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Relevant bibliographies by topics / MicroRNA-223

Academic literature on the topic 'MicroRNA-223'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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Journal articles on the topic "MicroRNA-223"

1

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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Dissertations / Theses on the topic "MicroRNA-223"

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Gökeri, Cengiz [Verfasser]. "MicroRNA-223-mediated neutrophilic inflammation in Community Acquired Pneumonia / Cengiz Gökeri." Berlin : Freie Universität Berlin, 2019. http://d-nb.info/1199344052/34.

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Şen, Erkan [Verfasser], Inge [Gutachter] Bauer, and Payam [Gutachter] Akhyari. "Einfluss von Ischämie und ischämischer Präkonditionierung auf die Expression der microRNA-223 im Myokard der Ratte und Interaktion der microRNA-223 mit dem potentiellen Zielprotein PMCA1 / Erkan Sen ; Gutachter: Inge Bauer, Payam Akhyari." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/1148066780/34.

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Meng, Cong. "microRNA-223 Regulates Macrophage Polarization and Diet-induced Insulin Resistance." Thesis, 2013. http://hdl.handle.net/1969.1/149464.

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Macrophage activation plays a crucial role in regulating adipose tissue inflammation and is a major contributor to the pathogenesis of obesity-associated cardiovascular diseases. On various types of stimuli, macrophages respond with either classic (M1) or alternative (M2) activation. M1- and M2-mediated signaling pathways and corresponding cytokine production profiles are not completely understood. The discovery of microRNAs provides a new opportunity to understand this complicated but crucial network for macrophage activation and adipose tissue function. We have examined the activity of microRNA-223 (miR-223) and its role in controlling macrophage functions in adipose tissue inflammation and systemic insulinresistance. miR-223-/- mice on a high-fat diet exhibited an increased severity of systemic insulin resistance compared with wild-type mice that was accompanied by a marked increase in adipose tissue inflammation. The specific regulatory effects of miR-223 in myeloid cell-mediated regulation of adipose tissue inflammation and insulin resistance were then confirmed by transplantation analysis. Moreover, using bone marrow-derived macrophages, we demonstrated that miR-223 is a novel regulator of macrophage polarization, which suppresses classic pro-inflammatory pathways and enhances the alternative anti-inflammatory responses. In addition, we identified Pknox1 as a genuine miR-223 target gene and an essential regulator for macrophage polarization. For the first time, this study demonstrates that miR-223 acts to inhibit Pknox 1,suppressing pro-inflammatory activation of macrophages; thus, it is a crucial regulator of macrophage polarization and protects against diet-induced adipose tissue inflammatory response and systemic insulin resistance.

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Yun-ChiaoDing and 丁云喬. "Role of microRNA-223 and its regulation in rheumatoid arthritis." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/nz8z39.

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Zhang, Bihong. "T Regulatory Cells in Early Pregnancy in Mice." Thesis, 2017. http://hdl.handle.net/2440/117928.

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To accommodate the semi-allogeneic fetus, a state of maternal immune tolerance to paternally-derived conceptus alloantigens is required. Tolerance is initially established when the same antigens are contacted following seminal fluid exposure, and increases in tolerogenic CD4+Foxp3+ T regulatory (Treg) cells are elicited. Clinical studies demonstrate the importance of seminal fluid contact in human pregnancy, where pathologies of pregnancy including preeclampsia are more likely with a short period of sexual cohabitation. Despite the pivotal role of Treg cells in pregnancy, the factors which regulate their response are yet to be fully understood. In this thesis, we describe experiments using mouse models that investigate regulators of the Treg cell pool and their impact on pregnancy success. Initially, we examined the contribution of number of seminal fluid exposures to Treg cell generation. Our data demonstrate that repeated exposure to the same male alloantigens strengthens the Treg cell pool, and increases its stability. These changes were not observed after repeated mating to syngeneic males or following switching from syngeneic to allogeneic partners. Changes to the Treg cell population was also linked with greater resistance to inflammatory challenge in mid-gestation. These findings may provide a mechanistic explanation for clinical observations linking long-term seminal fluid exposure in women with improved outcomes of pregnancy. We then assessed the contribution of a number of key immune regulatory factors on the female Treg cell response in early pregnancy. Prominent among the tolerance-inducing cytokines is IL10, which protects against fetal loss and alters key immune cells in early gestation including Treg cells. In this study we demonstrate that maternal as opposed to fetal IL10 deficiency causes increases susceptibility to fetal loss following inflammatory challenge in mid-gestation. The transcriptome of Treg cells is altered in IL10 deficiency with increased Ctse (cathepsin E), Il1r1, Il12rb2 and Ifng. These findings highlight the pivotal contribution of maternal IL10 in facilitating robust Treg cell generation and immune protection of the fetus from inflammatory challenge. Recent studies demonstrate that microRNAs (miRNA) also play a role in Treg cell generation. miR-155 and miR-223 are both regulated by seminal fluid following coitus and are postulated to play important roles in the peri-conception immune environment. Using mir-155 null mutant mice, we demonstrate that miR-155 deficiency substantially alters the local Treg cell and antigen presenting cell populations after mating. Using mir-223 null mice, we demonstrate that miR-223 also contributes to the peri-conception immune environment with alterations to the Treg cell and antigen presenting cell populations after mating. Furthermore, deficiency in either miR-155 or miR-223 increases susceptibility to fetal loss following pro-inflammatory challenge in mid-gestation. These findings indicate that both miR-155 and miR-223 have pivotal roles in establishing the appropriate maternal immune environment during the peri-conception period, and in activating sufficient immune tolerance to protect against inflammatory challenge in later gestation. Collectively, these data build understanding of key factors contributing to Treg cell generation and function in the peri-conception environment. The findings may be beneficial in informing new approaches to diagnosis and treatment of human gestational disorders associated with immune dysregulation.
Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2018

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Lisi, Véronique. "Modélisation de réseaux d'interactions des microARN et analyse et validation expérimentale de leurs boucles minimales avec des facteurs de transcription." Thèse, 2012. http://hdl.handle.net/1866/10139.

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Les microARN (miARN) sont de petits ARN non-codants qui répriment la traduction de leurs gènes cibles par hybridation à leur ARN messager (ARNm). L'identification de cibles biologiquement actives de miARN est cruciale afin de mieux comprendre leurs rôles. Ce problème est cependant difficile parce que leurs sites ne sont définis que par sept nucléotides. Dans cette thèse je montre qu'il est possible de modéliser certains aspects des miARN afin d'identifier leurs cibles biologiquement actives à travers deux modélisations d'un aspect des miARN. La première modélisation s'intéresse aux aspects de la régulation des miARN par l'identification de boucles de régulation entre des miARN et des facteurs de transcription (FT). Cette modélisation a permis, notamment, d'identifier plus de 700 boucles de régulation miARN/FT, conservées entre l'humain et la souris. Les résultats de cette modélisation ont permis, en particulier, d'identifier deux boucles d'auto-régulation entre LMO2 et les miARN miR-223 et miR-363. Des expériences de transplantation de cellules souches hématopoïétiques et de progéniteurs hématopoïétiques ont ensuite permis d'assigner à ces deux miARN un rôle dans la détermination du destin cellulaire hématopoïétique. La deuxième modélisation s'intéresse directement aux interactions des miARN avec les ARNm afin de déterminer les cibles des miARN. Ces travaux ont permis la mise au point d'une méthode simple de prédiction de cibles de miARN dont les performances sont meilleures que les outils courant. Cette modélisation a aussi permis de mettre en lumière certaines conséquences insoupçonnées de l'effet des miARN, telle que la spécificité des cibles de miARN au contexte cellulaire et l'effet de saturation de certains ARNm par les miARN. Cette méthode peut également être utilisée pour identifier des ARNm dont la surexpression fait augmenter un autre ARNm par l'entremise de miARN partagés et dont les effets sur les ARNm non ciblés seraient minimaux.
microRNAs (miRNAs) are small non coding RNAs that repress the translation of their target genes by pairing to their messenger RNA (mRNA). The identification of miRNAs' biologically active targets is a difficult problem because their binding sites are defined by only seven nucleotides. In this thesis, I show that it is possible to model specific aspects of miRNAs to identify their biologically active targets through two modeling of each one aspect of miRNAs. The first modeling considers the miRNAs regulations through the identification of regulatory loops between miRNAs and transcription factors (TFs). Through this modeling, we identified over 700 miRNA/TF regulatory loops conserved between human and mouse. With the results of this modeling, we were able to identify, in particular, two regulatory loops between LMO2 and the miRNAs miR-223 and miR-363. Using hematopoietic stem cells and progenitor cells transplantation experiment we showed that miR-223 and miR-363 are involved in hematopoietic cell fate determination. The second modeling focuses directly on the interaction between miARN and messenger RNA (mRNA) to determine the miRNA targets. With this work, we developed a simple method for predicting miRNA targets that outperforms the current state of the art tool. This modeling also highlighted some unsuspected consequences of miRNA effects such as the cell context specificity and the saturation of mRNA targets by miRNA. This method can also be used to identify mRNAs whose overexpression increases the expression level of another mRNA through their shared miRNA and whose global effects on other genes are minimal.

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Conference papers on the topic "MicroRNA-223"

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Victoria, L., A. Shim, A. Gupta, N. Li, X. Yan, A. Wang, and J. L. Gomez. "Transcriptional Profiling of Airway Epithelial Cells Overexpressing MicroRNA-223-3p." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3232.

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Leuenberger, Caroline, Claudio Schuoler, Célia Mignan, Thomas Rechsteiner, Malcolm Kohler, Lars Huber, and Matthias Brock. "microRNA-223 suppresses histone deacetylase 2 in chronic obstructive pulmonary disease." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa2931.

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Shim, A., A. Gupta, and J. L. Gomez. "The MicroRNA miR-223-3p Induces Pro-Inflammatory Changes in the Airway Epithelium." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1060.

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Gomez, J. L., A. Chen, X. Yan, L. E. Cohn, and G. L. Chupp. "MicroRNA miR-223 Is Associated with Lung Function Impairment and TH17 Inflammation in Asthma." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2929.

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Kurashige, Junji, Masayuki Watanabe, Masaaki Iwatsuki, Yoshifumi Baba, and Hideo Baba. "Abstract 2306: Overexpression of microRNA-223 regulates the ubiquitin ligase FBXW7 in esophageal squamous cell carcinoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2306.

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Chen, Li, Xiuzhi Zhu, Ling Yao, and Zonghua Wang. "Abstract PS6-21: High expression of MicroRNA-223 indicates better prognosis in triple negative breast cancer." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps6-21.

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Hocevar, A., J. Pizem, M. Tomsic, and D. Glavac. "OP0136 Microrna-223-3p expression in affected skin of adult iga vasculitis correlates with the severity of skin involvement." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2250.

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Qing, Yu-Feng, Dan Zhu, Ting Yi, Jian-Xiong Zheng, Qin Xiong, and Quan-Bo Zhang. "THU0004 MICRORNA-223 NEGATIVELY REGULATE GOUTY INFLAMMATION BY TARGETING THE NLRP3 INFLAMMASOME WITHOUT INFLUENCING IL-37 AND TGF-î’1." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3450.

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Fukumoto, Ichiro, Akira Kurozumi, Yusuke Goto, Ryosuke Matsushita, Mayuko Kato, Rika Nishikawa, Shinichi Sakamoto, Tomohiko Ichikawa, and Naohiko Seki. "Abstract 1100: Targeting ITGA3/ITGB1 signaling by tumor-suppressive microRNA-223 inhibits cancer cell migration and invasion in prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1100.

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