Toxoplasma gondii Cyclophilin 18 Regulates the Proliferation and Migration of Murine Macrophages and Spleen Cells

ABSTRACT Toxoplasma gondii is an intracellular parasite that shows a unique capacity to infect a variety of cell types in warm-blooded animals. It can invade and survive well inside immune cells, such as macrophages, that disseminate the parasite around the body because of their migratory properties. The aim of the present study was to evaluate the role of T. gondii cyclophilin 18 (TgCyp18) in the proliferation and migration of macrophages and spleen cells (mainly T lymphocytes) in order to understand the effects of TgCyp18 on the dynamics of the infection. A high dose of TgCyp18 enhanced the proliferation of macrophages and spleen cells in a cysteine-cysteine chemokine receptor 5 (CCR5)-independent way. In contrast, TgCyp18 controlled the migration of macrophages and spleen cells in dose- and CCR5-dependent manners. Our data suggest that TgCyp18 recruits cells and enhances the growth of host cells at the site of infection for maintenance of the interaction between the parasite and host.

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Downregulated MiR-206 expression promotes the proliferation and migration of macrophages by regulating IL-17A/REG3A pathway

European Journal of Inflammation ◽

10.1177/2058739220917490 ◽

2020 ◽

Vol 18 ◽

pp. 205873922091749

Author(s):

Xuan Huang ◽

Fang Gong ◽

Zhixian Lu ◽

Jie Zhu ◽

Qun Yu

Keyword(s):

Pcr Analysis ◽

Chain Reaction ◽

Inflammatory Infiltration ◽

Interleukin 17A ◽

Polymerase Chain ◽

And Migration ◽

Cell Migration And Proliferation ◽

Migration Of Macrophages ◽

Proliferation And Migration

This study sought to investigate the role of miR-206 in polymyositis/dermatomyositis (PM/DM) development. Transwell and 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium inner salt (MTS) assay were performed to investigate cell migration and proliferation. Real-time polymerase chain reaction (PCR) analysis was used to determine the expression of miR-206, interleukin-17A (IL-17A), IL-17 receptor A (IL-17RA), and regenerating islet-derived protein 3-alpha (REG3A). Significantly, miR-206 mimics decreased macrophage migration and proliferation, while miR-206 inhibitors exhibited the opposite effects. Indeed, elevating IL-17RA levels resulted in increased REG3A expression, which was inhibited by IL-17RA siRNA. Besides, miR-206 mimics decreased IL-17A and REG3A expressions, but miR-206 inhibitors showed opposite effects. Moreover, miR-206 expression in PM/DM patients was significantly reduced compared with the healthy controls, while IL-17A and REG3A expressions substantially increased among PM/DM patients. These findings suggested that downregulation of miR-206 increased the migration and proliferation of macrophages via IL-17A/REG3A signaling pathway, which could promote the inflammatory infiltration in PM/DM.

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The Potential of Mesothelial Cells in Tissue Engineering and Regenerative Medicine Applications

The International Journal of Artificial Organs ◽

10.1177/039139880703000611 ◽

2007 ◽

Vol 30 (6) ◽

pp. 527-540 ◽

Cited By ~ 21

Author(s):

S.E. Herrick ◽

S.E. Mutsaers

Keyword(s):

Tissue Engineering ◽

Regenerative Medicine ◽

Progenitor Cells ◽

Adhesion Formation ◽

Cell Types ◽

Mesothelial Cells ◽

Formation Mechanisms ◽

And Migration ◽

Proliferation And Migration

Injury to the serosa through injurious agents such as radiation, surgery, infection and disease results in the loss of the protective surface mesothelium and often leads to fibrous adhesion formation. Mechanisms that increase the rate of mesothialisation are therefore actively being investigated in order to reduce the formation of adhesions. These include intraperitoneal delivery of cultured mesothelial cells as well as administration of factors that are known to increase mesothelial proliferation and migration. An exciting alternative that has only recently received attention, is the possible role of mesothelial progenitor cells in the repair and regeneration of denuded serosal areas. Accumulating evidence suggests that such a population exists and under certain conditions is able to form a number of defined cell types indicating a degree of plasticity. Such properties may explain the extensive use of mesothelial cells in various tissue engineering applications including the development of vascular conduits and peripheral nerve replacements. It is likely that with the rapid explosion in the fields of tissue engineering and regenerative medicine, a greater understanding of the potential of mesothelial progenitor cells to repair, replace and possibly regenerate damaged or defective tissue will be uncovered.

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Role of microenvironment on proliferation and migration of an SDHB silenced murine Pheochromocytoma cell line

Endocrine Abstracts ◽

10.1530/endoabs.49.ep93 ◽

2017 ◽

Author(s):

Serena Martinelli ◽

Vanessa D'Antongiovanni ◽

Susan Richter ◽

Letizia Canu ◽

Tonino Ercolino ◽

...

Keyword(s):

Cell Line ◽

Pheochromocytoma Cell ◽

And Migration ◽

Proliferation And Migration

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Exosomal miR-214-5p Released from Glioblastoma Cells Modulates Inflammatory Response of Microglia after Lipopolysaccharide Stimulation through Targeting CXCR5

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527317666181105112009 ◽

2019 ◽

Vol 18 (1) ◽

pp. 78-87 ◽

Cited By ~ 7

Author(s):

Jian-kai Yang ◽

Hong-jiang Liu ◽

Yuanyu Wang ◽

Chen Li ◽

Ji-peng Yang ◽

...

Keyword(s):

Inflammatory Response ◽

Critical Role ◽

Luciferase Reporter ◽

Clinical Prognosis ◽

Direct Target ◽

And Migration ◽

High Level ◽

Cxcr5 Expression ◽

Proliferation And Migration

Background and Objective: Exosomes communicate inter-cellularly and miRNAs play critical roles in this scenario. MiR-214-5p was implicated in multiple tumors with diverse functions uncovered. However, whether miR-214-5p is mechanistically involved in glioblastoma, especially via exosomal pathway, is still elusive. Here we sought to comprehensively address the critical role of exosomal miR-214-5p in glioblastoma (GBM) microenvironment.Methods:The relative expression of miR-214-5p was determined by real-time PCR. Cell viability and migration were measured by MTT and transwell chamber assays, respectively. The secretory cytokines were measured with ELISA kits. The regulatory effect of miR-214-5p on CXCR5 expression was interrogated by luciferase reporter assay. Protein level was analyzed by Western blot.Results:We demonstrated that miR-214-5p was aberrantly overexpressed in GBM and associated with poorer clinical prognosis. High level of miR-214-5p significantly contributed to cell proliferation and migration. GBM-derived exosomal miR-214-5p promoted inflammatory response in primary microglia upon lipopolysaccharide challenge. We further identified CXCR5 as the direct target of miR-214- 5p in this setting.Conclusion:Overexpression of miR-214-5p in GBM modulated the inflammatory response in microglia via exosomal transfer.

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Extracellular-Vesicle-Based Coatings Enhance Bioactivity of Titanium Implants—SurfEV

Nanomaterials ◽

10.3390/nano11061445 ◽

2021 ◽

Vol 11 (6) ◽

pp. 1445

Author(s):

Taisa Nogueira Pansani ◽

Thanh Huyen Phan ◽

Qingyu Lei ◽

Alexey Kondyurin ◽

Bill Kalionis ◽

...

Keyword(s):

Cell Proliferation ◽

Titanium Surface ◽

Wound Closure ◽

Cell Types ◽

Extracellular Vesicle ◽

Tissue Growth ◽

Titanium Implants ◽

The Body ◽

High Concentrations ◽

And Migration

Extracellular vesicles (EVs) are nanoparticles released by cells that contain a multitude of biomolecules, which act synergistically to signal multiple cell types. EVs are ideal candidates for promoting tissue growth and regeneration. The tissue regenerative potential of EVs raises the tantalizing possibility that immobilizing EVs on implant surfaces could potentially generate highly bioactive and cell-instructive surfaces that would enhance implant integration into the body. Such surfaces could address a critical limitation of current implants, which do not promote bone tissue formation or bond bone. Here, we developed bioactive titanium surface coatings (SurfEV) using two types of EVs: secreted by decidual mesenchymal stem cells (DEVs) and isolated from fermented papaya fluid (PEVs). For each EV type, we determined the size, morphology, and molecular composition. High concentrations of DEVs enhanced cell proliferation, wound closure, and migration distance of osteoblasts. In contrast, the cell proliferation and wound closure decreased with increasing concentration of PEVs. DEVs enhanced Ca/P deposition on the titanium surface, which suggests improvement in bone bonding ability of the implant (i.e., osteointegration). EVs also increased production of Ca and P by osteoblasts and promoted the deposition of mineral phase, which suggests EVs play key roles in cell mineralization. We also found that DEVs stimulated the secretion of secondary EVs observed by the presence of protruding structures on the cell membrane. We concluded that, by functionalizing implant surfaces with specialized EVs, we will be able to enhance implant osteointegration by improving hydroxyapatite formation directly at the surface and potentially circumvent aseptic loosening of implants.

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Syndecans and Pancreatic Ductal Adenocarcinoma

Biomolecules ◽

10.3390/biom11030349 ◽

2021 ◽

Vol 11 (3) ◽

pp. 349

Author(s):

Nausika Betriu ◽

Juan Bertran-Mas ◽

Anna Andreeva ◽

Carlos E. Semino

Keyword(s):

Extracellular Matrix ◽

Pancreatic Ductal Adenocarcinoma ◽

Cell Types ◽

Ductal Adenocarcinoma ◽

Physiological Processes ◽

Extracellular Matrix Components ◽

Detection And Diagnosis ◽

And Migration ◽

Early Detection And Diagnosis

Pancreatic Ductal Adenocarcinoma (PDAC) is a fatal disease with poor prognosis because patients rarely express symptoms in initial stages, which prevents early detection and diagnosis. Syndecans, a subfamily of proteoglycans, are involved in many physiological processes including cell proliferation, adhesion, and migration. Syndecans are physiologically found in many cell types and their interactions with other macromolecules enhance many pathways. In particular, extracellular matrix components, growth factors, and integrins collect the majority of syndecans associations acting as biochemical, physical, and mechanical transducers. Syndecans are transmembrane glycoproteins, but occasionally their extracellular domain can be released from the cell surface by the action of matrix metalloproteinases, converting them into soluble molecules that are capable of binding distant molecules such as extracellular matrix (ECM) components, growth factor receptors, and integrins from other cells. In this review, we explore the role of syndecans in tumorigenesis as well as their potential as therapeutic targets. Finally, this work reviews the contribution of syndecan-1 and syndecan-2 in PDAC progression and illustrates its potential to be targeted in future treatments for this devastating disease.

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Role of the endogenous obestatin/G-protein coupled receptor 39 (GPR39) system in the regulation of proliferation and migration of activated human pancreatic stellate cells

Pancreatology ◽

10.1016/j.pan.2018.05.317 ◽

2018 ◽

Vol 18 (4) ◽

pp. S118

Author(s):

Lara Estévez-Perez ◽

Saul Leal-lopez ◽

Agustin Sanchez-Temprano ◽

Begoña Otero-Alen ◽

Carlos Seoane-Mosteiro ◽

...

Keyword(s):

G Protein ◽

Stellate Cells ◽

Pancreatic Stellate Cells ◽

G Protein Coupled Receptor ◽

Regulation Of Proliferation ◽

And Migration ◽

G Protein Coupled ◽

Proliferation And Migration

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FAM196B promotes proliferation and migration via regulating epithelial-mesenchymal transition in esophageal cancer

Cancer Biomarkers ◽

10.3233/cbm-203023 ◽

2021 ◽

pp. 1-8

Author(s):

Haifeng Xia ◽

Fang Hu ◽

Liangbin Pan ◽

Chengcheng Xu ◽

Haitao Huang ◽

...

Keyword(s):

Esophageal Cancer ◽

Western Blot ◽

Cox Regression ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition ◽

Cox Regression Analysis ◽

Ec Cells ◽

And Migration ◽

Proliferation And Migration

BACKGROUND: EC (esophageal cancer) is a common cancer among people in the world. The molecular mechanism of FAM196B (family with sequence similarity 196 member B) in EC is still unclear. This article aimed to clarify the role of FAM196B in EC. METHODS: The expression of FAM196B in EC tissues was detected using qRT-PCR. The prognosis of FAM196B in EC patients was determined by log-rank kaplan-Meier survival analysis and Cox regression analysis. Furthermore, shRNA was used to knockdown the expression of FAM196B in EC cell lines. MTT, wound healing assays and western blot were used to determine the role of FAM196B in EC cells. RESULTS: In our research, we found that the expression of FAM196B was up-regulated in EC tissues. The increased expression of FAM196B was significantly correlated with differentiation, lymph node metastasis, stage, and poor survival. The proliferation and migration of EC cells were inhibited after FAM196B-shRNA transfection in vitro and vivo. The western blot result showed that FAM196B could regulate EMT. CONCLUSION: These results suggested that FAM196B severs as an oncogene and promotes cell proliferation and migration in EC. In addition, FAM196B may be a potential therapeutic target for EC patients.

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Paradoxical role of high mobility group box 1 in glioma: a suppressor or a promoter?

Oncology Reviews ◽

10.4081/oncol.2017.325 ◽

2017 ◽

Cited By ~ 14

Author(s):

Richard A. Seidu ◽

Min Wu ◽

Zhaoliang Su ◽

Huaxi Xu

Keyword(s):

Molecular Mechanisms ◽

High Mobility ◽

Treatment Resistance ◽

High Mobility Group ◽

Tissue Invasion ◽

Self Sufficiency ◽

Glycation End Products ◽

And Migration ◽

Proliferation And Migration

Gliomas represent 60% of primary intracranial brain tumors and 80% of all malignant types, with highest morbidity and mortality worldwide. Although glioma has been extensively studied, the molecular mechanisms underlying its pathology remain poorly understood. Clarification of the molecular mechanisms involved in their development and/or treatment resistance is highly required. High mobility group box 1 protein (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation and migration, through receptor for advanced glycation end products and toll like receptors in a number of cancers including gliomas. It is known that excessive release of HMGB1 in cancer leads to unlimited replicative potential, ability to develop blood vessels (angiogenesis), evasion of programmed cell death (apoptosis), self-sufficiency in growth signals, insensitivity to inhibitors of growth, inflammation, tissue invasion and metastasis. In this review we explore the mechanisms by which HMGB1 regulates apoptosis and autophagy in glioma. We also looked at how HMGB1 mediates glioma regression and promotes angiogenesis as well as possible signaling pathways with an attempt to provide potential therapeutic targets for the treatment of glioma.

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