Articles de revues : « Migration camp »

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Foley, J. F. « Control cAMP to control migration ». Science 351, n^o 6276 (25 février 2016) : 929–30. http://dx.doi.org/10.1126/science.351.6276.929-h.

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Lorenowicz, Magdalena J., Mar Fernandez-Borja et Peter L. Hordijk. « cAMP Signaling in Leukocyte Transendothelial Migration ». Arteriosclerosis, Thrombosis, and Vascular Biology 27, n^o 5 (mai 2007) : 1014–22. http://dx.doi.org/10.1161/atvbaha.106.132282.

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Stoufflet, Julie, Maxime Chaulet, Mohamed Doulazmi, Coralie Fouquet, Caroline Dubacq, Christine Métin, Sylvie Schneider-Maunoury, Alain Trembleau, Pierre Vincent et Isabelle Caillé. « Primary cilium-dependent cAMP/PKA signaling at the centrosome regulates neuronal migration ». Science Advances 6, n^o 36 (septembre 2020) : eaba3992. http://dx.doi.org/10.1126/sciadv.aba3992.

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The primary cilium (PC) is a small centrosome-assembled organelle, protruding from the surface of most eukaryotic cells. It plays a key role in cell migration, but the underlying mechanisms are unknown. Here, we show that the PC regulates neuronal migration via cyclic adenosine 3’-5’ monosphosphate (cAMP) production activating centrosomal protein kinase A (PKA). Biosensor live imaging revealed a periodic cAMP hotspot at the centrosome of embryonic, postnatal, and adult migrating neurons. Genetic ablation of the PC, or knockdown of ciliary adenylate cyclase 3, caused hotspot disappearance and migratory defects, with defective centrosome dynamics and altered nucleokinesis. Delocalization of PKA from the centrosome phenocopied the migratory defects. Our results show that the PC and centrosome form a single cAMP signaling unit dynamically regulating migration, further highlighting the centrosome as a signaling hub.

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Yokoyama, Utako, Susumu Minamisawa, Hong Quan, Toru Akaike, Meihua Jin, Koji Otsu, Coskun Ulucan et al. « Epac1 is upregulated during neointima formation and promotes vascular smooth muscle cell migration ». American Journal of Physiology-Heart and Circulatory Physiology 295, n^o 4 (octobre 2008) : H1547—H1555. http://dx.doi.org/10.1152/ajpheart.01317.2007.

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Vascular remodeling after mechanoinjury largely depends on the migration of smooth muscle cells, an initial key step to wound healing. However, the role of the second messenger system, in particular, the cAMP signal, in regulating such remodeling remains controversial. Exchange protein activated by cAMP (Epac) has been identified as a new target molecule of the cAMP signal, which is independent from PKA. We thus examined whether Epac plays a distinct role from PKA in vascular remodeling. To examine the role of Epac and PKA in migration, we used primary culture smooth muscle cells from both the fetal and adult rat aorta. A cAMP analog selective to PKA, 8-(4-parachlorophenylthio)-cAMP (pCPT-cAMP), decreased cell migration, whereas an Epac-selective analog, 8-pCPT-2′- O-Me-cAMP, enhanced migration. Adenovirus-mediated gene transfer of PKA decreased cell migration, whereas that of Epac1 significantly enhanced cell migration. Striking morphological differences were observed between pCPT-cAMP- and 8-pCPT-2′- O-Me-cAMP-treated aortic smooth muscle cells. Furthermore, overexpression of Epac1 enhanced the development of neointimal formation in fetal rat aortic tissues in organ culture. When the mouse femoral artery was injured mechanically in vivo, we found that the expression of Epac1 was upregulated in vascular smooth muscle cells, whereas that of PKA was downregulated with the progress of neointimal thickening. Our findings suggest that Epac1, in opposition to PKA, increases vascular smooth muscle cell migration. Epac may thus play an important role in advancing vascular remodeling and restenosis upon vascular injury.

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Raymond, Daniel R., Rhonda L. Carter, Christopher A. Ward et Donald H. Maurice. « Distinct phosphodiesterase-4D variants integrate into protein kinase A-based signaling complexes in cardiac and vascular myocytes ». American Journal of Physiology-Heart and Circulatory Physiology 296, n^o 2 (février 2009) : H263—H271. http://dx.doi.org/10.1152/ajpheart.00425.2008.

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Numerous cAMP-elevating agents regulate events required for efficient migration of arterial vascular smooth muscle cells (VSMCs). Interestingly, when the impact of cAMP-elevating agents on individual migration-related events is studied, these agents have been shown to have distinct, and sometimes unexpected, effects. For example, although cAMP-elevating agents inhibit overall migration, they promote VSMC adhesion to extracellular matrix proteins and the formation of membrane extensions, which are both events that are essential for and promote migration. Herein, we extend previous observations that identified phosphodiesterase-4D3 (PDE4D3) as an integral component of a PKA/A kinase-anchoring protein (AKAP) complex in cultured/hypertrophied rat cardiac myocytes to the case for nonhypertrophied cardiac myocytes. Moreover, we show that while rat aortic VSMCs also express PDE4D3, this protein is not detected in PKA/AKAP complexes isolated from these cells. In contrast, we show that another PDE4D splice variant expressed in arterial vascular myocytes, namely, PDE4D8, integrates into PKA/AKAP-based signaling complexes in VSMCs. Consistent with the idea that a PDE4D8/PKA/AKAP complex regulates specific VSMC functions, PKA and PDE4D8 were each recruited to leading-edge structures in migrating VSMCs, and inhibition of PDE4D8 recruitment to pseudopodia of migrating cells caused localized changes in actin dynamics. Our data are presented in the context that cardiac myocytes and arterial VSMCs may use distinct PDE4D variants to regulate selected pools of targeted PKA activity and that disruption of this complex may allow selective regulation of cAMP-dependent events between these two cardiovascular cell types.

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KOHNO, MASAKAZU, KENICHI YASUNARI, MIEKO MINAMI, HIROAKI KANO, KENSAKU MAEDA, ANIL K. MANDAL, KEN INOKI, MASAKAZU HANEDA et JUNICHI YOSHIKAWA. « Regulation of Rat Mesangial Cell Migration by Platelet-Derived Growth Factor, Angiotensin II, and Adrenomedullin ». Journal of the American Society of Nephrology 10, n^o 12 (décembre 1999) : 2495–502. http://dx.doi.org/10.1681/asn.v10122495.

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Abstract. This study sought to determine whether platelet-derived growth factor (PDGF) and angiotensin II (AngII) stimulate migration of cultured rat glomerular mesangial cells. After finding that this was so, the effects of adrenomedullin (ADM) and cAMP-elevating agents on basal and stimulated mesangial cell migration were examined. Two isoforms of PDGF, AB and BB, stimulated migration in a concentration-dependent manner between 1 and 50 ng/ml, while the AA isoform lacked significant effect. AngII modestly but significantly stimulated migration in a concentration-dependent manner between 10-7 and 10-6 mol/L. Rat ADM significantly inhibited the PDGF BB- and AngII-stimulated migration in a concentration-dependent manner between 10-8 and 10-7 mol/L. Inhibition by rat ADM was accompanied by an increase in cellular cAMP. cAMP agonists or inducers such as 8-bromo cAMP, forskolin, and prostaglandin I2 also significantly reduced the stimulated migration. H 89, a protein kinase A (PKA) inhibitor, attenuated the inhibitory effect of ADM, and a calcitonin gene-related peptide (CGRP) receptor antagonist, human CGRP (8-37), abolished the inhibitory effects of rat ADM. These results suggest that PDGF AB and BB as well as AngII stimulate rat mesangial cell migration and that ADM can inhibit PDGF BB- and AngII-stimulated migration, at least in part through cAMP-dependent mechanisms likely to involve specific ADM receptors with which CGRP interacts. The adenylate cyclase/cAMP/PKA system may be involved in the migration-inhibitory effect of ADM in these cells.

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Brzezinska, Paulina, et Donald H. Maurice. « An EPAC1/PDE1C-Signaling Axis Regulates Formation of Leading-Edge Protrusion in Polarized Human Arterial Vascular Smooth Muscle Cells ». Cells 8, n^o 12 (20 novembre 2019) : 1473. http://dx.doi.org/10.3390/cells8121473.

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Pharmacological activation of protein kinase A (PKA) reduces migration of arterial smooth muscle cells (ASMCs), including those isolated from human arteries (HASMCs). However, when individual migration-associated cellular events, including the polarization of cells in the direction of movement or rearrangements of the actin cytoskeleton, are studied in isolation, these individual events can be either promoted or inhibited in response to PKA activation. While pharmacological inhibition or deficiency of exchange protein activated by cAMP-1 (EPAC1) reduces the overall migration of ASMCs, the impact of EPAC1 inhibition or deficiency, or of its activation, on individual migration-related events has not been investigated. Herein, we report that EPAC1 facilitates the formation of leading-edge protrusions (LEPs) in HASMCs, a critical early event in the cell polarization that underpins their migration. Thus, RNAi-mediated silencing, or the selective pharmacological inhibition, of EPAC1 decreased the formation of LEPs by these cells. Furthermore, we show that the ability of EPAC1 to promote LEP formation by migrating HASMCs is regulated by a phosphodiesterase 1C (PDE1C)-regulated “pool” of intracellular HASMC cAMP but not by those regulated by the more abundant PDE3 or PDE4 activities. Overall, our data are consistent with a role for EPAC1 in regulating the formation of LEPs by polarized HASMCs and show that PDE1C-mediated cAMP hydrolysis controls this localized event.

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Aumo, Linda, Marte Rusten, Gunnar Mellgren, Marit Bakke et Aurélia E. Lewis. « Functional Roles of Protein Kinase A (PKA) and Exchange Protein Directly Activated by 3′,5′-Cyclic Adenosine 5′-Monophosphate (cAMP) 2 (EPAC2) in cAMP-Mediated Actions in Adrenocortical Cells ». Endocrinology 151, n^o 5 (16 mars 2010) : 2151–61. http://dx.doi.org/10.1210/en.2009-1139.

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In the adrenal cortex, the biosynthesis of steroid hormones is controlled by the pituitary-derived hormone ACTH. The functions of ACTH are principally relayed by activating cAMP-dependent signaling pathways leading to the induction of genes encoding enzymes involved in the conversion of cholesterol to steroid hormones. Previously, protein kinase A (PKA) was thought to be the only direct effector of cAMP. However, the discovery of the cAMP sensors, exchange proteins directly activated by cAMP (EPAC1 and 2), has led to a reevaluation of this assumption. In the present study, we demonstrate the occurrence of the EPAC2 splicing variant EPAC2B in adrenocortical cancer cells. Immunocytochemistry demonstrated that EPAC2B is localized predominantly in the nucleus. EPAC2B is functional because it activates Rap1 in these cells. Using the cAMP analogs 8-p-chlorophenylthio-2′-O-methyl-cAMP and N6-benzoyl-cAMP, which specifically activate EPAC1/2 and PKA, respectively, we evaluated the contribution of these factors in steroid hormone production, cell morphology, actin reorganization, and migration. We demonstrate that the expression of cAMP-inducible factors involved in steroidogenesis (steroidogenic acute regulatory protein, cytochrome P450 11A1 and 17, and nerve growth factor-induced clone B) and the cAMP-induced biosynthesis of steroid hormones (cortisol and aldosterone) are mediated by PKA and not by EPAC2B. In contrast, both PKA- and EPAC-specific cAMP analogs induced cell rounding, loss of stress fibers, and blocked migration. Taken together, the presented data confirm PKA as the central cAMP mediator in steroid hormone production and reveal the involvement of EPAC2B in cAMP-induced effects on cytoskeleton integrity and cell migration.

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Lima, Thaline F. A., Juliana D. B. Rocha, Anderson B. Guimarães-Costa, José M. Barbosa-Filho, Débora Decoté-Ricardo, Elvira M. Saraiva, Luciana B. Arruda, Marcia R. Piuvezam et Ligia M. T. Peçanha. « Warifteine, an Alkaloid Purified fromCissampelos sympodialis, Inhibits Neutrophil MigrationIn VitroandIn Vivo ». Journal of Immunology Research 2014 (2014) : 1–12. http://dx.doi.org/10.1155/2014/752923.

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Cissampelos sympodialisEichl is a plant from the Northeast and Southeast of Brazil. Its root infusion is popularly used for treatment of inflammatory and allergic diseases. We investigated whether warifteine, its main alkaloid, would have anti-inflammatory effect due to a blockage of neutrophil function.In vivowarifteine treatment inhibited casein-induced neutrophil migration to the peritoneal cavity but did not inhibit neutrophil mobilization from the bone marrow. Analysis of the direct effect of warifteine upon neutrophil adherence and migrationin vitrodemonstrated that the alkaloid decreased cell adhesion to P and E-selectin-transfected cells. In addition, fLMP-induced neutrophil migration in a transwell system was blocked by warifteine; this effect was mimicked by cAMP mimetic/inducing substances, and warifteine increased intracellular cAMP levels in neutrophils. The production of DNA extracellular traps (NETs) was also blocked by warifteine but there was no alteration on PMA-induced oxidative burst or LPS-stimulated TNFαsecretion. Taken together, our data indicate that the alkaloid warifteine is a potent anti-inflammatory substance and that it has an effect on neutrophil migration through a decrease in both cell adhesion and migration.

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Yang, Jing-Xing, Te-Chih Hsiung, Fu-Chun Weng, Shiau-Li Ding, Chin-Pyng Wu, Marco Conti, Tsung-Hsien Chuang et S.-L. Catherine Jin. « Synergistic effect of phosphodiesterase 4 inhibitor and serum on migration of endotoxin-stimulated macrophages ». Innate Immunity 24, n^o 8 (novembre 2018) : 501–12. http://dx.doi.org/10.1177/1753425918809155.

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Macrophage migration is an essential step in host defense against infection and wound healing. Elevation of cAMP by inhibiting phosphodiesterase 4 (PDE4), enzymes that specifically degrade cAMP, is known to suppress various inflammatory responses in activated macrophages, but the role of PDE4 in macrophage migration is poorly understood. Here we show that the migration of Raw 264.7 macrophages stimulated with LPS was markedly and dose-dependently induced by the PDE4 inhibitor rolipram as assessed by scratch wound healing assay. Additionally, this response required the involvement of serum in the culture medium as serum starvation abrogated the effect. Further analysis revealed that rolipram and serum exhibited synergistic effect on the migration, and the influence of serum was independent of PDE4 mRNA expression in LPS-stimulated macrophages. Moreover, the enhanced migration by rolipram was mediated by activating cAMP/exchange proteins directly activated by cAMP (Epac) signaling, presumably via interaction with LPS/TLR4 signaling with the participation of unknown serum components. These results suggest that PDE4 inhibitors, together with serum components, may serve as positive regulators of macrophage recruitment for more efficient pathogen clearance and wound repair.

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Oppenheimer-Marks, N., A. F. Kavanaugh et P. E. Lipsky. « Inhibition of the transendothelial migration of human T lymphocytes by prostaglandin E2. » Journal of Immunology 152, n^o 12 (15 juin 1994) : 5703–13. http://dx.doi.org/10.4049/jimmunol.152.12.5703.

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Abstract To determine whether part of the anti-inflammatory effects of prostaglandin E2 (PGE2) was related to inhibition of T cell interactions with endothelial cells (EC), the effects of PGE2 and other cAMP-elevating agents on the transendothelial migration of human T cells was examined. Although PGE2 did not effect T cell binding to EC, concentration-dependent inhibition of the transendothelial migration of T cells through unstimulated or IL-1-activated EC was observed. PGE2 inhibited the function of both T cells and EC, with maximal inhibition observed when both T cells and EC were treated with PGE2. However, the inhibitory action of PGE2 could not be ascribed to an effect on the adhesion receptor pair, CD11a/CD18-CD54. The inhibitory effect of PGE2 seemed to relate to its capacity to elevate cellular cAMP levels, because 3-isobutyl-1-methylxanthine enhanced PGE2 activity and dibutyryl cAMP and forskolin also inhibited transendothelial migration. The inhibitory effect of PGE2 and the other cAMP-elevating agents on the function of T cells related in part to suppression of their intrinsic locomotory behavior as random migration in the absence of EC was blocked. In EC, PGE2 and the other cAMP-elevating agents increased the barrier function of EC as evidenced by a decrease in the diffusion of [3H]mannitol through the endothelium. These results indicate that part of the anti-inflammatory action of PGE2 relates to its capacity to suppress the transendothelial migration of T cells by cAMP-mediated alterations in the function of both T cells and EC.

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Huang, Qianwu, Jun Lv, Ting Dong, Haijun Liu, Lei Xu et Mingcai Wu. « Cryptochrome 1 Alleviates the Antiproliferative Effect of Isoproterenol on Human Gastric Cancer Cells ». Dose-Response 18, n^o 3 (1 juillet 2020) : 155932582093902. http://dx.doi.org/10.1177/1559325820939022.

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Background: Cryptochrome 1 (CRY1) is a key protein that regulates the feedback loop of circadian clock. The abnormal expression of CRY1 was reported in numerous cancers, and contributed to tumorigenesis and progression. But the underlying mechanism remains undefined. Methods: CRY1 overexpression was constructed by lentivirus vector. Gene and protein expression was detected by reverse transcription quantitative polymerase chain reaction and Western blot. Cell proliferation was analyzed by CCK-8 assay. Cell migration ability was analyzed by scratch assay and transwell migration assay. The cAMP concentration was measured by intracellular cAMP assay. Results: Overexpression of CRY1 showed slightly effect on the proliferation and migration of HGC-27 cells. Upon exposure to isoproterenol (ISO), a β-adrenergic receptor agonist, cell proliferation, and migration were inhibited while the cAMP/PKA pathway was activated and ERK1/2 phosphorylation was suppressed. CRY1 overexpression reduced cAMP accumulation, retained ERK1/2 phosphorylation level and alleviated the antiproliferative effect upon exposure to ISO. However, CRY1 overexpression was inoperative on the antiproliferative effect of forskolin (FSK), a direct activator of adenyl cyclase (AC), or 3-isobutyl-1-methylxanthine (IBMX), a phosphodiesterase (PDE) inhibitor. Conclusions: Our results suggest CRY1 overexpression may protect cells from the antiproliferative effects via activation of the cAMP/PKA pathway through interrupting signal transduction from G protein-coupled receptors to AC.

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Whyte, Zachary, Rebecca Campbell et Heidi Overgaard. « Paradoxical infrastructures of asylum : Notes on the rise and fall of tent camps in Denmark ». Migration Studies 8, n^o 2 (13 juin 2018) : 143–60. http://dx.doi.org/10.1093/migration/mny018.

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AbstractAsylum policies in the Global North have increasingly turned towards populist policies of deterrence, as states attempt to make themselves seem as unattractive as possible to would-be asylum seekers. This article examines one such case: the tent camps for asylum seekers that were hastily erected in Denmark in early 2016. However, while the tent camps surely are an instance of symbolic politics, we argue that to understand their daily operation, attention must also be paid to their infrastructural qualities. Drawing on two months of fieldwork at a tent camp in Næstved, this article examines the ways in which asylum policy and infrastructure interact to shape the daily lives and interactions of camp residents and staff. We propose two paradoxical frames for the analysis, which we term ‘spectacular obscurity’ and ‘successful failure’. The tent camps were trumpeted as symbolic politics, while their daily operation remained obscured, only to burst in to scandal as reports emerged of threatening and violent behaviour on the part of the staff. The tent camps’ infrastructure was constantly failing, as both material and social support broke down, but at the same time these failures successfully formed the basis for the everyday interactions that structured life in the camps. We conclude by questioning the effect of the policies of deterrence as mediated through particular infrastructures, suggesting that the materialities of the tent camps played a more significant role than supposed by policy makers, and that paradoxes of infrastructure provide a useful perspective through which to analyse migration management more broadly.

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Kriebel, Paul W., Ritankar Majumdar, Lisa M. Jenkins, Hiroshi Senoo, Weiye Wang, Sonia Ammu, Song Chen, Kedar Narayan, Miho Iijima et Carole A. Parent. « Extracellular vesicles direct migration by synthesizing and releasing chemotactic signals ». Journal of Cell Biology 217, n^o 8 (8 juin 2018) : 2891–910. http://dx.doi.org/10.1083/jcb.201710170.

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Chemotactic signals are relayed to neighboring cells through the secretion of additional chemoattractants. We previously showed in Dictyostelium discoideum that the adenylyl cyclase A, which synthesizes the chemoattractant cyclic adenosine monophosphate (cAMP), is present in the intraluminal vesicles of multivesicular bodies (MVBs) that coalesce at the back of cells. Using ultrastructural reconstructions, we now show that ACA-containing MVBs release their contents to attract neighboring cells. We show that the released vesicles are capable of directing migration and streaming and are central to chemotactic signal relay. We demonstrate that the released vesicles not only contain cAMP but also can actively synthesize and release cAMP to promote chemotaxis. Through proteomic, pharmacological, and genetic approaches, we determined that the vesicular cAMP is released via the ABCC8 transporter. Together, our findings show that extracellular vesicles released by D. discoideum cells are functional entities that mediate signal relay during chemotaxis and streaming.

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Dormann, Dirk, et Cornelis J. Weijer. « Propagating chemoattractant waves coordinate periodic cell movement inDictyosteliumslugs ». Development 128, n^o 22 (15 novembre 2001) : 4535–43. http://dx.doi.org/10.1242/dev.128.22.4535.

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Migration and behaviour of Dictyostelium slugs results from coordinated movement of its constituent cells. It has been proposed that cell movement is controlled by propagating waves of cAMP as during aggregation and in the mound. We report the existence of optical density waves in slugs; they are initiated in the tip and propagate backwards. The waves reflect periodic cell movement and are mediated by cAMP, as injection of cAMP or cAMP phosphodiesterase disrupts wave propagation and results in effects on cell movement and, therefore, slug migration. Inhibiting the function of the cAMP receptor cAR1 blocks wave propagation, showing that the signal is mediated by cAR1. Wave initiation is strictly dependent on the tip; in decapitated slugs no new waves are initiated and slug movement stops until a new tip regenerates. Isolated tips continue to migrate while producing waves. We conclude from these observations that the tip acts as a pacemaker for cAMP waves that coordinate cell movement in slugs.Movies available on-line

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O'Connor, Kathleen L., Leslie M. Shaw et Arthur M. Mercurio. « Release of cAMP Gating by the α6β4 Integrin Stimulates Lamellae Formation and the Chemotactic Migration of Invasive Carcinoma Cells ». Journal of Cell Biology 143, n^o 6 (14 décembre 1998) : 1749–60. http://dx.doi.org/10.1083/jcb.143.6.1749.

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The α6β4 integrin promotes carcinoma in-vasion by its activation of a phosphoinositide 3-OH (PI3-K) signaling pathway (Shaw, L.M., I. Rabinovitz, H.H.-F. Wang, A. Toker, and A.M. Mercurio. Cell. 91: 949–960). We demonstrate here using MDA-MB-435 breast carcinoma cells that α6β4 stimulates chemotactic migration, a key component of invasion, but that it has no influence on haptotaxis. Stimulation of chemotaxis by α6β4 expression was observed in response to either lysophosphatidic acid (LPA) or fibroblast conditioned medium. Moreover, the LPA-dependent formation of lamellae in these cells is dependent upon α6β4 expression. Both lamellae formation and chemotactic migration are inhibited or “gated” by cAMP and our results reveal that a critical function of α6β4 is to suppress the intracellular cAMP concentration by increasing the activity of a rolipram-sensitive, cAMP-specific phosphodiesterase (PDE). This PDE activity is essential for lamellae formation, chemotactic migration and invasion based on data obtained with PDE inhibitors. Although PI3-K and cAMP-specific PDE activities are both required to promote lamellae formation and chemotactic migration, our data indicate that they are components of distinct signaling pathways. The essence of our findings is that α6β4 stimulates the chemotactic migration of carcinoma cells through its ability to influence key signaling events that underlie this critical component of carcinoma invasion.

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Kryczka, Jakub, Ewelina Sochacka, Izabela Papiewska-Pająk et Joanna Boncela. « Implications of ABCC4–Mediated cAMP Efflux for CRC Migration ». Cancers 12, n^o 12 (27 novembre 2020) : 3547. http://dx.doi.org/10.3390/cancers12123547.

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Colorectal cancer (CRC) presents significant molecular heterogeneity. The cellular plasticity of epithelial to mesenchymal transition (EMT) is one of the key factors responsible for the heterogeneous nature of metastatic CRC. EMT is an important regulator of ATP binding cassette (ABC) protein expression; these proteins are the active transporters of a broad range of endogenous compounds and anticancer drugs. In our previous studies, we performed a transcriptomic and functional analysis of CRC in the early stages of metastasis induced by the overexpression of Snail, the transcription factor involved in EMT initiation. Interestingly, we found a correlation between the Snail expression and ABCC4 (MRP4) protein upregulation. The relationship between epithelial transition and ABCC4 expression and function in CRC has not been previously defined. In the current study, we propose that the ABCC4 expression changes during EMT and may be differentially regulated in various subpopulations of CRC. We confirmed that ABCC4 upregulation is correlated with the phenotype conversion process in CRC. The analysis of Gene Expression Omnibus (GEO) sets showed that the ABCC4 expression was elevated in CRC patients. The results of a functional study demonstrated that, in CRC, ABCC4 can regulate cell migration in a cyclic nucleotide-dependent manner.

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Davies, Thom, et Arshad Isakjee. « Geography, migration and abandonment in the Calais refugee camp ». Political Geography 49 (novembre 2015) : 93–95. http://dx.doi.org/10.1016/j.polgeo.2015.08.003.

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Howe, Alan K. « Regulation of actin-based cell migration by cAMP/PKA ». Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1692, n^o 2-3 (juillet 2004) : 159–74. http://dx.doi.org/10.1016/j.bbamcr.2004.03.005.

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Fukai, Nozomi, Masayoshi Shichiri, Naoko Ozawa, Mika Matsushita et Yukio Hirata. « Coexpression of Calcitonin Receptor-Like Receptor and Receptor Activity-Modifying Protein 2 or 3 Mediates the Antimigratory Effect of Adrenomedullin ». Endocrinology 144, n^o 2 (1 février 2003) : 447–53. http://dx.doi.org/10.1210/en.2002-220463.

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Three isoforms of the receptor activity-modifying protein (RAMP) are thought to transport the calcitonin receptor-like receptor (CRLR) to the plasma membrane to function as calcitonin gene-related peptide or adrenomedullin receptors, but their role remains largely unknown. We investigated whether coexpression of RAMP and CRLR are involved in the regulation of cell migration using a monolayer-wounding protocol. Quantification of gene transcripts revealed expression of all RAMP isoforms and CRLR in cultured rat vascular smooth muscle cells (VSMCs), RAMP2 and RAMP3 in rat endothelial cells, and RAMP1 in rat fibroblasts. CRLR expression was minimal in endothelial cells and fibroblasts. Adrenomedullin potently suppressed the migration of VSMCs, whereas calcitonin gene-related peptide did not suppress migration in any cell type. The antimigratory effect of adrenomedullin on VSMCs was potentiated by transfecting CRLR cDNA. Cotransfection of RAMP2 or RAMP3 with CRLR into VSMCs resulted in a slower migratory rate, and this effect was enhanced by adrenomedullin. Migration of fibroblasts was also suppressed after cotransfection of RAMP2 or RAMP3 with CRLR. cAMP agonists had no effect on VSMC migration, and a cAMP antagonist failed to abrogate the antimigratory effect of adrenomedullin. Thus, coexpression of CRLR and RAMP2 or RAMP3 mediates the inhibitory effect of adrenomedullin on cell migration, independent of cAMP-dependent signaling pathways.

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Spurzem, John R., Jitendrakumar Gupta, Thomas Veys, Kristen R. Kneifl, Stephen I. Rennard et Todd A. Wyatt. « Activation of protein kinase A accelerates bovine bronchial epithelial cell migration ». American Journal of Physiology-Lung Cellular and Molecular Physiology 282, n^o 5 (1 mai 2002) : L1108—L1116. http://dx.doi.org/10.1152/ajplung.00148.2001.

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Bronchial epithelial cell migration is required for the repair of damaged airway epithelium. We hypothesized that bronchial epithelial cell migration during wound repair is influenced by cAMP and the activity of its cyclic nucleotide-dependent protein kinase, protein kinase A (PKA). We found that, when confluent monolayers of bronchial epithelial cells are wounded, an increase in PKA activity occurs. Augmentation of PKA activity with a cell-permeable analog of cAMP, dibutyryl adenosine 3′,5′-cyclic monophosphate, isoproterenol, or a phosphodiesterase inhibitor accelerated migration of normal bronchial epithelial cells in in vitro wound closure assays and Boyden chamber migration assays. A role for PKA activity was also confirmed with a PKA inhibitor, KT-5720, which reduced stimulated migration. Augmentation of PKA activity reduced the levels of active Rho and the formation of focal adhesions. These studies suggest that PKA activation modulates Rho activity, migration mechanisms, and thus bronchial epithelial repair mechanisms.

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Gajpal, L. S. « Rethinking about Tribal Marriage, Family and Kinship of Chhattisgarh State (With special reference to tribes of base camp in Dantewada district) ». Journal of Ravishankar University (PART-A) 23, n^o 1 (1 février 2020) : 23–32. http://dx.doi.org/10.52228/jrua.2017-23-1-3.

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Present paper is based on the findings of major research project “Tribal life in base camp and structural change.” Researcher has been try to find out what are the factor responsible for migration of large number of tribal people from native places to nearby the district and block head quarters. The study is focused on impact of migration on tribal marriage and family in base camp. A comparative study of social life of tribal people before coming in base camps and changes after boarding in base camps. The findings of the study show that due to naxal movement and residing in the base camp tribal marriage, family and kinship system is highly affected.

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Kohyama, Tadashi, Xiangde Liu, Hui Jung Kim, Tetsu Kobayashi, Ronald F. Ertl, Fu-Qiang Wen, Hajime Takizawa et Stephen I. Rennard. « Prostacyclin analogs inhibit fibroblast migration ». American Journal of Physiology-Lung Cellular and Molecular Physiology 283, n^o 2 (1 août 2002) : L428—L432. http://dx.doi.org/10.1152/ajplung.00432.2001.

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The controlled accumulation of fibroblasts to sites of inflammation is crucial to effective tissue repair after injury. Either inadequate or excessive accumulation of fibroblasts could result in abnormal tissue function. Prostacyclin (PGI2) is a potent mediator in the coagulation and inflammatory processes. The aim of this study was to investigate the effect of PGI2on chemotaxis of human fetal lung fibroblasts (HFL-1). Using the blind well chamber technique, we found that the PGI2analog carbaprostacyclin (10−6M) inhibited HFL-1 chemotaxis to human plasma fibronectin (20 μg/ml) 58.0 ± 13.2% ( P < 0.05) and to platelet-derived growth factor (PDGF)-BB (10 ng/ml) 48.7 ± 4.6% ( P < 0.05). Checkerboard analysis demonstrated that carbaprostacyclin inhibits both directed and undirected migration. The inhibitory effect of the carbaprostacyclin was concentration dependent and blocked by the cAMP-dependent protein kinase (PKA) inhibitor KT-5720, suggesting that a cAMP-PKA pathway may be involved in the process. Two other PGI2analogs, ciprostene and dehydro-15-cyclohexyl carbaprostacyclin (both 10−6M), significantly inhibited fibroblast migration to fibronectin. In summary, PGI2appears to inhibit fibroblast chemotaxis to fibronectin and PDGF-BB. Such an effect may contribute to the regulation of fibroblasts in wound healing and could contribute to the pathogenesis of diseases characterized by abnormal tissue repair remodeling.

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Wallace, Clare. « The Camp and the Journey : Aesthetic Encounters with Forced Migration ». Litteraria Pragensia 17, n^o 35 (10 août 2021) : 60–79. http://dx.doi.org/10.14712/2571452x.2021.61.5.

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Favot, Laure, Thérèse Keravis, Vincent Holl, Alain Bec et Claire Lugnier. « VEGF-induced HUVEC migration and proliferation are decreased by PDE2 and PDE4 inhibitors ». Thrombosis and Haemostasis 90, n^o 08 (2003) : 334–43. http://dx.doi.org/10.1160/th03-02-0084.

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SummaryMigration and proliferation of endothelial cells in response to VEGF play an important role in angiogenesis associated to pathologies such as atherosclerosis, diabetes and tumor development. Elevation of cAMP in endothelial cells has been shown to inhibit growth factor-induced proliferation. Our hypothesis was that inactivation of cAMP-specific phosphodiesterases (PDEs) would inhibit angiogenesis. The purpose of this study was to evaluate the effect of PDE inhibitors on in vitro and in vivo angiogenesis, using human umbilical vein endothelial cell (HUVEC) and chick chorioallantoic membrane (CAM) models respectively. Here, we report that: 1) PDE2, PDE3, PDE4 and PDE5 are expressed in HUVEC; 2) EHNA (20 µM), PDE2 selective inhibitor, and RP73401 (10 µM), PDE4 selective inhibitor, are able to increase the intracellular cAMP level in HUVEC; 3) EHNA and RP73401 are able to inhibit proliferation, cell cycle progression and migration of HUVEC stimulated by VEGF; 4) these in vitro effects can be mimic by treating HUVEC with the cAMP analogue, 8-Br-cAMP (600 µM); 5) only the association of EHNA and RP73401 inhibits in vivo angiogenesis, indicating that both migration and proliferation must be inhibited. These data strongly suggest that PDE2 and PDE4 represent new potential therapeutic targets in pathological angiogenesis.

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Zuo, Haoxiao, Marina Trombetta-Lima, Irene H. Heijink, Christina H. T. J. van der Veen, Laura Hesse, Klaas Nico Faber, Wilfred J. Poppinga, Harm Maarsingh, Viacheslav O. Nikolaev et Martina Schmidt. « A-Kinase Anchoring Proteins Diminish TGF-β1/Cigarette Smoke-Induced Epithelial-To-Mesenchymal Transition ». Cells 9, n^o 2 (3 février 2020) : 356. http://dx.doi.org/10.3390/cells9020356.

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Epithelial-to-mesenchymal transition (EMT) plays a role in chronic obstructive pulmonary diseases (COPD). Cyclic adenosine monophosphate (cAMP) can inhibit transforming growth factor-β1 (TGF-β1) mediated EMT. Although compartmentalization via A-kinase anchoring proteins (AKAPs) is central to cAMP signaling, functional studies regarding their therapeutic value in the lung EMT process are lacking. The human bronchial epithelial cell line (BEAS-2B) and primary human airway epithelial (pHAE) cells were exposed to TGF-β1. Epithelial (E-cadherin, ZO-1) and mesenchymal markers (collagen Ӏ, α-SMA, fibronectin) were analyzed (mRNA, protein). ELISA measured TGF-β1 release. TGF-β1-sensitive AKAPs Ezrin, AKAP95 and Yotiao were silenced while using siRNA. Cell migration was analyzed by wound healing assay, xCELLigence, Incucyte. Prior to TGF-β1, dibutyryl-cAMP (dbcAMP), fenoterol, rolipram, cilostamide, and forskolin were used to elevate intracellular cAMP. TGF-β1 induced morphological changes, decreased E-cadherin, but increased collagen Ӏ and cell migration, a process that was reversed by the inhibitor of δ/epsilon casein kinase I, PF-670462. TGF-β1 altered (mRNA, protein) expression of Ezrin, AKAP95, and Yotiao. St-Ht31, the AKAP antagonist, decreased E-cadherin (mRNA, protein), but counteracted TGF-β1-induced collagen Ӏ upregulation. Cigarette smoke (CS) increased TGF-β1 release, activated TGF signaling, augmented cell migration, and reduced E-cadherin expression, a process that was blocked by TGF-β1 neutralizing antibody. The silencing of Ezrin, AKAP95, and Yotiao diminished TGF-β1-induced collagen Ӏ expression, as well as TGF-β1-induced cell migration. Fenoterol, rolipram, and cilostamide, in AKAP silenced cells, pointed to distinct cAMP compartments. We conclude that Ezrin, AKAP95, and Yotiao promote TGF-β1-mediated EMT, linked to a TGF-β1 release by CS. AKAP members might define the ability of fenoterol, rolipram, and cilostamide to modulate the EMT process, and they might represent potential relevant targets in the treatment of COPD.

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Szilágyi, Béla. « Refugee Camp : A Tool for Dignity and Security ». Belügyi Szemle 69, n^o 4. ksz. (19 octobre 2021) : 31–52. http://dx.doi.org/10.38146/bsz.spec.2021.4.3.

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Migration is the main challenge of the 21st century. With 272 million people migrating in 2019, of whom 80 million people are forcibly displaced worldwide, their security and the security of those living in the destination countries or regions is a major concern. One of the decisive factors in protection and security is the planning and management of the camps where millions of refugees and internally displaced people are hosted, in several cases, for many years. Well planned and well-organized camps do not only provide assistance and ensure the dignity to those displaced, help the effective work of the aid workers, but can also contribute to reducing crime and gender-based violence, furthermore decrease security threats and concerns. This paper examines how migrant settlement options, especially camps can be a tool for upholding the dignity of those in the camp whether they are refugees, internally displaced persons or different kinds of migrants, but at the same time how they can provide the safety and security for both the hosted population and the hosting community. For this very reason, the purpose of a shelter, the advantages and disadvantages of camps, furthermore setting and planning of camps will be discussed.

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Suh, Han Na, et Ho Jae Han. « Laminin regulates mouse embryonic stem cell migration : involvement of Epac1/Rap1 and Rac1/cdc42 ». American Journal of Physiology-Cell Physiology 298, n^o 5 (mai 2010) : C1159—C1169. http://dx.doi.org/10.1152/ajpcell.00496.2009.

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Laminin is the first extracellular matrix (ECM) component to be expressed in the developing mammalian embryo. However, the roles of laminin or the related signal pathways are not well known in mouse embryonic stem cells (mESCs). Presently, we examined the effect of laminin on mESC migration. Laminin (10 μg/ml) decreased cell aggregation, whereas migration was increased. Laminin bound α6β1 integrin and laminin receptor 1 (LR1), decreasing their mRNA levels. Laminin increased focal adhesion kinase (FAK) and paxillin phosphorylation, cAMP intracellular concentration, and the protein levels of exchange factor directly activated by cAMP (Epac1) and Rap1. These increases were completely blocked by α6β1 integrin and LR1 neutralizing antibody, indicating that laminin-bound LR1 assists laminin-induced α6β1 integrin activity and initiates signal. As a downstream signal molecule, laminin activated small G protein such as Rac1/cdc42 and its effector protein p21-activated kinase (PAK). Subsequently, laminin stimulated E-cadherin complex disruption. Inhibition of each pathway such as those for α6β1 integrin and LR1, FAK, Rap1, and PAK1 blocked laminin-induced migration. We conclude that laminin binds both α6β1 integrin and LR1 and induces signaling FAK/paxillin and cAMP/Epac1/Rap1. These signaling merge at Rac1/cdc42 subsequently activate PAK1. Activated PAK1 enhances E-cadherin complex disruption and finally increases mESCs migration.

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Sullivan, G. W., J. Linden, E. L. Hewlett, H. T. Carper, J. B. Hylton et G. L. Mandell. « Adenosine and related compounds counteract tumor necrosis factor-alpha inhibition of neutrophil migration : implication of a novel cyclic AMP-independent action on the cell surface. » Journal of Immunology 145, n^o 5 (1 septembre 1990) : 1537–44. http://dx.doi.org/10.4049/jimmunol.145.5.1537.

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Abstract Human rTNF-alpha (greater than or equal to U/ml) decreased PMN nondirected and directed migration to FMLP to approximately 50% of control. Adenosine (100 microM) almost completely restored hrTNF-inhibited migration (nondirected from 54 to 92% and directed migration to from 54 to 93% of control). The lowest concentration of adenosine that restored hrTNF-inhibited migration was 3 microM, and the adenosine analogue, 5'-(N-cyclopropyl)-carboxamido-adenosine (CPCA) was more potent than adenosine. Although CPCA binds to A2-receptors and stimulates adenylate cyclase, the reversal of hrTNF-inhibited chemotaxis was found to be independent of both PMN cAMP content and binding to A2-receptors, because neither 8-Br-cAMP nor pertussis adenylate cyclase restored hrTNF-inhibited PMN chemotaxis and the A2-receptor antagonist, 1,3-dipropyl-7-methylxanthine decreased CPCA stimulated cAMP but enhanced CPCA-restoration of hrTNF-inhibited chemotaxis. The effect of adenosine could be augmented by inhibition of adenosine uptake and decreased by adenosine deamination. Pentoxifylline, (3,7 dimethyl-1-[5 oxo-hexyl] xanthine), like adenosine also restored PMN chemotaxis inhibited by hrTNF. The adenosine receptor antagonist, 1,3-dipropyl-8(phenyl-p-acrylate)-xanthine (BW A1433U), decreased restoration of hrTNF-inhibited chemotaxis by CPCA or pentoxifylline. Thus, the inhibitory effect of hrTNF on PMN migration can be counteracted by adenosine, CPCA, pentoxifylline, and compounds that increase adenosine availability to the surface of the PMN. Inasmuch as an A1-selective agonist N6-cyclopentyladenosine was less active, and the action of the A2-selective agonist CPCA was enhanced by an A2-receptor antagonist, we hypothesize that neither A1 or A2 receptors are involved in adenosine restoration of hrTNF-inhibited chemotaxis. Further, increased cAMP, an A2-regulated event, does not cause the effect, and adenosine restoration of hrTNF-inhibited migration does not appear to be mediated by changes in PMN [F-actin], FMLP receptor expression, or cytosolic calcium. Hence, the restoration of hrTNF-inhibited chemotaxis is controlled by a novel cyclic AMP-independent action on the PMN surface.

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King-Smith, C., P. Chen, D. Garcia, H. Rey et B. Burnside. « Calcium-independent regulation of pigment granule aggregation and dispersion in teleost retinal pigment epithelial cells ». Journal of Cell Science 109, n^o 1 (1 janvier 1996) : 33–43. http://dx.doi.org/10.1242/jcs.109.1.33.

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In the eyes of teleosts and amphibians, melanin pigment granules of the retinal pigment epithelium (RPE) migrate in response to changes in light conditions. In the light, pigment granules disperse into the cells' long apical projections, thereby shielding the rod photoreceptor outer segments and reducing their extent of bleach. In darkness, pigment granules aggregate towards the base of the RPE cells. In vitro, RPE pigment granule aggregation can be induced by application of nonderivatized cAMP, and pigment granule dispersion can be induced by cAMP washout. In previous studies based on RPE-retina co-cultures, extracellular calcium was found to influence pigment granule migration. To examine the role of calcium in regulation of RPE pigment granule migration in the absence of retinal influences, we have used isolated RPE sheets and dissociated, cultured RPE cells. Under these conditions depletion of extracellular or intracellular calcium ([Ca2+]o, [Ca2+]i) had no effect on RPE pigment granule aggregation or dispersion. Using the intracellular calcium dye fura-2 and a new dye, fura-pe3, to monitor calcium dynamics in isolated RPE cells, we found that [Ca2+]i did not change from basal levels when pigment granule aggregation was triggered by cAMP, or dispersion was triggered by cAMP washout. Also, no change in [Ca2+]i was detected when dispersion was triggered by cAMP washout in the presence of 10 microM dopamine, a treatment previously shown to enhance dispersion. In addition, elevation of [Ca2+]i by addition of ionomycin neither triggered pigment movements, nor interfered with pigment granule motility elicited by cAMP addition or washout. Since other studies have indicated that actin plays a role in both pigment granule dispersion and aggregation in RPE, our findings suggest that RPE pigment granule migration depends on an actin-based motility system that is not directly regulated by calcium.

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Sung, Bong Hwan, et Alissa M. Weaver. « Directed migration : Cells navigate by extracellular vesicles ». Journal of Cell Biology 217, n^o 8 (5 juillet 2018) : 2613–14. http://dx.doi.org/10.1083/jcb.201806018.

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Directional cell motility toward a chemical gradient, chemotaxis, is critical during inflammation, embryogenesis, and cancer metastasis. In this issue, Kriebel et al. (2018. J. Cell Biol. https://doi.org/10.1083/jcb.201710170) demonstrate that the key cAMP chemoattractant for Dictyostelium discoideum amoebas is synthesized within and released from extracellular vesicles to promote chemotaxis.

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Wyatt, Todd A., Jill A. Poole, Tara M. Nordgren, Jane M. DeVasure, Art J. Heires, Kristina L. Bailey et Debra J. Romberger. « cAMP-dependent protein kinase activation decreases cytokine release in bronchial epithelial cells ». American Journal of Physiology-Lung Cellular and Molecular Physiology 307, n^o 8 (15 octobre 2014) : L643—L651. http://dx.doi.org/10.1152/ajplung.00373.2013.

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Lung injury caused by inhalation of dust from swine-concentrated animal-feeding operations (CAFO) involves the release of inflammatory cytokine interleukin 8 (IL-8), which is mediated by protein kinase C-ε (PKC-ε) in airway epithelial cells. Once activated by CAFO dust, PKC-ε is responsible for slowing cilia beating and reducing cell migration for wound repair. Conversely, the cAMP-dependent protein kinase (PKA) stimulates contrasting effects, such as increased cilia beating and an acceleration of cell migration for wound repair. We hypothesized that a bidirectional mechanism involving PKA and PKC regulates epithelial airway inflammatory responses. To test this hypothesis, primary human bronchial epithelial cells and BEAS-2B cells were treated with hog dust extract (HDE) in the presence or absence of cAMP. PKC-ε activity was significantly reduced in cells that were pretreated for 1 h with 8-bromoadenosine 3′,5′-cyclic monophosphate (8-Br-cAMP) before exposure to HDE ( P < 0.05). HDE-induced IL-6, and IL-8 release was significantly lower in cells that were pretreated with 8-Br-cAMP ( P < 0.05). To exclude exchange protein activated by cAMP (EPAC) involvement, cells were pretreated with either 8-Br-cAMP or 8-(4-chlorophenylthio)-2'- O-methyladenosine-3',5'-cyclic monophosphate (8-CPT-2Me-cAMP) (EPAC agonist). 8-CPT-2Me-cAMP did not activate PKA and did not reduce HDE-stimulated IL-6 release. In contrast, 8-Br-cAMP decreased HDE-stimulated tumor necrosis factor (TNF)-α-converting enzyme (TACE; ADAM-17) activity and subsequent TNF-α release ( P < 0.001). 8-Br-cAMP also blocked HDE-stimulated IL-6 and keratinocyte-derived chemokine release in precision-cut mouse lung slices ( P < 0.05). These data show bidirectional regulation of PKC-ε via a PKA-mediated inhibition of TACE activity resulting in reduced PKC-ε-mediated release of IL-6 and IL-8.

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Miura, S., H. Serizawa, Y. Tsuzuki, I. Kurose, M. Suematsu, H. Higuchi, T. Shigematsu et al. « Vasoactive intestinal peptide modulates T lymphocyte migration in Peyer's patches of rat small intestine ». American Journal of Physiology-Gastrointestinal and Liver Physiology 272, n^o 1 (1 janvier 1997) : G92—G99. http://dx.doi.org/10.1152/ajpgi.1997.272.1.g92.

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Although vasoactive intestinal peptide (VIP) has been postulated to function in modulation of T cell trafficking, the exact mechanism has not been elucidated in vivo. In the present study, the effects of VIP on T lymphocyte migration were examined in rat Peyer's patches. T lymphocytes collected from intestinal lymph of rats were labeled with carboxyfluorescein diacetate succinimidyl ester and injected into the jugular vein. Peyer's patches of the recipient rats were observed with intravital fluorescence microscopy. In vivo intra-arterial infusion of or in vitro incubation with VIP did not affect the initial lymphocyte interaction with postcapillary venules of Peyer's patches. However, these treatments with VIP significantly inhibited transendothelial migration and also significantly blocked the interstitial migration of T cells and inhibited their subsequent appearance in the interfollicular lymphatics. Treatment with adenosine 3',5'-cyclic monophosphate (cAMP)-inducing agents resulted in similar inhibitory effect on T lymphocyte migration in Peyer's patches. In conclusion, VIP has significant inhibitory effects on T lymphocyte migration in Peyer's patches, possibly mediated by elevation of the intracellular cAMP concentrations.

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Stoufflet, Julie, et Isabelle Caillé. « The Primary Cilium and Neuronal Migration ». Cells 11, n^o 21 (26 octobre 2022) : 3384. http://dx.doi.org/10.3390/cells11213384.

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The primary cilium (PC) is a microtubule-based tiny sensory organelle emanating from the centrosome and protruding from the surface of most eukaryotic cells, including neurons. The extremely severe phenotypes of ciliopathies have suggested their paramount importance for multiple developmental events, including brain formation. Neuronal migration is an essential step of neural development, with all neurons traveling from their site of birth to their site of integration. Neurons perform a unique type of cellular migration called cyclic saltatory migration, where their soma periodically jumps along with the stereotyped movement of their centrosome. We will review here how the role of the PC on cell motility was first described in non-neuronal cells as a guide pointing to the direction of migration. We will see then how these findings are extended to neuronal migration. In neurons, the PC appears to regulate the rhythm of cyclic saltatory neuronal migration in multiple systems. Finally, we will review recent findings starting to elucidate how extracellular cues sensed by the PC could be intracellularly transduced to regulate the machinery of neuronal migration. The PC of migrating neurons was unexpectedly discovered to display a rhythmic extracellular emergence during each cycle of migration, with this transient exposure to the external environment associated with periodic transduction of cyclic adenosine monophosphate (cAMP) signaling at the centrosome. The PC in migrating neurons thus uniquely appears as a beat maker, regulating the tempo of cyclic saltatory migration.

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Lodewyks, Carly, Jose Rodriguez, Jing Yan, Betty Lerner, Jeremy Lipschitz, Charles Nfon, Julia Darlene Rempel, Julia Uhanova et Gerald Yosel Minuk. « GABA-B receptor activation inhibits the in vitro migration of malignant hepatocytes ». Canadian Journal of Physiology and Pharmacology 89, n^o 6 (juin 2011) : 393–400. http://dx.doi.org/10.1139/y11-031.

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There are conflicting data regarding whether activation of γ-aminobutyric acid-B (GABA-B) receptors results in inhibition of tumor growth and invasion. The objectives of this study were to document the effects of the GABA-B receptor agonist baclofen on malignant hepatocyte proliferation and migration. We also sought to determine whether any effects on cell migration were mediated by changes in cyclic adenosine monophosphate (cAMP) signaling or matrix metalloproteinase (MMP) expression. Finally, GABA-B1 and -B2 receptor expression was documented in 2 malignant hepatocyte cell lines (PLC/PRF/5 and Huh-7) and 12 sets of human hepatocellular carcinoma and adjacent nontumor tissues. Cell proliferative activity was documented by WST-1 absorbance, migration by wound healing assays, cAMP levels by enzyme-linked immunoassay (ELISA), MMP by immunohistochemistry and ELISA, and GABA-B receptor expression by flow cytometry and reverse transcriptase – polymerase chain reaction. Although baclofen had no effect on cell proliferation, wound healing was delayed, an effect that was reversed by the GABA-B receptor antagonist CGP. cAMP levels were decreased in Huh-7 but not PLC cells exposed to baclofen. MMP expression remained unaltered in both cell lines. Finally, GABA-B1 receptor expression was present and consistently expressed, but GABA-B2 expression was limited and varied with the number of cell passages and (or) duration of culture. In conclusion, activation of GABA-B receptors has no effect on malignant hepatocyte proliferation but does decrease cell migration. This inhibitory effect may involve cAMP signaling but not MMP expression. GABA-B2 receptor expression is limited and variable, which may help to explain discrepancies with previously published results.

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Chen, Yongchang, Ying Wang, Hao Yu, Fengwei Wang et Wenrong Xu. « The Cross Talk Between Protein Kinase A– and RhoA-Mediated Signaling in Cancer Cells ». Experimental Biology and Medicine 230, n^o 10 (novembre 2005) : 731–41. http://dx.doi.org/10.1177/153537020523001006.

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The cross talk between cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) and RhoA-mediated signal transductions and the effect of this cross talk on biologic features of human prostate and gastric cancer cells were investigated. In the human gastric cancer cell line, SGC-7901, lysophosphatidic acid (LPA) increased RhoA activity in a dosedependent manner. The cellular permeable cAMP analog, 8-chlorophenylthio-cAMP (CPT-cAMP), inhibited the LPA-induced RhoA activation and caused phosphorylation of RhoA at serine188. Immunofluorescence microscopy, Western blotting, and green fluorescent protein (GFP)-tagged RhoA location assay in live cells revealed that RhoA was distributed in both the cytoplasm and nucleus of SGC-7901 cells. Treatment with LPA and/or CPT-cAMP did not induce obvious translocation of RhoA in the cells. The LPA treatment caused formation of F-actin in SGC-7901 cells, and CPT-cAMP inhibited the formation. In a modified Boyden chamber assay, LPA stimulated the migration of SGC-7901 cells, and CPT-cAMP dose-dependently inhibited the stimulating effect of LPA. In soft agar assay, LPA stimulated early proliferation of SGC-7901 cells, and CPT-cAMP significantly inhibited the growth of LPA-stimulated cells. In the prostate cancer cell line, PC-3, LPA caused morphologic changes from polygonal to round, and transfection with plasmid DNA encoding constitutively active RhoA(63L) caused a similar change. Treatment with CPT-cAMP inhibited the changes in both cases. However, in PC-3 cells transfected with a plasmid encoding mutant RhoA188A, LPA induced rounding, but CPT-cAMP could not prevent the change. Results of this experiment indicated that cAMP/PKA inhibited RhoA activation, and serine188 phosphorylation on RhoA was necessary for PKA to exert its inhibitory effect on RhoA activation. The cross talk between cAMP/PKA and RhoA-mediated signal transductions had significant affect on biologic features of gastric and prostate cancer cells, such as morphologic and cytoskeletal change, migration, and anchorage-independent growth. The results may be helpful in implementing novel therapeutic strategies for invasive and metastatic prostate and gastric cancers.

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Joyce, N. C., et B. Meklir. « PGE2 : a mediator of corneal endothelial wound repair in vitro ». American Journal of Physiology-Cell Physiology 266, n^o 1 (1 janvier 1994) : C269—C275. http://dx.doi.org/10.1152/ajpcell.1994.266.1.c269.

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Maintenance of the integrity of the corneal endothelial monolayer is essential for corneal clarity. Aging, trauma, inflammation, and diseases, such as diabetes, can compromise monolayer integrity, resulting in corneal edema and loss of visual acuity. In adult humans, repair of the monolayer occurs mainly by two forms of cell movement: "migration," in which individual cells move from the wound edge to repopulate the defect, and "spreading," in which cells enlarge and flatten, causing movement of the monolayer as a sheet to cover the defect. Previous studies from this laboratory have shown that these two forms of movement can be pharmacologically separated. In the current studies, an established tissue culture model was used to determine the effect of prostaglandin E2 (PGE2) and of mediators of the adenosine 3',5'-cyclic monophosphate (cAMP) pathway on individual cell migration. Indomethacin, an inhibitor of prostaglandin synthesis, significantly decreased individual cell migration below levels obtained when wounds were exposed to culture medium alone. PGE2, but not PGF2 alpha, restored this response in a dose-dependent manner. In the presence of indomethacin, forskolin, a direct adenylate cyclase activator, stimulated individual cell migration. 2',5'-Dideoxyadenosine, an adenylate cyclase inhibitor, reversed the stimulatory effects of both forskolin and PGE2. Dibutyryl cAMP (DBcAMP) also stimulated individual cell migration in the presence of indomethacin, whereas, H89, a protein kinase A inhibitor, reversed both the DBcAMP and PGE2-induced effects. These results provide evidence that stimulation of the cAMP pathway enhances individual cell migration and that PGE2, acting via this pathway, may be an endogenous stimulator of this response during corneal endothelial wound repair.

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Dong, Hongli, Kevin P. Claffey, Stefan Brocke et Paul M. Epstein. « Inhibition of breast cancer cell migration by activation of cAMP signaling ». Breast Cancer Research and Treatment 152, n^o 1 (29 mai 2015) : 17–28. http://dx.doi.org/10.1007/s10549-015-3445-9.

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Blindt, Rüdiger, Anja-K. Bosserhoff, Jürgen vom Dahl, Peter Hanrath, Karsten Schrör, Thomas Hohlfeld et Jutta Meyer-Kirchrath. « Activation of IP and EP3 receptors alters cAMP-dependent cell migration ». European Journal of Pharmacology 444, n^o 1-2 (mai 2002) : 31–37. http://dx.doi.org/10.1016/s0014-2999(02)01607-2.

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Millner, Naomi. « Routing the camp : experiential authority in a politics of irregular migration ». Journal of Political Power 6, n^o 1 (avril 2013) : 87–105. http://dx.doi.org/10.1080/2158379x.2013.774978.

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Chen, Lin, J. Jillian Zhang et Xin-Yun Huang. « cAMP Inhibits Cell Migration by Interfering with Rac-induced Lamellipodium Formation ». Journal of Biological Chemistry 283, n^o 20 (19 mars 2008) : 13799–805. http://dx.doi.org/10.1074/jbc.m800555200.

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Lim, Chinten J., Kristin H. Kain, Eugene Tkachenko, Lawrence E. Goldfinger, Edgar Gutierrez, Michael D. Allen, Alex Groisman, Jin Zhang et Mark H. Ginsberg. « Integrin-mediated Protein Kinase A Activation at the Leading Edge of Migrating Cells ». Molecular Biology of the Cell 19, n^o 11 (novembre 2008) : 4930–41. http://dx.doi.org/10.1091/mbc.e08-06-0564.

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cAMP-dependent protein kinase A (PKA) is important in processes requiring localized cell protrusion, such as cell migration and axonal path finding. Here, we used a membrane-targeted PKA biosensor to reveal activation of PKA at the leading edge of migrating cells. Previous studies show that PKA activity promotes protrusion and efficient cell migration. In live migrating cells, membrane-associated PKA activity was highest at the leading edge and required ligation of integrins such as α4β1 or α5β1 and an intact actin cytoskeleton. α4 integrins are type I PKA-specific A-kinase anchoring proteins, and we now find that type I PKA is important for localization of α4β1 integrin-mediated PKA activation at the leading edge. Accumulation of 3′ phosphorylated phosphoinositides [PtdIns(3,4,5)P3] products of phosphatidylinositol 3-kinase (PI3-kinase) is an early event in establishing the directionality of migration; however, polarized PKA activation did not require PI3-kinase activity. Conversely, inhibition of PKA blocked accumulation of a PtdIns(3,4,5)P3-binding protein, the AKT-pleckstrin homology (PH) domain, at the leading edge; hence, PKA is involved in maintaining cell polarity during migration. In sum, we have visualized compartment-specific PKA activation in migrating cells and used it to reveal that adhesion-mediated localized activation of PKA is an early step in directional cell migration.

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Bradley, Megan. « The International Organization for Migration (IOM) : Gaining Power in the Forced Migration Regime ». Refuge : Canada's Journal on Refugees 33, n^o 1 (23 mars 2017) : 97–106. http://dx.doi.org/10.25071/1920-7336.40452.

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The International Organization for Migration (IOM) remains understudied, despite its dramatic growth in recent decades, particularly in the humanitarian sphere. In this article I examine key factors driving IOM’s expansion, and implications for the forced migration regime. Despite lacking a formal protection mandate, IOM has thrived by acting as an entrepreneur, capitalizing on its malleability and reputation for efficiency, and carving out distinctive roles in activities including post-disaster camp management, data collection, and assistance for migrant workers in crises. I reflect on IOM’s efforts to accrue increased authority and power, and suggest that understanding IOM’s humanitarian engagements is now essential to understanding the organization itself and, increasingly, the forced migration regime.

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Yarwood, S. J. « Microtubule-associated proteins (MAPs) regulate cAMP signalling through exchange protein directly activated by cAMP (EPAC) ». Biochemical Society Transactions 33, n^o 6 (26 octobre 2005) : 1327–29. http://dx.doi.org/10.1042/bst0331327.

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cAMP is an essential signalling molecule whose concentration in cells is regulated by a wide range of hormones. A large number of diseases, including cancer and asthma, are linked to improper regulation of the cAMP signalling system, and manipulation of cAMP levels by pharmaceutical agents has proven therapeutic benefit. The action of cAMP in cells is mediated through the signalling enzymes PKA (protein kinase A) and EPAC (exchange protein directly activated by cAMP). The study of the function of these proteins is essential to understand the role of cAMP in controlling disease. We have found that EPAC interacts with an ancillary protein, called LC2 (light chain 2), and this interaction enhances EPAC's ability to activate its substrate protein, Rap1 GTPase. This is an important finding because Rap1 is involved in the control of cell migration and cell shape, functions that are disrupted in diseases like cancer. LC2 appears to enhance EPAC activity towards Rap1 by increasing the ability of EPAC to interact with cAMP, so that EPAC activation occurs at lower concentrations of cAMP. The design of inhibitors that disrupt or enhance EPAC1–LC2 interaction may therefore form the basis of future therapeutics for diseases where cAMP signalling through Rap1 is improperly regulated.

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Liu, Chunfeng, Hao Wang, Mo Yang, Yiheng Liang, Li Jiang, Siman Sun et Shangrong Fan. « Downregulation of cAMP-Dependent Protein Kinase Inhibitor-b Promotes Preeclampsia by Decreasing Phosphorylated Akt ». Reproductive Sciences 28, n^o 1 (16 juillet 2020) : 178–85. http://dx.doi.org/10.1007/s43032-020-00258-8.

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AbstractPreeclampsia is a multi-system disease that is unique to human pregnancy. Impaired extravillous trophoblast migration and invasion accompanied by poor spiral vascular remodeling is thought to be the initial reason. This study investigated cAMP-dependent protein kinase inhibitor-b(PKIB) expression in placentas and its involvement in the pathogenesis of PE. We used immunohistochemistry and western blotting to calculate PKIB levels in the placentas. Then we knocked down PKIB by siRNA and used real-time cell analysis to assess the invasion and migration ability of trophoblasts. Tube formation assay and spheroid sprouting assay were utilized to identify the ability to form vessels of trophoblasts. At last, western blotting was used to demonstrate the level of phosphorylated Akt, as well as downstream-related genes of Akt signaling pathway in trophoblasts. We first found that PKIB expression level was lower in the PE placentas than in the normal placentas. In addition, we found that downregulation of PKIB can inhibit the migration, invasion, and the ability to form vessels of HTR8/SVneo cells. Downregulation of PKIB leaded to a decrease in phosphorylated Akt, as well as downstream proteins such as matrix metalloproteinase 2, matrix metalloproteinase 9, and glycogen synthase kinase 3β, which are related to migration and invasion. Our study revealed that the downregulation of PKIB expression resulted in decreased migration, invasion, and vessel formation ability by regulating Akt signaling pathway in placental trophoblasts in PE.

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Ndiaye, M., C. Rébé, A. Ilie, L. Ménégaut, T. Pilot et F. Ghiringhelli. « P07.02 Enhanced glycolysis in glioblastomas is associated with tumor cells migration ». Neuro-Oncology 21, Supplement_3 (août 2019) : iii36—iii37. http://dx.doi.org/10.1093/neuonc/noz126.126.

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Abstract BACKGROUND Glioblastoma is the most common primary brain tumor. Its prognosis remains poor even with the standard treatment - the Stupp protocol.The classic Warburg effect in cancers leads to increased glycolysis which causes acidification of the tumor environment. This phenomenon may favor migration of tumor cells as already reported in pancreatic ductal adenocarcinoma. We therefore hypothesized that enhanced glycolysis in glioblastomas could favor the tumor cell migration. MATERIAL AND METHODS We measured glycolysis by the extracellular acidification rate (ECAR) of several human glioblastomas cell lines (LN229, LN18, T98-G, U87-MG, U373-MG, U118-MG) with the Seahorse Analyzer. To confirm these results, we also measured the intracellular cAMP rates using the Cayman’s Elisa kit and we analyzed by RT-PCR the expression of the main genes coding for enzymes involved in glycolysis in these glioblastomas cell lines. Cell migration was measured with a scratch wound healing assay during 24 hours. RESULTS U118-MG was the glioblastoma cell line with the highest glycolysis rate, the highest production of cAMP and showed a strong expression of glycolysis-associated genes. LN229 was the glioblastoma cell line with the less important glycolysis rate, the lower production of cAMP and showed a weaker expression of glycolysis-associated genes. According to the scratch wound healing assay, U118-MG cells showed a more important migration than LN229 cells at 24 hours. CONCLUSION Glycolysis may be an attractive target to prevent effectively tumor cell migration in glioblastomas. Coupling the evaluation of glycolysis with histomolecular characterization of glioblastomas, could help to identify patients to whom adjuvant therapies that inhibit glycolysis such as fenofibrate could be proposed.

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Lindberg, Annika. « Feeling difference : Race, migration, and the affective infrastructure of a Danish detention camp ». Incarceration 3, n^o 1 (mars 2022) : 263266632210845. http://dx.doi.org/10.1177/26326663221084590.

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Migration-related detention, the administrative incarceration of people lacking legal authorisation to remain, has become a standardised technique used by states to violently regulate and discipline undesired mobility. As carceral junctions, migration detention camps serve to identify, confine, symbolically punish and expel people deemed ‘out of place’ in the national order of things. As bordering mechanisms, they are techniques of sorting and controlling populations, and sites where we can observe the enforcement of state racism. These processes of racialisation and expulsion operate corporally and affectively. Drawing on ethnographic fieldwork with prison officers working inside Denmark's migration-related detention camp, and engaging with the literature on race, emotion and border criminology, the article traces the role of racial affect in forging the identities of people interacting inside the camp. It demonstrates how prison officers’ racialised suspicion, compromised compassion, and passionate nationalism partake in making incarcerated migrants into expellable subjects, and in ordering them in accordance with matrices of racial differentiation. The officers’ emotions, I argue, should be understood as part of the camp's infrastructure, and productive for the border regime.

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McKean, Jenny S., Fiona Murray, George Gibson, Derryck A. Shewan, Steven J. Tucker et Graeme F. Nixon. « The cAMP-producing agonist beraprost inhibits human vascular smooth muscle cell migration via exchange protein directly activated by cAMP ». Cardiovascular Research 107, n^o 4 (19 juin 2015) : 546–55. http://dx.doi.org/10.1093/cvr/cvv176.

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Nová, Monika. « Dimension of Migration – Challenge or Concern for European Future ? » INTERNATIONAL JOURNAL OF INNOVATION AND ECONOMIC DEVELOPMENT 5, n^o 3 (2019) : 19–24. http://dx.doi.org/10.18775/ijied.1849-7551-7020.2015.53.2002.

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Migration is a significant process through which the dynamics of population on the move substantially affect the long-term development of mankind. During the recent sixty years, a host of citizens of the world have enjoyed improvements in the key indicators of development, such as the life expectancy and access to education and/or medical services, though, admittedly, this rule does not apply to all countries and all regions. Relying on her argument on historical facts complemented by current events, the author of the paper presents the chosen subject of migration as it relates to the European future and to the demographic patterns of migration. The article deals with the current wave of migration – it is about integration and people on the road. The arguments that the author puts forward rely, inter alia, on her personal experience gathered in a refugee camp a.k.a. the hotspot.

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Kilanowska, Agnieszka, Agnieszka Ziółkowska, Piotr Stasiak et Magdalena Gibas-Dorna. « cAMP-Dependent Signaling and Ovarian Cancer ». Cells 11, n^o 23 (29 novembre 2022) : 3835. http://dx.doi.org/10.3390/cells11233835.

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cAMP-dependent pathway is one of the most significant signaling cascades in healthy and neoplastic ovarian cells. Working through its major effector proteins—PKA and EPAC—it regulates gene expression and many cellular functions. PKA promotes the phosphorylation of cAMP response element-binding protein (CREB) which mediates gene transcription, cell migration, mitochondrial homeostasis, cell proliferation, and death. EPAC, on the other hand, is involved in cell adhesion, binding, differentiation, and interaction between cell junctions. Ovarian cancer growth and metabolism largely depend on changes in the signal processing of the cAMP-PKA-CREB axis, often associated with neoplastic transformation, metastasis, proliferation, and inhibition of apoptosis. In addition, the intracellular level of cAMP also determines the course of other pathways including AKT, ERK, MAPK, and mTOR, that are hypo- or hyperactivated among patients with ovarian neoplasm. With this review, we summarize the current findings on cAMP signaling in the ovary and its association with carcinogenesis, multiplication, metastasis, and survival of cancer cells. Additionally, we indicate that targeting particular stages of cAMP-dependent processes might provide promising therapeutic opportunities for the effective management of patients with ovarian cancer.

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