scholarly journals EZH2-Inhibited MicroRNA-454-3p Promotes M2 Macrophage Polarization in Glioma

2020 ◽  
Vol 8 ◽  
Author(s):  
Bin Qi ◽  
Cheng Yang ◽  
Zhanpeng Zhu ◽  
Hao Chen
Keyword(s):  
Macrophage Polarization ◽  
Glioma Cells ◽  
Luciferase Reporter ◽  
Clinical Samples ◽  
M2 Macrophage ◽  
Incidence And Mortality ◽  
High Incidence ◽  
M2 Macrophage Polarization ◽  
Primary Intracranial Tumor

Glioma is a primary intracranial tumor with high incidence and mortality. The oncogenic role of EZH2 has been reported in glioma. EZH2 inhibited microRNA-454-3p (miR-454-3p) by binding to its promoter in chondrosarcoma cells. Therefore, our study aimed to identify whether EZH2 regulated M2 macrophage polarization in glioma via miR-454-3p. Clinical samples of different grades of glioma and glioma cells were collected and immunohistochemistry and RT-qPCR demonstrated that EZH2 was highly expressed in glioma tissues. Expression of EZH2 was positively correlated with the degree of M2 macrophage polarization in glioma tissues. EZH2 was silenced by lentivirus in glioma cells, which were subsequently co-cultured with macrophages to evaluate its effect on macrophage polarization. miR-454-3p, a down-regulated miR in glioma, was found to be increased after silencing of EZH2. Furthermore, MethPrimer analysis showed that EZH2 silencing inhibited the DNA methylation level of miR-454-3p. Additionally, MS-PCR, dual-luciferase reporter, RIP and RNA pull down assays revealed that miR-454-3p promoted PTEN expression by inhibiting m6A modification through binding to the enzyme YTHDF2. Either inhibition of miR-454-3p or PTEN resulted in promotion of M2 macrophage polarization. Collectively, histone methyltransferase EZH2 inhibited miR-454-3p through methylation modification and promoted m6A modification of PTEN to induce glioma M2 macrophage polarization.

scholarly journals MiR-6869-5p Induces M2 Polarization by Regulating PTPRO in Gestational Diabetes Mellitus

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Pingping Wang ◽  
Zhenzhi Ma ◽  
Zengyan Wang ◽  
Ximei Wang ◽  
Guifeng Zhao ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Macrophage Polarization ◽  
Luciferase Reporter ◽  
M2 Macrophage ◽  
M2 Polarization ◽  
M2 Macrophage Polarization

The role of microRNA (miRNA) in gestational diabetes mellitus has been widely investigated during the last decade. However, the altering effect of miR-6869-5p on immunity and placental microenvironment in gestational diabetes mellitus is largely unknown. In our study, the expression of miR-6869-5p was documented to be significantly decreased in placenta-derived mononuclear macrophages, which was also negatively related to PTPRO. Besides, PTPRO was negatively regulated by miR-6869-5p in placenta-derived mononuclear macrophages. In vitro, miR-6869-5p inhibited macrophage proliferation demonstrated by EdU and CCK-8 experiments. The inflammatory response in macrophages was also significantly inhibited by miR-6869-5p, which could regulate PTPRO as a target documented by luciferase reporter assay. Moreover, miR-6869-5p promoted M2 macrophage polarization and thus restrain inflammation. Accordingly, miR-6869-5p is involved in maintaining placental microenvironment balance by preventing from inflammation and inducing M2 macrophages in gestational diabetes mellitus.

scholarly journals miR-657 Promotes Macrophage Polarization toward M1 by Targeting FAM46C in Gestational Diabetes Mellitus

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Pingping Wang ◽  
Zengfang Wang ◽  
Guojie Liu ◽  
Chengwen Jin ◽  
Quan Zhang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Macrophage Polarization ◽  
Vital Role ◽  
Luciferase Reporter ◽  
M2 Macrophage ◽  
And Migration

MicroRNA (miRNA) has been widely suggested to play a vital role of in the pathogenesis of gestational diabetes mellitus (GDM). We have previously demonstrated that miR-657 can regulate macrophage inflammatory response in GDM. However, the role of miR-657 on M1/M2 macrophage polarization in GDM pathogenesis is not clear yet. This study is aimed at elucidating this issue and identifying novel potential GDM therapeutic targets based on miRNA network. miR-657 is found to be upregulated in placental macrophages demonstrated by real-time PCR, which can enhance macrophage proliferation and migration in vitro. Luciferase reporter assay shows the evidence that FAM46C is a target of miR-657. In addition, miR-657 can promote macrophage polarization toward the M1 phenotype by downregulating FAM46C in macrophages. The present study strongly suggests miR-657 is involved in GDM pathogenesis by regulating macrophage proliferation, migration, and polarization via targeting FAM46C. miR-657/FAM46C may serve as promising targets for GDM diagnosis and treatment.

scholarly journals MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice

2021 ◽  
Vol 7 ◽  
Author(s):  
Jing Rui Qi ◽  
Dian Ru Zhao ◽  
Li Zhao ◽  
Fan Luo ◽  
Mei Yang
Keyword(s):  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Treatment Target ◽  
Vessel Disease ◽  
Novel Treatment ◽  
M1 Macrophage ◽  
Apolipoprotein E Knockout Mice ◽  
The World ◽  
M2 Macrophage Polarization

Atherosclerosis (AS), a kind of chronic inflammatory blood vessel disease, is a main cause of cardiovascular disease, which is a leading cause of mortality around the world. Accumulation of macrophages induced by inflammation contributes to AS development. It has been indicated that microRNAs (miRNAs) are involved in the process of AS. However, the pathway and gene miRNAs targeting are poorly understood. Here we reported that miR-520a-3p was increased in mice with AS and silencing of miR-520a-3p attenuated AS process. Furthermore, inhibition of miR-520a-3p increased the expression of α-SMA and collagen. In addition, miR-520a-3p silencing inhibited the expression of M1 macrophage polarization markers and pro-inflammatory genes and promoted the M2 macrophage polarization. What’s more, forced expression of miR-520a-3p diminished IL4/IL13 induced macrophage autophagy via targeting UVRAG. Collectively, our study reveals the role of miR-520a-3p in macrophage polarization and suggests the potential of miRNA as a novel treatment target of AS.

The role of M1 and M2 macrophage polarization in progression of medication-related osteonecrosis of the jaw

2020 ◽  
Author(s):  
Polytimi Paschalidi ◽  
Ioannis Gkouveris ◽  
Akrivoula Soundia ◽  
Evangelos Kalfarentzos ◽  
Emmanouil Vardas ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Osteonecrosis Of The Jaw ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization

Potential role of M2 macrophage polarization in ventilator-induced lung fibrosis

2019 ◽  
Vol 75 ◽  
pp. 105795
Author(s):  
Lu Wang ◽  
Yi Zhang ◽  
Nannan Zhang ◽  
Jingen Xia ◽  
Qingyuan Zhan ◽  
...  
Keyword(s):  
Lung Fibrosis ◽  
Potential Role ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization

scholarly journals Co-culture of Platelets with Monocytes Induced M2 Macrophage Polarization and Formation of Foam Cells: Shedding Light on the Crucial Role of Platelets in Monocyte Differentiation

2019 ◽  
Vol 36 (2) ◽  
pp. 97-105 ◽  
Author(s):  
Mahdeih Mehrpouri ◽  
Davood Bashash ◽  
Mohammad Hossein Mohammadi ◽  
Mohammad Esmail Gheydari ◽  
Esmaeil Shahabi Satlsar ◽  
...  
Keyword(s):  
Crucial Role ◽  
Macrophage Polarization ◽  
Foam Cells ◽  
M2 Macrophage ◽  
Monocyte Differentiation ◽  
M2 Macrophage Polarization

scholarly journals MiR-98-5p expression inhibits polarization of macrophages to an M2 phenotype by targeting Trib1 in inflammatory bowel disease

2020 ◽  
Author(s):  
Yunhua Peng ◽  
Qingyuan Wang ◽  
Wei Yang ◽  
Qiqi Yang ◽  
Ynani Pei ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Macrophage Polarization ◽  
Luciferase Reporter ◽  
Marker Genes ◽  
M2 Macrophage ◽  
M1 Macrophage ◽  
Inflammatory Bowel ◽  
M2 Macrophage Polarization ◽  
M2 Phenotype

Herein, we unfolded miR-98-5p mechanism in inflammatory bowel disease (IBD). IBD mouse model was established. The severity of colitis was assessed daily using the disease activity index (DAI). Murine peritoneal macrophages were stimulated by lipopolysaccharide (LPS). MiR-98-5p, tribbles homolog 1 (Trib1), M1 and M2 macrophage marker genes mRNA expression was analyzed. The relationship between miR-98-5p and Trib1 was explored using a luciferase reporter assay. The strategy of loss-of-function was used to explore the mechanism of miR-98-5p in macrophage polarization, inflammation and IBD. The results revealed that IBD mice had higher DAI index and miR-98-5p expression when compared to the Sham group. MiR-98-5p and Trib1 displayed a targeted regulation relationship. Knockdown of miR-98-5p transformed LPS-induced M1 macrophage polarization into M2 macrophage polarization and inhibited inflammation via up-regulating Trib1. However, shTrib1 reversed the effects. In vivo experiment, silencing of miR-98-5p, diminished the DAI and promoted M2 macrophage polarization. In conclusion, knockdown of miR-98-5p changed macrophage polarization to the M2 phenotype by increasing Trib1 expression, thereby alleviating IBD symptoms.

scholarly journals Glioblastoma cell-derived extracellular vesicle miR-27a-3p facilitates M2 macrophage polarization

2020 ◽  
Author(s):  
Guifang Zhao ◽  
Hongquan Yu ◽  
Lijuan Ding ◽  
Weiyao Wang ◽  
Huang Wang ◽  
...  
Keyword(s):  
Target Genes ◽  
Macrophage Polarization ◽  
Tissue Growth ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
M2 Macrophage ◽  
Glioblastoma Cell ◽  
Human Glioblastoma ◽  
Gene Assay ◽  
M2 Macrophage Polarization

Abstract Background: M2 macrophage polarization has been found to be correlated with malignancy of glioblastoma. In this study, we investigated the potential role of microRNA (miRNA) derived from extracellular vesicles of glioblastoma (glioblastoma-EVs) in M2 macrophage polarization.Methods: After isolation of human glioblastoma-EVs, transmission electron microscopy (TEM) and Nano-particle tracking analysis (NTA) were performed to identify the EVs. Besides, the proliferation, migration and invasion of glioma cells were analyzed by CCK8 and Transwell assays, respectively. The target genes of miR-27a-3p were predicted through bioinformatics analysis and verified by dual-luciferase reporter gene assay. ChIP assay was applied to detect the binding of enhancer of zeste homologue 1 (EZH1) to lysine-specific demethylase 3A (KDM3A) promoter region and the interaction between KDM3A and connective tissue growth factor (CTGF). Glioblastoma mouse models were established followed by the implement of hematoxylin-eosin (HE) and ELISA staining on pathological changes of mouse brain tissues.Results: Human glioblastoma-EVs were successfully isolated. The high expression of miR-27a-3p was found in glioblastoma tissues as well as glioblastoma-EVs, which could induce M2 polarization, thus promoting glioblastoma cell proliferation, migration and invasion. It was also shown that miR-27a-3p targeted EZH1 and promoted KDM3A expression to elevate the expression of CTGF. Glioblastoma-EVs delivered miR-27a-3p to promote the KDM3A-upregulated CTGF by downregulating EZH1, thereby promoting M2 macrophage polarization and development of glioblastoma in vivo.Conclusion: These findings highlight that EV miR-27a-3p may promote M2 macrophage polarization, which is associated with the progression of tumors.

scholarly journals Ablation of Galectin-12 Inhibits Atherosclerosis through Enhancement of M2 Macrophage Polarization

2020 ◽  
Vol 21 (15) ◽  
pp. 5511
Author(s):  
En-Shyh Lin ◽  
Yu-An Hsu ◽  
Ching-Yao Chang ◽  
Hui-Ju Lin ◽  
Chih Sheng Chen ◽  
...  
Keyword(s):  
Foam Cell ◽  
Macrophage Polarization ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Atp Binding ◽  
M2 Macrophage ◽  
Murine Macrophages ◽  
M2 Macrophage Polarization ◽  
Atp Binding Cassette

The formation of foam cells, which are macrophages that have engulfed oxidized low-density lipoprotein (OxLDL), constitutes the first stage in the development of atherosclerosis. Previously, we found that knocking down galectin-12, a negative regulator of lipolysis, leads to reduced secretion of monocyte chemoattractant protein-1 (MCP-1), a chemokine that plays an important role in atherosclerosis. This prompted us to study the role of galectin-12 in atherosclerosis. With that aim, we examined foam cell formation in Gal12‒/‒ murine macrophages exposed to OxLDL and acetylated LDL (AcLDL). Then, we generated an LDL receptor and galectin-12 double knockout (DKO) mice and studied the effect of galectin-12 on macrophage function and atherosclerosis. Lastly, we evaluated the role of galectin-12 in human THP-1 macrophages using a doxycycline-inducible conditional knockdown system. Galectin-12 knockout significantly inhibited foam cell formation in murine macrophages through the downregulation of cluster of differentiation 36 (CD36), and the upregulation of ATP Binding Cassette Subfamily A Member 1 (ABCA1), ATP Binding Cassette Subfamily G Member 1 (ABCG1), and scavenger receptor class B type 1 (SRB1). Consistent with this, galectin-12 knockdown inhibited foam cell formation in human macrophages. In addition, the ablation of galectin-12 promoted M2 macrophage polarization in human and murine macrophages as evidenced by the upregulation of the M2 marker genes, CD206 and CD163, and downregulation of the M1 cytokines, tumor necrosis factor α (TNF- α), interleukin-6 (IL-6), and MCP-1. Moreover, the ablation of galectin-12 decreased atherosclerosis formation in DKO mice. Based on these results, we propose galectin-12 as a potential therapeutic target for atherosclerosis.

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