Neutrophil cell function and migration inhibition studies in Nigerian patients with tropical pyomyositis

Cold shock Y-box binding protein-1 (YB-1) coordinates several molecular processes between the nucleus and the cytoplasm and plays a crucial role in cell function. Moreover, it is involved in cancer progression, invasion, and metastasis. As trophoblast cells share similar characteristics with cancer cells, we hypothesized that YB-1 might also be necessary for trophoblast functionality. In samples of patients with intrauterine growth restriction, YB-1 mRNA levels were decreased, while they were increased in preeclampsia and unchanged in spontaneous abortions when compared to normal pregnant controls. Studies with overexpression and downregulation of YB-1 were performed to assess the key trophoblast processes in two trophoblast cell lines HTR8/SVneo and JEG3. Overexpression of YB-1 or exposure of trophoblast cells to recombinant YB-1 caused enhanced proliferation, while knockdown of YB-1 lead to proliferative disadvantage in JEG3 or HTR8/SVneo cells. The invasion and migration properties were affected at different degrees among the trophoblast cell lines. Trophoblast expression of genes mediating migration, invasion, apoptosis, and inflammation was altered upon YB-1 downregulation. Moreover, IL-6 secretion was excessively increased in HTR8/SVneo. Ultimately, YB-1 directly binds to NF-κB enhancer mark in HTR8/SVneo cells. Our data show that YB-1 protein is important for trophoblast cell functioning and, when downregulated, leads to trophoblast disadvantage that at least in part is mediated by NF-κB.

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MicroRNA‐33b replacement effect on growth and migration inhibition in ovarian cancer cells

Chemical Biology & Drug Design ◽

10.1111/cbdd.13964 ◽

2021 ◽

Author(s):

Jin Liu ◽

Weiming Wang ◽

Limin Chen ◽

Yachai Li ◽

Shuimiao Zhao ◽

...

Keyword(s):

Ovarian Cancer ◽

Cancer Cells ◽

Ovarian Cancer Cells ◽

Migration Inhibition ◽

And Migration ◽

Effect On Growth

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Requirement for T cells in the production of migration inhibitory factor.

Journal of Experimental Medicine ◽

10.1084/jem.142.5.1306 ◽

1975 ◽

Vol 142 (5) ◽

pp. 1306-1311 ◽

Cited By ~ 25

Author(s):

B R Bloom ◽

E Shevach

Keyword(s):

T Cells ◽

T Cell ◽

B Lymphocytes ◽

Cell Function ◽

Plaque Assay ◽

Quantitative Measure ◽

Immune Response Gene ◽

Migration Inhibition ◽

Qualitative Assay ◽

Gene Restriction

The question whether B lymphocytes are capable of being activated by antigen in the absence of functional T cells was investigated in a model that excludes participation of T cells by virtue of an immune response gene restriction. Strain 2 guinea pigs are capable of responding to immunization with DNP-PLL, whereas strain 13 animals are not. In the present experiments, animals of both strains were immunized with DNP-PLL complexed to ovalbumin (DNP-PLL-Ova) under conditions in which equal titers of antibodies to DNP were produced by both strains. The failure of T cells of strain 13 animals to respond to DNP-PLL was confirmed by the virus plaque assay. While spleen cells from both strains produced MIF after stimulation with DNP-PLL-Ova, in response to DNP-PLL only strain 2 spleens were able to produce MIF. Cells from neither strain could be activated by DNP-guinea pig albumin to produce MIF. We conclude that B lymphocytes are incapable of being stimulated by antigen in the absence of T cells, and that MIF production is a thymus-dependent response. While the results indicate that MIF production is a valid qualitative assay for T-cell competence, since MIF can be produced by B and T cells, the degree of migration inhibition cannot be regarded as a quantitative measure of T-cell function.

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Abstract 101: MiR-4260 Promotes the Proliferation, Migration, and Tube Formation of Human Umbilical Vein Endothelial Cells

Circulation Research ◽

10.1161/res.117.suppl_1.101 ◽

2015 ◽

Vol 117 (suppl_1) ◽

Author(s):

Qi Sun ◽

Dongcao Lv ◽

Qiulian Zhou ◽

Yihua Bei ◽

Junjie Xiao

Keyword(s):

Endothelial Cells ◽

Target Genes ◽

Cell Function ◽

Umbilical Vein ◽

Tube Formation ◽

Endothelial Cell Function ◽

Human Umbilical Vein ◽

And Migration ◽

Umbilical Vein Endothelial Cells

MicroRNAs (miRNAs, miRs), endogenous small non-coding RNA, have been shown to act as essential regulators in angiogenesis which plays important roles in improving blood flow and cardiac function following myocardial infarction. The current study investigated the potential of miR-4260 in endothelial cell function and angiogenesis using human umbilical vein endothelial cells (HUVEC). Our data demonstrated that overexpression of miR-4260 was associated with increased proliferation and migration of HUVEC using EdU incorporation assay (17.25%±1.31 vs 25.78%±1.24 in nc-mimics vs miR-4260 mimics, respectively) and wound healing assay, respectively. While downregulation of miR-4260 inhibited the proliferation (17.90%±1.37 vs 10.66%±1.41 in nc-inhibitor vs miR-4260 inhibitor, respectively) and migration of HUVEC. Furthermore, we found that miR-4260 mimics increased (129.75±3.68 vs 147±3.13 in nc-mimics vs miR-4260 mimics, respectively), while miR-4260 inhibitor decreased the tube formation of HUVECs in vitro (123.25±2.17 vs 92±4.45 in nc-inhibitor vs miR-4260 inhibitor expression, respectively). Our data indicate that miR-4260 contributes to the proliferation, migration and tube formation of endothelial cells, and might be essential regulators for angiogenesis. Further study is needed to investigate the underlying mechanism that mediates the role of miR-4260 in angiogenesis by identifying its putative downstream target genes.

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Silencing of ELK3 Induces S-M Phase Arrest and Apoptosis and Upregulates SERPINE1 Expression Reducing Migration in Prostate Cancer Cells

BioMed Research International ◽

10.1155/2020/2406159 ◽

2020 ◽

Vol 2020 ◽

pp. 1-9 ◽

Cited By ~ 1

Author(s):

Yuanshen Mao ◽

Wenfeng Li ◽

Bao Hua ◽

Xin Gu ◽

Weixin Pan ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Cancer Progression ◽

Prostate Cancer Cells ◽

Migration Inhibition ◽

Akt Inhibitor ◽

Phase Arrest ◽

M Phase ◽

And Migration

ELK3, an ETS domain-containing transcription factor, participates in various physiological and pathological processes including cell proliferation, migration, angiogenesis, and malignant progression. However, the role of ELK3 in prostate cancer cells and its mechanism are not fully understood. The contribution of ELK3 to prostate cancer progression was investigated in the present study. We showed that silencing of ELK3 by siRNA in prostate cancer cell DU145 induced S-M phase arrest, promoted apoptosis, inhibited cell proliferation and migration in vitro, and suppressed xenograft growth in mice in vivo. In accordance with its ability to arrest cells in S-M phase, the expression of cyclin A and cyclin B was downregulated. In addition, the expression of p53 was upregulated following ELK3 knockdown, while that of antiapoptotic Bcl-2 was decreased. The migration inhibition may partly due to upregulation of SERPINE1 (a serine protease inhibitor) followed ELK3 knockdown. Consistently, downregulation of SERPINE1 resulted in a modest elimination of migration inhibition resulted from ELK3 knockdown. Furthermore, we found that the AKT signaling was activated in ELK3 knockdown cells, and treatment these cells with AKT inhibitor attenuated SERPINE1 expression induced by ELK3 silencing, suggesting that activation of AKT pathway may be one of the reasons for upregulation of SERPINE1 after ELK3 knockdown. In conclusion, modulation of ELK3 expression may control the progression of prostate cancer partly by regulating cell growth, apoptosis, and migration.

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LncRNA MRAK048635_P1 is critical for vascular smooth muscle cell function and phenotypic switching in essential hypertension

Bioscience Reports ◽

10.1042/bsr20182229 ◽

2019 ◽

Vol 39 (3) ◽

Cited By ~ 10

Author(s):

Genqiang Fang ◽

Jia Qi ◽

Liya Huang ◽

Xianxian Zhao

Keyword(s):

Smooth Muscle ◽

Essential Hypertension ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Vascular Remodeling ◽

Cell Function ◽

Phenotypic Switching ◽

And Migration ◽

Proliferation And Migration

AbstractVascular remodeling caused by essential hypertension is a leading cause of death in patients, and vascular smooth muscle cell (VSMC) dysfunction and phenotypic switching result in vascular remodeling. Therefore, inhibiting cell dysfunction and phenotypic switching in VSMCs may be a new treatment strategy for essential hypertension. The aim of the current study is to explore the roles of long non-coding RNA (lncRNA) MRAK048635_P1 in VSMC function and phenotypic switching. The MRAK048635_P1 level was determined in spontaneously hypertensive rats (SHRs) and VSMCs isolated from SHRs. MRAK048635_P1 was knocked down using a specific siRNA in VSMCs isolated from the thoracic aorta of SHRs and Wistar–Kyoto rats. Then, the proliferation and migration of VSMCs were determined using a cell counting kit-8 (CCK-8), a 3H labeling method, a transwell assay, and a wound healing assay. Flow cytometry was used to test the effect of MRAK048635_P1 on VSMC apoptosis. The protein and mRNA levels of associated genes were measured through Western blotting, immunofluorescence, and Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). MRAK048635_P1 showed low expression during hypertension in vivo and in vitro. Down-regulation of lncRNA MRAK048635_P1 promoted proliferation and migration and inhibited apoptosis in VSMCs isolated from healthy rat vascular tissue and SHR-derived VSMCs. Importantly, we also found that down-regulation of MRAK048635_P1 could induce VSMC phenotypic switching from a contractile to a secretory phenotype. In conclusion, our findings reveal that decreased MRAK048635_P1 is probably an important factor for vascular remodeling by affecting VSMC cell function and phenotypic switching in essential hypertension.

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Fish telocytes and their relation to rodlet cells in ruby-red-fin shark (rainbow shark) Epalzeorhynchos frenatum (Teleostei: Cyprinidae)

Scientific Reports ◽

10.1038/s41598-020-75677-3 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Hanan H. Abd-Elhafeez ◽

Walied Abdo ◽

Basma Mohamed Kamal ◽

Soha A. Soliman

Keyword(s):

Stem Cells ◽

Progenitor Cells ◽

Direct Contact ◽

Cell Function ◽

Cell Contact ◽

Migration Ability ◽

Thin Sections ◽

3D Network ◽

And Migration ◽

Rodlet Cells

Abstract Telocytes comprise the major constituents of the supportive interstitial framework within the various organs. They form a 3D network between different types of stromal and non-stromal cells, which makes them distinctively vital. We have previously explored the origin of the peculiar rodlet cells, especially on their differential stages in aquatic species. The current study aimed at highlighting the relation of telocytes with different rodlet stages. Samples of fish, olfactory organs, and gills were processed for semi thin sections, transmission electron microscopy, and immunohistochemistry. It was evident in the study that telocytes formed a 3D interstitial network, entrapping stem cells and differentiating rodlet cells, to establish direct contact with stem cells. Differentiated stem cells and rodlet progenitor cells, practically in the granular and transitional stages, also formed ultrastructure junctional modifications, by which nanostructures are formed to establish cell contact with telocytes. Telocytes in turn also connected with macrophage progenitor cells. Telocytes (TCs) expressed CD34, CD117, VEGF, and MMP-9. In conclusion, telocytes established direct contact with the stem and rodlet cells in various differential stages. Telocytes may vitally influence stem/progenitor cell differentiation, regulate rodlet cell function, and express MPP-9 that may regulate immune cells functions especially, including movement and migration ability.

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Phosphorylation of Yes-associated protein impairs trophoblast invasion and migration: implications for the pathogenesis of fetal growth restriction†

Biology of Reproduction ◽

10.1093/biolre/ioaa112 ◽

2020 ◽

Vol 103 (4) ◽

pp. 866-879

Author(s):

Hao Wang ◽

Ping Xu ◽

Xiaofang Luo ◽

Mingyu Hu ◽

Yamin Liu ◽

...

Keyword(s):

Fetal Growth ◽

Fetal Growth Restriction ◽

Cell Function ◽

Hippo Pathway ◽

Growth Restriction ◽

Growth Potential ◽

Biomechanical Analysis ◽

Trophoblast Invasion ◽

Invasion And Migration ◽

And Migration

Abstract Fetal growth restriction (FGR) is a condition in which a newborn fails to achieve his or her prospective hereditary growth potential. This condition is associated with high newborn mortality, second only to that associated with premature birth. FGR is associated with maternal, fetal, and placental abnormalities. Although the placenta is considered to be an important organ for supplying nutrition for fetal growth, research on FGR is limited, and treatment through the placenta remains challenging, as neither proper uterine intervention nor its pathogenesis have been fully elucidated. Yes-associated protein (YAP), as the effector of the Hippo pathway, is widely known to regulate organ growth and cancer development. Therefore, the correlation of the placenta and YAP was investigated to elucidate the pathogenic mechanism of FGR. Placental samples from humans and mice were collected for histological and biomechanical analysis. After investigating the location and role of YAP in the placenta by immunohistochemistry, we observed that YAP and cytokeratin 7 have corresponding locations in human and mouse placentas. Moreover, phosphorylated YAP (p-YAP) was upregulated in FGR and gradually increased as gestational age increased during pregnancy. Cell function experiments and mRNA-Seq demonstrated impaired YAP activity mediated by extracellular signal-regulated kinase inhibition. Established FGR-like mice also recapitulated a number of the features of human FGR. The results of this study may help to elucidate the association of FGR development with YAP and provide an intrauterine target that may be helpful in alleviating placental dysfunction.

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ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS

Journal of Experimental Medicine ◽

10.1084/jem.140.2.383 ◽

1974 ◽

Vol 140 (2) ◽

pp. 383-395 ◽

Cited By ~ 18

Author(s):

Shlomo Z. Ben-Sasson ◽

Ethan Shevach ◽

Ira Green ◽

William E. Paul

Keyword(s):

T Cell ◽

Guinea Pigs ◽

Opposite Effect ◽

Cell Function ◽

Migration Inhibition Factor ◽

Immune Response Gene ◽

Migration Inhibition ◽

Inhibition Factor ◽

Controlled Systems

We have previously demonstrated that alloantisera prepared by reciprocal immunization of strain 2 and strain 13 guinea pigs specifically block stimulation of in vitro DNA synthesis in genetically controlled systems. In order to determine whether this blockade extends to other T-lymphocyte functions, we examined the effect of alloantisera on the production of migration inhibition factor (MIF). (2 x 13)F1 guinea pigs were immunized with a DNP derivative of the copolymer of L-glutamic acid and L-lysine (DNP-GL) and with DNP guinea pig albumin (GPA). The response to the former is controlled by a 2-linked Ir gene while that to the latter is mainly controlled by a 13-linked Ir gene. MIF production was assayed by an indirect procedure in which the migrating cell population lacked the histocompatibility antigen against which the alloantiserum was directed. Our results showed that anti-2 serum blocked MIF production by F1 cells in response to DNP-GL but not DNP-GPA while anti-13 serum had the opposite effect. These experiments show that expression of a second major T-cell function is specifically blocked by alloantisera and suggest that Ir-gene products may act as antigen recognition substances on more than one type of T cell.

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