 (January 15, 2010): 410–20. http://dx.doi.org/10.1093/cvr/cvq010.

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Wen, Dezhong, Ping Qiao, and Li Wang. "Circulating microRNA-223 as a potential biomarker for obesity." Obesity Research & Clinical Practice 9, no. 4 (July 2015): 398–404. http://dx.doi.org/10.1016/j.orcp.2015.01.006.

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Wu, Li Hui, Qian Qian Cai, Yi Wei Dong, Rong Wang, Bao Mei He, Bing Qi, Chang Jun Xu, and Xing Zhong Wu. "Decoy Oligonucleotide Rescues IGF1R Expression from MicroRNA-223 Suppression." PLoS ONE 8, no. 12 (December 4, 2013): e82167. http://dx.doi.org/10.1371/journal.pone.0082167.

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Chen, Shih-Yao. "MicroRNA-223: a double-edged sword in rheumatoid arthritis." Rheumatology International 34, no. 2 (March 21, 2013): 285–86. http://dx.doi.org/10.1007/s00296-013-2720-5.

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Sugatani, T., and K. A. Hruska. "MicroRNA-223 is a key factor in osteoclast differentiation." Journal of Cellular Biochemistry 101, no. 4 (2007): 996–99. http://dx.doi.org/10.1002/jcb.21335.

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Brovkina, A. F., and N. D. Tsybikova. "MicroRNA - biomarker of aggressiveness of choroidal melanoma." Russian Ophthalmological Journal 15, no. 1 (March 25, 2022): 7–12. http://dx.doi.org/10.21516/2072-0076-2022-15-1-7-12.

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Almost 50 % of microRNAs (a family of small noncoding RNAs) are associated with the regions of the genome responsible for the development of tumors. These microRNAs play the role of oncogenes or tumor suppressor genes. In 2008, there were reports of the possibility of using microRNA as a predictive biomarker of the metastatic risk of uveal melanoma. Initially, microRNAs were investigated in melanoma samples; later, the possibility of using blood plasma for these purposes was shown.Purpose: to study the character of expression of miRNA- 146a, miRNA-155, miRNA-223, miRNA-126, miRNA-27b in the blood plasma of patients with choroidal melanoma (CM) and determine their significance in predicting possible hematogenous metastases. Material and methods. The study included 84 patients with CM aged 35–86 (ave 63.4 ± 1.2 yrs). The thickness of the CM varied in the range of 0.77–17.19 mm (ave 7.21 ± 0.43 mm). The control group consisted of 28 volunteers aged 45-78 (62.90 ± 1.42 yrs). MicroRNA expression levels were determined by quantitative PCR.Results. An increase in the expression level of miRNA-155, miRNA-146a, miRNA-126, miRNA-223, and miRNA-27b in blood plasma in all 84 patients with CM was revealed.Conclusion. The study of miRNA levels (miRNA-146, miRNA-155, miRNA-223, miRNA-126 and miRNA-27b) in the blood plasma of patients with CM can be used both to confirm the diagnosis of CM in difficult diagnostic cases and to determine the aggressiveness of the course tumor and prediction of metastasis.

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Anto Pulikkan, John, Viola Dengler, Philomina Sona Peramangalam, Abdul A. Peer Zada, Carsten Müller tidow, Stefan K. Bohlander, Daniel G. Tenen, and Gerhard Behre. "The Interplay Between Microrna-223 and E2F1 Regulates Cell Cycle Control During Granulopoiesis." Blood 114, no. 22 (November 20, 2009): 255. http://dx.doi.org/10.1182/blood.v114.22.255.255.

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Abstract Abstract 255 Transcription factor CCAAT enhancer binding protein α (C/EBPα) functions as a master regulator of granulocyte development by co-ordinating cell cycle inhibition and differentiation. Recent findings demonstrate that deregulation of C/EBPα is a critical step in the development of acute myeloid leukemia (AML). Inhibition of E2F1, the key regulator of cell cycle progression by C/EBPα is essential for granulopoiesis and disruption of this function of C/EBPα leads to leukemia. The mechanism with which C/EBPα inhibits E2F1 in granulopoiesis is poorly understood. Recent advances in our understanding about microRNAs suggest that these molecules have profound impact in gene expression programmes. Also, deregulation of microRNAs has been shown as a hall mark of many cancers including leukemia. microRNA-223 (miR-223) is upregulated by C/EBPα during granulopoiesis. The pivotal role of miR-223 in granulopoiesis is shown by the finding that mice deficient for miR-223 display defects in granulopoiesis. In this study, we explored the role of miR-223 in the cell cycle inhibition function of C/EBPα. Computational analysis by using programmes such as Target Scan suggests that E2F1 is a putative target of miR-223. Luciferase assays using 3'UTR of E2F1 suggest E2F1 is a potential target of miR-223. Western blot analysis using bone marrow cells isolated from miR-223 null mice shows accumulation of E2F1 protein levels. Interestingly, E2F1 protein levels were downregulated during miR-223 overexpression in myeloid cells. Analysis of miR-223 by quantitative Real-Time RT-PCR in AML patient samples shows that miR-223 is downregulated in different subtypes of AML. Proliferation assays, cell cycle analysis and BrdU assays show that miR-223 functions as an inhibitor of myeloid cell cycle progression. Several studies have reported the ability of E2F1 to block granulocytic differentiation. We next analysed whether E2F1 is inhibiting myeloid differentiation through miR-223. Promoter assays show that E2F1 inhibits the miR-223 promoter activity. By using Chromatin immunoprecipitation assays, we found that E2F1 binds to miR-223 promoter in leukemia derived cell lines and this binding is reversed during granulocytic differentiation. We also observed that E2F1 is bound to the miR-223 promoter in blast cells isolated from AML patients as analysed by chromatin immunoprecipitation assays. In addition, we show that overexpression of E2F1 leads to down regulation of miR-223 levels in myeloid cells. All these data suggest that E2F1 functions as a transcriptional repressor of the miR-223 gene. Taken together, our data suggest that granulopoiesis is regulated by the interplay between miR-223 and E2F1 and deregulation of this interplay may lead to the development of AML. Overexpression of miR-223 could be a potential strategy in the treatment of AML patients in which E2F1 inhibition by C/EBPα is deregulated. Disclosures: No relevant conflicts of interest to declare.

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Ariyachet, Chaiyaboot, Nattaya Chuaypen, Pornchai Kaewsapsak, Naphat Chantaravisoot, Depicha Jindatip, Saranyapin Potikanond, and Pisit Tangkijvanich. "MicroRNA-223 Suppresses Human Hepatic Stellate Cell Activation Partly via Regulating the Actin Cytoskeleton and Alleviates Fibrosis in Organoid Models of Liver Injury." International Journal of Molecular Sciences 23, no. 16 (August 19, 2022): 9380. http://dx.doi.org/10.3390/ijms23169380.

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MicroRNAs (miRNAs) are small, non-coding RNAs that negatively regulate target mRNA expression, and altered expression of miRNAs is associated with liver pathological conditions. Recent studies in animal models have shown neutrophil/myeloid-specific microRNA-223 (miR-223) as a key regulator in the development of various liver diseases including fibrosis, where hepatic stellate cells (HSCs) are the key player in pathogenesis. However, the precise roles of miR-223 in human HSCs and its therapeutic potential to control fibrosis remain largely unexplored. Using primary human HSCs, we demonstrated that miR-223 suppressed the fibrogenic program and cellular proliferation while promoting features of quiescent HSCs including lipid re-accumulation and retinol storage. Furthermore, induction of miR-223 in HSCs decreased cellular motility and contraction. Mechanistically, miR-223 negatively regulated expression of smooth muscle α-actin (α-SMA) and thus reduced cytoskeletal activity, which is known to promote amplification of fibrogenic signals. Restoration of α-SMA in miR-223-overexpressing HSCs alleviated the antifibrotic effects of miR-223. Finally, to explore the therapeutic potential of miR-233 in liver fibrosis, we generated co-cultured organoids of HSCs with Huh7 hepatoma cells and challenged them with acetaminophen (APAP) or palmitic acid (PA) to induce hepatotoxicity. We showed that ectopic expression of miR-223 in HSCs attenuated fibrogenesis in the two human organoid models of liver injury, suggesting its potential application in antifibrotic therapy.

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Cheng, Zhouyang, Yang Cao, Qingfeng Ni, and Jun Qin. "miR-223 Promotes Proliferation of Colon Cancer Cells by Down-Regulating Bcl-2-Like Protein 11 (BIM) Expression." Journal of Biomaterials and Tissue Engineering 9, no. 10 (December 1, 2019): 1424–28. http://dx.doi.org/10.1166/jbt.2019.2161.

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Colorectal cancer is one of malignant tumors. microRNA plays an important role in various diseases. In this study, we evaluated miR-223's effect on the proliferation of colon cancer cells. Protein and RNA expression levels in patients with clinical colorectal cancer were determined by western blot and real-time quantitative PCR respectively. In addition, the mechanism of miR-223 action was explored by combining transfection methods in cell lines. Colon cancer tissues showed significantly elevated miR-223 expression compared with adjacent tissues. Meanwhile, FOXO3a and BIM protein levels were significantly lower in cancer tissues compared to adjacent tissues. In colon cancer cell lines, knockdown of miR-223 increased cell proliferation and decreased BIM expression. The luciferase reporter gene showed that miR-223 down-regulates BIM expression through targeting FOXO3a. In colon cancer cells, miR-223 can down-regulate BIM expression through FOXO3a, thereby promoting the proliferation of colon cancer cells, indicating that targeting miR-223-regulated FOXO3a pathway might lead to the development of a number of drugs, and it is feasible to have a purpose to regulate the behavior of malignant cells.

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Vu, Ly P., Xinyang Zhao, Fabiana Perna, and Stephen D. Nimer. "Downregulation of Protein Arginine Methyltransferase – 4 (PRMT4) Promotes MiR-223 Expression and Myeloid Differentiation." Blood 116, no. 21 (November 19, 2010): 3632. http://dx.doi.org/10.1182/blood.v116.21.3632.3632.

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Abstract Abstract 3632 Protein arginine methyltransferase 4 is a Type I member of PRMT family, that catalyses the addition of a methyl-group to arginine residues of a wide range of proteins, including histones, transcription factors, and RNA binding proteins. PRMT4 has been shown to regulate gene expression through its interaction with various transcription factors and via methylation of numerous substrates. Although PRMT4 has been reported to play an important role in T cell development, lung development and adipocyte differentiation in mouse models, the function of PRMT4 during hematopoiesis has not been studied. To investigate the function of PRMT4 in the hematopoietic system, we utilized human CD34+ haematopoietic stem/progenitor cells (HSPCs). We observed that PRMT4 protein level is markedly downregulated during the myeloid differentiation of CD34+ cells without a significant change in the mRNA level. We then utilized a loss of function approach, using short hairpin RNAs, and found that knockdown of PRMT4 leads to an acceleration of myeloid differentiation, with a concomitant loss of the clonogenic potential of the cells. Interestingly, knocking down PRMT4 results in upregulation of miR-223, a myeloid specific microRNA. We also found that, during the myeloid differentiation of CD34+ cells, miR-223 expression steadily increased. Using a microRNA target prediction program, we identified a binding site for miR-223 in the 3′-UTR region of PRMT4 and found that when we over-expressed miR-223 in CD34+ cells, PRMT4 protein expression decreased. To determine the importance of PRMT4 downregulation in myeloid differentiation, we expressed the PRMT4-ORF (that should not be regulated by microRNAs) in CD34+ cells. The forced expression of PRMT4, that lacks the 3′-UTR region, leads to a block in myeloid differentiation and the inability of cells to up-regulate miR-223 during differentiation. Taken together, these data indicate a regulatory loop between PRMT4 and miR-223 that controls the differentiation of CD34+ toward the myeloid lineage. To examine how PRMT4 regulates transcription of miR-223, we examined the miR-223 locus and found a RUNX1 binding site in the promoter of pri-miR-223. We discovered that PRMT4 interacts with RUNX1 and methylates RUNX1 at a specific arginine residue. This results in the recruitment of several novel interacting partners, which appear to control the expression of miR-223. Thus our results indicate that PRMT4 regulate the transcription of miR-223 transcription via its effects on RUNX1. Our study demonstrates a novel function of PRMT4 in myeloid differentiation, through regulation of RUNX1 function and miR-223 expression. Disclosures: No relevant conflicts of interest to declare.

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Cheng, Naixuan, Chang Liu, Yulin Li, Shijuan Gao, Ying-Chun Han, Xiaonan Wang, Jie Du, and Congcong Zhang. "MicroRNA-223-3p promotes skeletal muscle regeneration by regulating inflammation in mice." Journal of Biological Chemistry 295, no. 30 (June 3, 2020): 10212–23. http://dx.doi.org/10.1074/jbc.ra119.012263.

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After injury, the coordinated balance of pro- and anti-inflammatory factors in the microenvironment contribute to skeletal muscle regeneration. However, the underlying molecular mechanisms regulating this balance remain incompletely understood. In this study, we examined the roles of microRNAs (miRNAs) in inflammation and muscle regeneration. miRNA-Seq transcriptome analysis of mouse skeletal muscle revealed that miR-223-3p is upregulated in the early stage of muscle regeneration after injury. miR-223-3p knockout resulted in increased inflammation, impaired muscle regeneration, and increased interstitial fibrosis. Mechanistically, we found that myeloid-derived miR-223-3p suppresses the target gene interleukin-6 (Il6), associated with the maintenance of the proinflammatory macrophage phenotype during injury. Administration of IL-6-neutralizing antibody in miR-223-3p-knockout muscle could rescue the impaired regeneration ability and reduce the fibrosis. Together, our results reveal that miR-223-3p improves muscle regeneration by regulating inflammation, indicating that miRNAs can participate in skeletal muscle regeneration by controlling the balance of pro- and anti-inflammatory factors in the skeletal muscle microenvironment.

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Xie, Yong, Lihai Zhang, Yanpan Gao, Wei Ge, and Peifu Tang. "The Multiple Roles of Microrna-223 in Regulating Bone Metabolism." Molecules 20, no. 10 (October 23, 2015): 19433–48. http://dx.doi.org/10.3390/molecules201019433.

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Morquette, Barbara, Camille A. Juźwik, Sienna S. Drake, Marc Charabati, Yang Zhang, Marc-André Lécuyer, Dylan A. Galloway, et al. "MicroRNA-223 protects neurons from degeneration in experimental autoimmune encephalomyelitis." Brain 142, no. 10 (August 14, 2019): 2979–95. http://dx.doi.org/10.1093/brain/awz245.

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Dysregulation of miRNAs has been observed in many neurodegenerative diseases, including multiple sclerosis. Morquette et al. show that overexpression of miR-223-3p prevents accumulation of axonal damage in a rodent model of multiple sclerosis, in part through regulation of glutamate receptor signalling. Manipulation of miRNA levels may have therapeutic potential.

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Li, Sufang, Hong Chen, Jingyi Ren, Qiang Geng, Junxian Song, Chongyou Lee, Chengfu Cao, Jing Zhang, and Ning Xu. "MicroRNA-223 inhibits tissue factor expression in vascular endothelial cells." Atherosclerosis 237, no. 2 (December 2014): 514–20. http://dx.doi.org/10.1016/j.atherosclerosis.2014.09.033.

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Mi, Qing-Sheng, Ying-Ping Xu, He Wang, Rui-Qun Qi, Zheng Dong, and Li Zhou. "Deletion of microRNA miR-223 increases Langerhans cell cross-presentation." International Journal of Biochemistry & Cell Biology 45, no. 2 (February 2013): 395–400. http://dx.doi.org/10.1016/j.biocel.2012.11.004.

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Zhang, Duo, Heedoo Lee, Xiaoyun Wang, Michael Groot, Lokesh Sharma, Charles S. Dela Cruz, and Yang Jin. "A potential role of microvesicle-containing miR-223/142 in lung inflammation." Thorax 74, no. 9 (July 22, 2019): 865–74. http://dx.doi.org/10.1136/thoraxjnl-2018-212994.

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BackgroundUncontrolled lung inflammation is one of the prominent features in the pathogenesis of lung infection- associated acute lung injury (ALI). Microvesicles (MVs) are extracellular nanovesicles that are generated via direct membrane budding.MethodsBronchoalveolar lavage fluid (BALF) samples were collected from mice with or without intratracheal lipopolysaccharide (LPS) instillation. BALF MVs were characterised and MV-containing microRNA (miRNA) profiles were assessed and confirmed. Secretion and function of MV-containing miR-223/142 (MV-miR-223/142) were analysed in vivo.ResultsIn BALF, MVs are mainly derived from macrophages in response to LPS. After intratracheal instillation (i.t.) of LPS or Klebsiella pneumoniae, MV-containing miR-223/142 are dramatically induced in both BALF and serum. Mechanistically, miRNA 3′ end uridylation mediates the packing of miR-223/142 into MVs. To investigate the functional role of MV-miR-223/142, we loaded miR-223/142 mimics into unstimulated MVs and delivered them into the murine lungs via i.t. The miR-223/142 mimics-enriched MVs selectively targeted lung macrophages and suppressed the inflammatory lung responses that were triggered by LPS or K. pneumoniae. Mechanistically, miR-223 and miR-142 synergistically suppress Nlrp3 inflammasome activation in macrophages via inhibition of Nlrp3 and Asc, respectively.ConclusionsIn the pathogenesis of lung macrophage-mediated inflammatory responses, MV-miR-223/142 secretion is robustly enhanced and detectable in BALF and serum. Furthermore, restoration of intracellular miR-223/142 via vesicle-mediated delivery suppresses macrophage activation and lung inflammation via inhibition of Nlrp3 inflammasome activation.

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Nuckel, Holger, Crista Ochsenfarth, Ludger Sellmann, Jan Duerig, Ulrich Duehrsen, and Ulrich Frey. "A New MicroRNA Risk Model for Prediction of Clinical Outcome In Chronic Lymphocytic Leukemia." Blood 116, no. 21 (November 19, 2010): 3592. http://dx.doi.org/10.1182/blood.v116.21.3592.3592.

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Abstract Abstract 3592 Introduction: Increasing experimental evidence supports the idea of aberrant microRNA (miRNA) expression in cancer pathogenesis, especially in chronic lymphocytic leukemia (CLL). Recently, aberrant expression of miR-29c and miR-223 has been associated with CLL outcome. Moreover, low expression of miR-34a in CLL is associated with p53 inactivation and also chemotherapy-refractory disease. Therefore, we investigated miR-29c, miR-223 and miR-34a expression in a large representative cohort of 110 CLL patients in order to assess the role of these miRNAs in risk prediction in B-CLL. Methods: Mononuclear cells of B-CLL were isolated from whole blood by centrifugation on a Ficoll/Hypaque gradient and cryopreserved in liquid nitrogen. MicroRNA was extracted from native liquid-nitrogen frozen cells using the QIAGEN miRNeasy® mini kit (Qiagen, Hilden, Germany). The relative expression of mature miRNAs was quantified using the TaqMan MicroRNA RT kit and TaqMan® MicroRNA Assays (Applied Biosystems, Foster City, California) on the ABI 7500 Real Time PCR System (Applied Biosystems, Foster City, California). RNU6B was used as internal control. The relative expression of each microRNA of interest to RNU6B was calculated using the formula miRNA of interest/RNU6B=2-deltaCt(miRNA-RNU6B). Result: The impact of the three miRNA expressions on treatment-free survival (TFS) and overall survival (OS) was assessed by performing “Receiver Operating Characteristics” (ROC) curve analysis. Patients with low miR-29c, miR-223 or miR-34a expression had a shorter TFS and OS than those patients with high expression: miR-29c: TFS 49 vs 91 months (p=0.081); OS 164 months vs not reached (p=0.093) miR-223: TFS 27 vs 84 months (p=0.035); OS 132 months vs not reached (p=0.001) miR-34a: TFS 46 vs 83 months (p=0.084); OS 132 months vs not reached (p=0.001) Furthermore, we investigated whether combining information on the expression of miRNAs could help refine the prognostic information provided by either of the three risk factors (RF) alone. Adding the number of risk factors this approach allowed for highly significant separation of our patient cohort into four subgroups, which differed significantly with regard to their clinical outcome. TFS: 0 RF 99 months; 1 RF 75 months; 2 RF 26 months; 3 RF 22 months (p=0.008) OS: 0 RF not reached; 1 RF not reached; 2 RF 164 months; 3 RF 132 months (p<0.0001) Moreover, in multivariate analysis the miRNA risk model was a significant independent prognostic factor (HR 1.3; 95%CI 1.0–1.8; p=0.04) next to the stage of Binet (HR 2.1; 95%CI 1.4–3.4; p=0.001) and ZAP-70 status (HR 3.0; 95%CI 1.5–5.9; p=0.002). Conclusion: Combined analysis of miR-29c, miR-223 and miR-34a expression in a risk model may help optimize currently available prognostic instruments. Future studies are warranted to elucidate the role of miRNAs as a prognostic factor for response and clinical outcome. Disclosures: No relevant conflicts of interest to declare.

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Journal articles on the topic 'MicroRNA-223'

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