GDF11 ameliorates severe acute pancreatitis through modulating macrophage M1 and M2 polarization by targeting the TGFβR1/SMAD-2 pathway

Duan, Feixiang; Wang, Xiaowu; Wang, Hongwei; Wang, Yongqiang; Zhang, Yan; Chen, Jiawei; Zhu, Xiandong; Chen, Bicheng

doi:10.1016/j.intimp.2022.108777

Cited by 25 publications

(8 citation statements)

References 40 publications

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“…To explore the mechanism of miR-3124-5p in regulating tumor metastasis and angiogenesis, we predicted the target genes of miR-3124-5p in CHOL by the TargetScan database. Among target genes, GDF11 has been shown to play a key role in diverse diseases, such as cardiovascular disease ( 20 ), acute pancreatitis ( 21 ), and colorectal cancer ( 22 ). However, the function of GDF11 in CHOL is largely unknown.…”

Section: Resultsmentioning

confidence: 99%

Exosome-transmitted miR-3124-5p promotes cholangiocarcinoma development via targeting GDF11

Gao

et al. 2022

Front. Oncol.

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ObjectiveCholangiocarcinoma (CHOL) is a deadly cancer worldwide with limited available therapies. The aim of this study was to investigate key exosomal miRNAs and their functions in CHOL development.MethodsSerum exosomes were isolated from patients with CHOL and healthy controls, followed by miRNA sequencing for identifying differentially expressed miRNAs (DEMs) and their functions. Then, the expression of key DEMs was experimentally validated in exosomes from clinical CHOL patients and CHOL cells. The effects of overexpression of key DEMs on CHOL cell migration and proliferation were investigated. A key exosomal DEM miR-3124-5p was identified. The effects of overexpression or knockdown of exosomal miR-3124-5p on the proliferation, migration, and angiogenesis of human umbilical vein endothelial cells (HUVECs) were investigated. Moreover, the function of exosomal miR-3124-5p on tumor growth in vivo was explored.ResultsA total of 632 exosomal DEMs were identified between CHOL and control samples. Target genes of DEMs were significantly enriched in pathways, such as the p53 signaling pathway. miR-3124-5p was upregulated in serum exosomes from CHOL patients and exosomes from CHOL cells, and overexpression of miR-3124-5p promoted RBE cell migration and viability. Moreover, overexpression of exosomal miR-3124-5p promoted the proliferation, migration, and angiogenesis of HUVECs, while knockdown of miR-3124-5p had the opposite effect. miR-3124-5p could target growth differentiation factor 11 (GDF11) and downregulate GDF11 expression. Furthermore, exosomal miR-3124-5p promoted tumor growth in vivo.ConclusionsOur findings revealed that exosome-encapsulated miR-3124-5p promoted the malignant progression of CHOL by targeting GDF11. Exosomal miR-3124-5p and GDF11 could be promising biomarkers or therapeutic targets for CHOL.

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Section: Resultsmentioning

confidence: 99%

Exosome-transmitted miR-3124-5p promotes cholangiocarcinoma development via targeting GDF11

Gao

et al. 2022

Front. Oncol.

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“…These results suggest that the GO coating may also have certain anti-inflammatory properties in addition to its nanomorphology and hydrophilicity. Previous studies have also shown that the polarization of macrophages may additionally depend on micro-environmental factors [42]. In a recent study, Han et al confirmed the regulatory effect of dispersed GO on macrophage polarization and showed that this material could be used for myocardial infarction repair [43].…”

Section: Discussionmentioning

confidence: 97%

Effect of graphene oxide loaded on TiO₂-nanotube-modified Ti on inflammatory responses

Cao,

Luo,

Wang

et al. 2024

Phys. Scr.

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Although a titanium matrix modified with titanium dioxide nanotube (TNT) arrays can have anti-inflammatory effects in vitro, these effects are limited. In this study, the TNT surface was modified by electrodepositing graphene oxide (GO) to enhance the anti-inflammatory effect of the material. Scanning electron microscopy (SEM), Raman spectroscopy, and X-ray diffraction were used to characterize each of these materials. Cell Counting Kit-8 (CCK-8) was used to determine the cell proliferation status. Enzyme-linked Immunosorbent Assay (ELISA), immunofluorescence staining, and RNA sequencing were used to assess the regulation of inflammation in each group. Raman spectroscopy confirmed that GO was successfully loaded onto the surface. The SEM, ELISA, fluorescence staining, and RNA sequencing results indicated that TNT-GO can effectively inhibit the inflammatory response and induce the M2 polarization of macrophages. TNT-GO can weaken the surface inflammatory responses of materials, suppress the secretion of pro-inflammatory factors, and promote the M2 polarization of macrophages. These advantageous properties render TNT-GO a promising material for dental implants.

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“…The activated Smad2/3 forms a heterodimer with Smad4 and enters the nucleus, where it can subsequently regulate the expression of M2 macrophage-related genes and facilitate the process of M2 macrophage polarization ( 32 ). Additionally, TGF-β can also promote M2 macrophage polarization through non-Smad pathways ( 33 ). In summary, TGF-β plays an important role in regulating M2 macrophage polarization and modulating immune responses.…”

Section: Regulation Of M2 Macrophage Polarizationmentioning

confidence: 99%

M2 macrophage polarization: a potential target in pain relief

Zhao,

Ma,

Deng

et al. 2023

Front. Immunol.

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Pain imposes a significant urden on patients, affecting them physically, psychologically, and economically. Despite numerous studies on the pathogenesis of pain, its clinical management remains suboptimal, leading to the under-treatment of many pain patients. Recently, research on the role of macrophages in pain processes has been increasing, offering potential for novel therapeutic approaches. Macrophages, being indispensable immune cells in the innate immune system, exhibit remarkable diversity and plasticity. However, the majority of research has primarily focused on the contributions of M1 macrophages in promoting pain. During the late stage of tissue damage or inflammatory invasion, M1 macrophages typically transition into M2 macrophages. In recent years, growing evidence has highlighted the role of M2 macrophages in pain relief. In this review, we summarize the mechanisms involved in M2 macrophage polarization and discuss their emerging roles in pain relief. Notably, M2 macrophages appear to be key players in multiple endogenous pathways that promote pain relief. We further analyze potential pathways through which M2 macrophages may alleviate pain.

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GDF11 ameliorates severe acute pancreatitis through modulating macrophage M1 and M2 polarization by targeting the TGFβR1/SMAD-2 pathway

Cited by 25 publications

References 40 publications

Exosome-transmitted miR-3124-5p promotes cholangiocarcinoma development via targeting GDF11

Exosome-transmitted miR-3124-5p promotes cholangiocarcinoma development via targeting GDF11

Effect of graphene oxide loaded on TiO₂-nanotube-modified Ti on inflammatory responses

M2 macrophage polarization: a potential target in pain relief

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GDF11 ameliorates severe acute pancreatitis through modulating macrophage M1 and M2 polarization by targeting the TGFβR1/SMAD-2 pathway

Cited by 25 publications

References 40 publications

Exosome-transmitted miR-3124-5p promotes cholangiocarcinoma development via targeting GDF11

Exosome-transmitted miR-3124-5p promotes cholangiocarcinoma development via targeting GDF11

Effect of graphene oxide loaded on TiO2-nanotube-modified Ti on inflammatory responses

M2 macrophage polarization: a potential target in pain relief

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Product

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Effect of graphene oxide loaded on TiO₂-nanotube-modified Ti on inflammatory responses