Articoli di riviste: "RANTES"

1

Hoover, David M., Jeffrey Shaw, Zygmunt Gryczynski, Amanda E. I. Proudfoot, Tim Wells e Jacek Lubkowski. "The crystal structure of met-rantes: comparison with native rantes and aop-rantes". Protein & Peptide Letters 7, n. 2 (aprile 2000): 73–82. http://dx.doi.org/10.2174/092986650702221206112548.

Testo completo

Abstract (sommario):

Abstract: Met-RANTES is a modified version of the chemokine RANTES, which has an additional amino acid at the amino terminus. To compare Met-RANTES with the native protein as well as with another antagonist, AOP RANTES, we have solved the structure of Met-RANTES at 1.6 A by X-ray crystallography and investigated the dimerization of all three proteins by fluorescence anisotropy. The dimerization of AOP-RANTES shows an altered aggregation profile. The delineation of slight differences in binding sulfate anions by Met- and AOP RANTES might be linked to specific yet different interactions between these proteins and glycosaminoglycans.

Gli stili APA, Harvard, Vancouver, ISO e altri

2

McLean, Adam. "Regulation with RANTES". Lancet 343, n. 8891 (gennaio 1994): 189–90. http://dx.doi.org/10.1016/s0140-6736(94)90985-7.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

3

Pattison, James M., Peter J. Nelson e Alan M. Krensky. "The RANTES Chemokine". Clinical Immunotherapeutics 4, n. 1 (luglio 1995): 1–8. http://dx.doi.org/10.1007/bf03259067.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

4

Proudfoot, Amanda E. I., Raphaële Buser, Fredéric Borlat, Sami Alouani, Dulce Soler, Robin E. Offord, Jens-Michel Schröder, Christine A. Power e Timothy N. C. Wells. "Amino-terminally Modified RANTES Analogues Demonstrate Differential Effects on RANTES Receptors". Journal of Biological Chemistry 274, n. 45 (5 novembre 1999): 32478–85. http://dx.doi.org/10.1074/jbc.274.45.32478.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

5

Rutherford, Adam, e Jonathan Weitzman. "Split-personality RANTES mutation". Trends in Molecular Medicine 7, n. 1 (gennaio 2001): 12. http://dx.doi.org/10.1016/s1471-4914(00)01893-1.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

6

Hayashi, Kunio, Shosaku Nomura, Atsuko Mugitani, Minoru Hasegawa, Nobuhiko Uoshima, Takayuki Takubo, Masahiro Kami, Tsunehiko Komatsu, Tamae Hamaki e Toshio Shimokawa. "Chemokine RANTES (Regulated upon Activation, Normal T Cell Expressed and Secreted) in Multiple Myeloma and MGUS (Monoclonal Gammopathy of Undetermined Significance)." Blood 110, n. 11 (16 novembre 2007): 4756. http://dx.doi.org/10.1182/blood.v110.11.4756.4756.

Testo completo

Abstract (sommario):

Abstract Introduction: Bone disease in patients with myeloma is the devastating complication. RANTES (CCR chemokine, Regulated upon Activation,Normal T Cell Expressed and Secreted) is involved in the bone remodeling that is made by coupled functions of osteoclasts and osteoblasts. Osteoclasts represent the RANTES receptor CCR1 and product RANTES. Osteoblasts express CCR1,3,4,5, and also product RANTES. Osteoblasts chemotaxicaly move to osteoclasts to repair the absorbed bone lesions (Shozo Yano et al., Endocrinology Vol.145, No.5, 2324–2335). The bone pathophysiology of multiple myeloma is the distortion of the well-balanced functions of osteoclast and osteobast. The change of RANTES may be representative of this distortion and the restoration of bone. Method: Blood samples were collected from 54 patients with Multiple Myeloma, 15 patients with MGUS, 41 from donors (30 healthy people or 11 people who have no bone disease). Plasma samples were separated and analyzed by ELISA to determine the levels of RANTES. Result: In healthy people, RANTES changes in proportion to ages with sexual difference. The value of RANTES is 155000pg/ml in20ys male, 51100pg/ml in 20ys female, 133000pg/ml in 40ys male and 78933 pg/ml in 40ys female. The difference of male and female becomes smaller and the value becomes nearly 60000pg/ml at sixty ages in male and female. Serum-bone specific alkaline phosphatase (BAP) is a biochemical indicator of bone turnover and urinary collagen type 1 cross-linked N-telopeptide (NTX) excretion normalized to creatinine (NTX/Cr) from urine sample is a bone resorption marker. At sixty ages, BAP and NTX/Cr become lower in accord with RANTES. In Myeloma cases, RANTES is about 20000pg/ml lower than the age-related value in female and about 75000pg/ml higher in male. After the treatment, RANRES increases in most of patients (both male and female) who have got response after chemotherapy. The rise of female is average 34566pg/ml but the rise of male is very small, average 5250pg/ml, because RANTES has already increased before chemotherapy. Beyond our expectation,RANTES of MGUS is almost the same as Myeloma. Discussion: The bone remodeling activity of male is higher than female and may be easily induced by the chance of bone absorption. The data suggest that tumor growth suppression produces the recovery of the remodeling. The value of RANTES of MGUS indicates why some patients with MGUS have the punched-out lesions like Myeloma. Conclusion: This study has turned out for the first time that RANTES is associated with the bone pathophysiology of multiple myeloma and MGUS.

Gli stili APA, Harvard, Vancouver, ISO e altri

7

Rodríguez-Frade, José M., Antonio J. Vila-Coro, Ana Martín, Marta Nieto, Francisco Sánchez-Madrid, Amanda E. I. Proudfoot, Timothy N. C. Wells, Carlos Martínez-A e Mario Mellado. "Similarities and Differences in RANTES- and (AOP)-RANTES–triggered Signals: Implications for Chemotaxis". Journal of Cell Biology 144, n. 4 (22 febbraio 1999): 755–65. http://dx.doi.org/10.1083/jcb.144.4.755.

Testo completo

Abstract (sommario):

Chemokines are a family of proinflammatory cytokines that attract and activate specific types of leukocytes. Chemokines mediate their effects via interaction with seven transmembrane G protein–coupled receptors (GPCR). Using CCR5-transfected HEK-293 cells, we show that both the CCR5 ligand, RANTES, as well as its derivative, aminooxypentane (AOP)- RANTES, trigger immediate responses such as Ca2+ influx, receptor dimerization, tyrosine phosphorylation, and Gαi as well as JAK/STAT association to the receptor. In contrast to RANTES, (AOP)-RANTES is unable to trigger late responses, as measured by the association of focal adhesion kinase (FAK) to the chemokine receptor complex, impaired cell polarization required for migration, or chemotaxis. The results are discussed in the context of the dissociation of the late signals, provoked by the chemokines required for cell migration, from early signals.

Gli stili APA, Harvard, Vancouver, ISO e altri

8

Mack, Matthias, Bruno Luckow, Peter J. Nelson, Josef Cihak, Graham Simmons, Paul R. Clapham, Nathalie Signoret et al. "Aminooxypentane-RANTES Induces CCR5 Internalization but Inhibits Recycling: A Novel Inhibitory Mechanism of HIV Infectivity". Journal of Experimental Medicine 187, n. 8 (20 aprile 1998): 1215–24. http://dx.doi.org/10.1084/jem.187.8.1215.

Testo completo

Abstract (sommario):

CCR5, a chemokine receptor expressed on T cells and macrophages, is the principal coreceptor for M-tropic HIV-1 strains. Recently, we described an NH2-terminal modification of the CCR5 ligand regulated on activation, normal T cell expressed and secreted (RANTES), aminooxypentane-RANTES (AOP-RANTES), that showed potent inhibition of macrophage infection by HIV-1 under conditions where RANTES was barely effective. To investigate the mechanism of AOP-RANTES inhibition of HIV infectivity we examined the surface expression of CCR5 using a monoclonal anti-CCR5 antibody, MC-1. We demonstrate that AOP-RANTES rapidly caused >90% decrease in cell surface expression of CCR5 on lymphocytes, monocytes/ macrophages, and CCR5 transfected Chinese hamster ovary (CHO) cells. RANTES also caused a loss of cell surface CCR5, although its effect was less than with AOP-RANTES. Significantly, AOP-RANTES inhibited recycling of internalized CCR5 to the cell surface, whereas RANTES did not. When peripheral blood mononuclear cells are cultured for prolonged periods of time in the presence of RANTES, CCR5 expression is comparable to that seen on cells treated with control medium, whereas there is no CCR5 surface expression on cells cultured in the presence of AOP-RANTES. Immunofluorescence indicated that both AOP-RANTES and RANTES induced downmodulation of cell surface CCR5, and that the receptor was redistributed into endocytic organelles containing the transferrin receptor. When RANTES was removed, the internalized receptor was recycled to the cell surface; however, the receptor internalized in the presence of AOP-RANTES was retained in endosomes. Using human osteosarcoma (GHOST) 34/CCR5 cells, the potency of AOP-RANTES and RANTES to inhibit infection by the M-tropic HIV-1 strain, SF 162, correlated with the degree of downregulation of CCR5 induced by the two chemokines. These differences between AOP-RANTES and RANTES in their effect on receptor downregulation and recycling suggest a mechanism for the potent inhibition of HIV infection by AOP-RANTES. Moreover, these results support the notion that receptor internalization and inhibition of receptor recycling present new targets for therapeutic agents to prevent HIV infection.

Gli stili APA, Harvard, Vancouver, ISO e altri

9

Terao, Satoshi. "Chemokine RANTES in brain infarction". Cerebral Blood Flow and Metabolism (Japanese journal of cerebral blood flow and metabolism) 28, n. 2 (2017): 327–31. http://dx.doi.org/10.16977/cbfm.28.2_327.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

10

Graziano, Frank M., Ellen B. Cook e James L. Stahl. "Cytokines, Chemokines, RANTES, and Eotaxin". Allergy and Asthma Proceedings 20, n. 3 (1 maggio 1999): 141–46. http://dx.doi.org/10.2500/108854199778553055.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

11

SNOWDEN, N. "RANTES role in rheumatoid arthritis". Lancet 343, n. 8896 (febbraio 1994): 547–48. http://dx.doi.org/10.1016/s0140-6736(94)91503-2.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

12

Arenberger, Petr, Peter Nelson, Anil Abraham e Richard O. Leder. "Anti-rantes immunoreactivity in skin". Journal of Dermatological Science 6, n. 1 (agosto 1993): 72. http://dx.doi.org/10.1016/0923-1811(93)91127-g.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

13

Bai, Bingxue, Keiko Tanaka, Takahiro Tazawa, Naoko Yamamoto e Hisashi Sugiura. "Association between RANTES promoter polymorphism −401A and enhanced RANTES production in atopic dermatitis patients". Journal of Dermatological Science 39, n. 3 (settembre 2005): 189–91. http://dx.doi.org/10.1016/j.jdermsci.2005.06.003.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

14

Mori, Naoki, Alan M. Krensky, Romas Geleziunas, Akihiro Wada, Toshiya Hirayama, Chihiro Sasakawa e Naoki Yamamoto. "Helicobacter pylori Induces RANTES through Activation of NF-κB". Infection and Immunity 71, n. 7 (luglio 2003): 3748–56. http://dx.doi.org/10.1128/iai.71.7.3748-3756.2003.

Testo completo

Abstract (sommario):

ABSTRACT Helicobacter pylori-infected gastric mucosa displays a conspicuous infiltration of mononuclear cells and neutrophils. RANTES (short for “regulated upon activation, normal T cell expressed and secreted”) is a chemoattractant cytokine (chemokine) important in the infiltration of T lymphocytes and monocytes. RANTES may therefore contribute to the cellular infiltrate in the H. pylori-infected gastric mucosa. The aim of this study was to analyze the molecular mechanism responsible for H. pylori-mediated RANTES expression. We observed that gastric epithelial cells produced RANTES upon coculture with H. pylori. In addition, H. pylori induced RANTES mRNA expression and an increase in luciferase activity in cells which were transfected with a luciferase reporter construct derived from the RANTES promoter, in gastric epithelial cells, indicating that the induction of RANTES production occurred at the transcriptional level. Induction of RANTES was dependent on an intact cag pathogenicity island. Activation of the RANTES promoter by H. pylori occurred through the action of NF-κB. Transfection of kinase-deficient mutants of IκB kinase (IKK) and NF-κB-inducing kinase (NIK) inhibited H. pylori-mediated RANTES activation. In contrast, tumor necrosis factor alpha- or interleukin-1/Toll-like receptor signaling molecules—such as mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1, MyD88, and interleukin-1 receptor-associated kinase—did not play a role in RANTES activation by H. pylori. Collectively, H. pylori induced NF-κB activation through an intracellular signaling pathway that involved IKK and NIK, leading to RANTES gene transcription. RANTES induction by H. pylori may play an important role in gastric inflammation.

Gli stili APA, Harvard, Vancouver, ISO e altri

15

FRANK, Stefan, Heiko KÄMPFER, Christian WETZLER, Birgit STALLMEYER e Josef PFEILSCHIFTER. "Large induction of the chemotactic cytokine RANTES during cutaneous wound repair: a regulatory role for nitric oxide in keratinocyte-derived RANTES expression". Biochemical Journal 347, n. 1 (27 marzo 2000): 265–73. http://dx.doi.org/10.1042/bj3470265.

Testo completo

Abstract (sommario):

We investigated the role of NO on expressional regulation of the chemotactic cytokine RANTES (regulated upon activation, normal T-cell expressed and secreted) during tissue regeneration using an excisional wound-healing model in mice. Wound repair was characterized by a large and sustained induction of RANTES expression, and inhibition of inducible nitric oxide synthase (iNOS) during repair only slightly decreased RANTES expression levels. Immunohistochemical analysis revealed keratinocytes of the wound margins and the hyperproliferative epithelium to be the main RANTES-expressing cell type within the wound. Therefore we analysed the regulation of RANTES expression in vitro in cultured human keratinocytes of the cell line HaCaT. Here we demonstrate that NO very efficiently suppressed interleukin-1β- and tumour-necrosis-factor-α-induced RANTES expression in keratinocytes. Furthermore, down-regulation of cytokine-induced RANTES mRNA in keratinocytes was dependent on endogenously produced NO, as inhibition of the co-induced iNOS by L-NG-monomethyl-L-arginine increased cytokine-triggered RANTES expression in the cells. Moreover, we observed strongest RANTES-immunopositive labelling in epithelial areas which were characterized by a NO-mediated low cellularity. Thus our data implicate NO as a negative regulator of RANTES expression during wound repair in vivo, as decreased numbers of keratinocytes observed in the absence of wound-derived NO might compensate for the high levels of RANTES expression which are associated with normal repair.

Gli stili APA, Harvard, Vancouver, ISO e altri

16

Gordon, Cynthia J., Mark A. Muesing, Amanda E. I. Proudfoot, Christine A. Power, John P. Moore e Alexandra Trkola. "Enhancement of Human Immunodeficiency Virus Type 1 Infection by the CC-Chemokine RANTES Is Independent of the Mechanism of Virus-Cell Fusion". Journal of Virology 73, n. 1 (1 gennaio 1999): 684–94. http://dx.doi.org/10.1128/jvi.73.1.684-694.1999.

Testo completo

Abstract (sommario):

ABSTRACT We have studied the effects of CC-chemokines on human immunodeficiency virus type 1 (HIV-1) infection, focusing on the infectivity enhancement caused by RANTES. High RANTES concentrations increase the infectivity of HIV-1 isolates that use CXC-chemokine receptor 4 for entry. However, RANTES can have a similar enhancing effect on macrophagetropic viruses that enter via CC-chemokine receptor 5 (CCR5), despite binding to the same receptor as the virus. Furthermore, RANTES enhances the infectivity of HIV-1 pseudotyped with the envelope glycoprotein of murine leukemia virus or vesicular stomatitis virus, showing that the mechanism of enhancement is independent of the route of virus-cell fusion. The enhancing effects of RANTES are not mediated via CCR5 or other known chemokine receptors and are not mimicked by MIP-1α or MIP-1β. The N-terminally modified derivative aminooxypentane RANTES (AOP-RANTES) efficiently inhibits HIV-1 infection via CCR5 but otherwise mimics RANTES by enhancing viral infectivity. There are two mechanisms of enhancement: one apparent when target cells are pretreated with RANTES (or AOP-RANTES) for several hours, and the other apparent when RANTES (or AOP-RANTES) is added during virus-cell absorption. We believe that the first mechanism is related to cellular activation by RANTES, whereas the second is an increase in virion attachment to target cells.

Gli stili APA, Harvard, Vancouver, ISO e altri

17

von Hundelshausen, Philipp, Rory R. Koenen, Markus Sack, Sebastian F. Mause, Wencke Adriaens, Amanda E. I. Proudfoot, Tilman M. Hackeng e Christian Weber. "Heterophilic interactions of platelet factor 4 and RANTES promote monocyte arrest on endothelium". Blood 105, n. 3 (1 febbraio 2005): 924–30. http://dx.doi.org/10.1182/blood-2004-06-2475.

Testo completo

Abstract (sommario):

AbstractThe chemokines platelet factor 4 (PF4) and RANTES (regulated on activation normal T cell expressed and secreted) are secreted by activated platelets and influence multiple cell types and biologic processes. For instance, PF4 inhibits progenitor cell proliferation and angiogenesis, while platelet-derived RANTES is involved in vascular recruitment of monocytes. However, little is known about functional interactions of PF4 and RANTES. Here we show that the presence of PF4 enhanced the arrest of RANTES-stimulated monocytes and monocytic cells on activated endothelial cells under flow conditions, while binding of PF4 to the monocyte surface was increased by RANTES. Both RANTES-triggered arrest and PF4 binding involved monocytic chondroitin sulfate. Ligand blots and surface plasmon resonance revealed a robust heterophilic interaction of PF4 with RANTES but not with RANTES variants defective in higher order oligomerization. The tetrameric mutant E26A bound to the monocyte surface without increasing PF4 binding, and monocyte arrest induced by E26A-RANTES was not enhanced by PF4. Stimulation of monocytes with supernatants of activated platelets triggered arrest involving RANTES and PF4, as shown by inhibition studies. Our results suggest that heterophilic interactions with PF4 require structural motifs important in RANTES oligomerization and amplify RANTES-triggered effects on monocyte adhesion. This may have implications for the modulation of inflammatory recruitment by platelet-derived chemokines.

Gli stili APA, Harvard, Vancouver, ISO e altri

18

Dairaghi, Daniel J., Kenneth S. Soo, Elizabeth R. Oldham, Brett A. Premack, Toshio Kitamura, Kevin B. Bacon e Thomas J. Schall. "RANTES-Induced T Cell Activation Correlates with CD3 Expression". Journal of Immunology 160, n. 1 (1 gennaio 1998): 426–33. http://dx.doi.org/10.4049/jimmunol.160.1.426.

Testo completo

Abstract (sommario):

Abstract The chemokine RANTES induces a unique biphasic cytoplasmic Ca2+ signal in T cells. The first phase of this signal, similar to that of other chemokines, is G-protein mediated and chemotaxis associated. The second phase of this signal, unique to RANTES and evident at concentrations greater than 100 nM, is tyrosine kinase linked and results in a spectrum of responses similar to those seen with antigenic stimulation of T cells. We show here that certain Jurkat T cells responded to RANTES solely through this latter pathway. A direct correlation between the RANTES-induced second phase response and CD3 expression was demonstrated in these cells. Sorting the Jurkat cells into CD3high and CD3low populations revealed that only the CD3high cells were responsive to RANTES. Furthermore, stimulation of these Jurkat cells with anti-CD3 mAb significantly depresses their subsequent response to RANTES. While a RANTES-specific chemokine receptor is expressed at a low level on these Jurkat cells, the RANTES-induced activation is dependent on the presence of the TCR. Thus, stimulation through TCR may partially account for RANTES’ unique pattern of signaling in T cells.

Gli stili APA, Harvard, Vancouver, ISO e altri

19

Allen, Jerilyn S., Roselle Eisma, Gerald Leonard, Denis Lafreniere e Donald Kreutzer. "Characterization of the Eosinophil Chemokine Rantes in Nasal Polyps". Annals of Otology, Rhinology & Laryngology 107, n. 5 (maggio 1998): 416–20. http://dx.doi.org/10.1177/000348949810700510.

Testo completo

Abstract (sommario):

Previous studies have demonstrated that the cytokine RANTES (Regulated And Normal T cell Expressed and Secreted) has been shown to be a potent mediator of eosinophil Chemotaxis in vitro and of leukocyte recruitment. Because eosinophils are the hallmark cells in nasal polyposis, we hypothesize that RANTES is locally produced within the nasal polyp microenvironment and is responsible for the eosinophil recruitment seen in nasal polyposis. To begin to test this hypothesis, we evaluated nasal polyps from 17 patients and 3 control specimens for distribution and content of RANTES using immunohistochemical techniques and enzyme-linked immunosorbent assay technology. Our immunohistochemical studies demonstrated that in nasal polyposis, RANTES antigen staining occurred predominantly within eosinophils and epithelial cells. To quantify the relative levels of RANTES in normal and nasal polyp specimens, tissue homogenates were prepared, quantified, and normalized to protein levels. We detected RANTES in all 17 nasal polyp tissue homogenates (566 ± 16 pg/mg total protein). The RANTES levels in nasal polyp homogenates were nearly 40-fold higher man the RANTES levels in normal tissue (15.7 ± 28.2 pg/mg total protein). Thus, it appears that increased expression of RANTES by eosinophils and epithelial cells within the nasal polyp microenvironment promotes eosinophil recruitment and activation within nasal polyps. We hypothesize that RANTES induces increased recruitment and activation of eosinophils, presumably contributing to the increased tissue changes associated with nasal polyposis.

Gli stili APA, Harvard, Vancouver, ISO e altri

20

Yano, Shozo, Romuald Mentaverri, Deepthi Kanuparthi, Sanghamitra Bandyopadhyay, Alicia Rivera, Edward M. Brown e Naibedya Chattopadhyay. "Functional Expression of β-Chemokine Receptors in Osteoblasts: Role of Regulated upon Activation, Normal T Cell Expressed and Secreted (RANTES) in Osteoblasts and Regulation of Its Secretion by Osteoblasts and Osteoclasts". Endocrinology 146, n. 5 (1 maggio 2005): 2324–35. http://dx.doi.org/10.1210/en.2005-0065.

Testo completo

Abstract (sommario):

Abstract The expression and functions of receptors for the β-chemokine, regulated upon activation, normal T cell expressed, and secreted (RANTES)/CCL5, were investigated in osteoblasts. Both primary osteoblasts and the MC3T3-E1 osteoblast cell line express the RANTES receptors, CCR1, 3, 4, and 5 (by RT-PCR), which encode functional receptors in osteoblasts as shown by [125I]-RANTES binding followed by Scatchard analysis. Expression of all four RANTES receptor mRNAs in osteoblast is in contrast to the reports of expression of CCR1 being the only RANTES receptor expressed by osteoclasts. Exogenous RANTES elicits chemotaxis of osteoblasts and promotes cell survival via phosphatidylinositol 3-kinase with attendant phosphorylation of Akt. Osteoclastic RANTES, obtained from the conditioned medium of receptor activator of nuclear factor-κB ligand-differentiated RAW264.7 cells also induces chemotaxis of MC3T3-E1 cells. Incubating the conditioned medium with an anti-RANTES neutralizing antibody attenuated this effect. RANTES secretion from osteoblast is inhibited by differentiation promoting hormones, e.g. 1,25 (OH)2D3 and dexamethasone, whereas macrophage inflammatory protein-1α (but not macrophage inflammatory protein-1β) and elevated calcium induce it. Elevated calcium also stimulated RANTES secretion by osteoclasts. Therefore, RANTES is an osteoblast chemoattractant and a survival-promoting molecule whose regulation in osteoblast is varied. Furthermore, RANTES secreted from osteoclasts induces osteoblast chemotaxis. Therefore, expression of RANTES and its receptors in both osteoblasts and osteoclasts could enable this chemokine to act in autocrine/paracrine modes.

Gli stili APA, Harvard, Vancouver, ISO e altri

21

Ayad, Onsy, James M. Stark, Michael M. Fiedler, Ingrid Y. Menendez, Marnie A. Ryan e Hector R. Wong. "The Heat Shock Response Inhibits RANTES Gene Expression in Cultured Human Lung Epithelium". Journal of Immunology 161, n. 5 (1 settembre 1998): 2594–99. http://dx.doi.org/10.4049/jimmunol.161.5.2594.

Testo completo

Abstract (sommario):

Abstract The chemokine RANTES is thought to be involved in the pathophysiology of inflammation-associated acute lung injury. Although much is known regarding signals that induce RANTES gene expression, relatively few data exist regarding signals that inhibit RANTES gene expression. The heat shock response, a highly conserved cellular defense mechanism, has been demonstrated to inhibit a variety of lung proinflammatory responses. We tested the hypothesis that induction of the heat shock response inhibits RANTES gene expression. Treatment of A549 cells with TNF-α induced RANTES gene expression in a concentration-dependent manner. Induction of the heat shock response inhibited subsequent TNF-α-mediated RANTES mRNA expression and secretion of immunoreactive RANTES. Transient transfection assays involving a RANTES promoter-luciferase reporter plasmid demonstrated that the heat shock response inhibited TNF-α-mediated activation of the RANTES promoter. Inhibition of NF-κB nuclear translocation with isohelenin inhibited TNF-α-mediated RANTES mRNA expression, indicating that RANTES gene expression is NF-κB dependent in A549 cells. Induction of the heat shock response inhibited degradation of the NF-κB inhibitory protein, I-κBα but did not significantly inhibit phosphorylation of I-κBα. We conclude that the heat shock response inhibits RANTES gene expression by a mechanism involving inhibition of NF-κB nuclear translocation and subsequent inhibition of RANTES promoter activation. The mechanism by which the heat shock response inhibits NF-κB nuclear translocation involves stabilization of I-κBα, without significantly affecting phosphorylation of I-κBα.

Gli stili APA, Harvard, Vancouver, ISO e altri

22

Jang, Yangsoo, Jey Sook Chae, Yae Jung Hyun, Soo Jeong Koh, Ji Young Kim, Min Ji Ko, Se-Joong Rim, Hyun-Joon Shin, Jose M. Ordovas e Jong Ho Lee. "The RANTES −403G>A promoter polymorphism in Korean men: association with serum RANTES concentration and coronary artery disease". Clinical Science 113, n. 8 (12 settembre 2007): 349–56. http://dx.doi.org/10.1042/cs20070014.

Testo completo

Abstract (sommario):

In the present study we investigated the association of the RANTES (regulated upon activation, normal T-cell expressed and secreted) −28C>G and −403G>A promoter polymorphisms with the concentration of serum RANTES and CAD (coronary artery disease) in Korean men. We included 553 male CAD patients with (n=176) or without (n=377) Type 2 diabetes, aged 40–65 years with previous myocardial infarction (∼50%) or angiographically confirmed CAD (∼50%), and 416 aged-matched healthy male controls. The main outcome measures were the OR (odds ratio) of CAD risk and the serum RANTES concentration evaluated by sandwich ELISA. Although the RANTES −28C>G genotype had no significant association with CAD risk, the presence of the minor allele of the RANTES −403G>A single nucleotide polymorphism was associated with a lower risk of CAD {OR 0.70 [95% CI (confidence interval) 0.54–0.92], P=0.011} after adjusting for age, BMI (body mass index), cigarette smoking and alcohol consumption. Serum RANTES concentrations were significantly associated with the −403G>A genotype in controls (G/G: 44.7±3.3 ng/ml, G/A: 36.5±2.0 ng/ml, A/A: 28.7±2.5 ng/ml; P<0.001), non-diabetic CAD patients (G/G: 50.9±3.0 ng/ml, G/A: 42.2±2.6 ng/ml, A/A: 41.3±4.4 ng/ml; P<0.05) and diabetic CAD patients (G/G: 58.5±3.5 ng/ml, G/A: 49.6±4.1 ng/ml, A/A: 42.2±4.3 ng/ml; P<0.05); however, such associations were not observed in the subgroup of CAD patients taking lipid-lowering medication. Moreover, serum RANTES was positively correlated with C-reactive protein (r=0.289, P<0.001) and platelet counts (r=0.253, P<0.001). The results of the present study demonstrate that the RANTES −403A allele is associated with lower serum RANTES concentrations and consequently with reduced CAD risk.

Gli stili APA, Harvard, Vancouver, ISO e altri

23

Signoret, Nathalie, Annegret Pelchen-Matthews, Matthias Mack, Amanda E. I. Proudfoot e Mark Marsh. "Endocytosis and Recycling of the HIV Coreceptor Ccr5". Journal of Cell Biology 151, n. 6 (11 dicembre 2000): 1281–94. http://dx.doi.org/10.1083/jcb.151.6.1281.

Testo completo

Abstract (sommario):

The chemokine receptor CCR5 is a cofactor for the entry of R5 tropic strains of human immunodeficiency viruses (HIV)-1 and -2 and simian immunodeficiency virus. Cells susceptible to infection by these viruses can be protected by treatment with the CCR5 ligands regulated on activation, normal T cell expressed and secreted (RANTES), MIP-1α, and MIP-1β. A major component of the mechanism through which chemokines protect cells from HIV infection is by inducing endocytosis of the chemokine receptor. Aminooxypentane (AOP)-RANTES, an NH2-terminal modified form of RANTES, is a potent inhibitor of infection by R5 HIV strains. AOP-RANTES efficiently downmodulates the cell surface expression of CCR5 and, in contrast with RANTES, appears to prevent recycling of CCR5 to the cell surface. Here, we investigate the cellular basis of this effect. Using CHO cells expressing human CCR5, we show that both RANTES and AOP-RANTES induce rapid internalization of CCR5. In the absence of ligand, CCR5 shows constitutive turnover with a half-time of 6–9 h. Addition of RANTES or AOP-RANTES has little effect on the rate of CCR5 turnover. Immunofluorescence and immunoelectron microscopy show that most of the CCR5 internalized after RANTES or AOP-RANTES treatment accumulates in small membrane-bound vesicles and tubules clustered in the perinuclear region of the cell. Colocalization with transferrin receptors in the same clusters of vesicles indicates that CCR5 accumulates in recycling endosomes. After the removal of RANTES, internalized CCR5 recycles to the cell surface and is sensitive to further rounds of RANTES-induced endocytosis. In contrast, after the removal of AOP-RANTES, most CCR5 remains intracellular. We show that these CCR5 molecules do recycle to the cell surface, with kinetics equivalent to those of receptors in RANTES-treated cells. However, these recycled CCR5 molecules are rapidly reinternalized. Our results indicate that AOP-RANTES–induced changes in CCR5 alter the steady-state distribution of the receptor and provide the first evidence for G protein–coupled receptor trafficking through the recycling endosome compartment.

Gli stili APA, Harvard, Vancouver, ISO e altri

24

Vila-Coro, Antonio J., Mario Mellado, Ana Martín de Ana, Carlos Martínez-A. e José Miguel Rodríguez-Frade. "Characterization of RANTES- and Aminooxypentane-RANTES- Triggered Desensitization Signals Reveals Differences in Recruitment of the G Protein-Coupled Receptor Complex". Journal of Immunology 163, n. 6 (15 settembre 1999): 3037–44. http://dx.doi.org/10.4049/jimmunol.163.6.3037.

Testo completo

Abstract (sommario):

Abstract The trafficking of lymphocyte populations is a complex process controlled by a vast array of molecules. In this process, cells must be able to sense small changes in chemoattractant gradients. Migration through a chemotactic gradient probably employs an on-off mechanism in which chemokine receptor desensitization, internalization, and recycling may be important steps. This multistep process requires the coordinated action of many factors, including G protein-coupled receptor kinases, arrestins, clathrin, and GTP-hydrolyzing proteins such as dynamin. In this report, we show that RANTES and its derivative, aminooxypentane (AOP)-RANTES, a potent RANTES antagonist as well as an inhibitor of HIV-1 infection, both promote CCR5 desensitization involving G protein-coupled receptor kinases-2 and β-arrestin equally well. An important difference between the two molecules is that (AOP)-RANTES is more efficient than RANTES in promoting Ser/Thr phosphorylation of the receptor and association of G protein-coupled receptor kinases-2, β-arrestin, and clathrin to the CCR5. After stimulation with either ligand, we observe rapid, transient association of dynamin to CCR5, implicating this protein in receptor sensitization, but this association is faster and longer-lasting following (AOP)-RANTES stimulation. In summary, we show that chemokine receptor internalization takes place through the formation of clathrin vesicles and involves dynamin activity. We provide compelling evidence that the differences between RANTES and (AOP)-RANTES in Gαi activation condition subsequent signaling events, including internalization and receptor recycling.

Gli stili APA, Harvard, Vancouver, ISO e altri

25

YING, S., Q. MENG, L. TABORDABARATA, C. CORRIGAN, J. BARKANS, B. ASSOUFI, R. MOQBEL, S. DURHAM e A. KAY. "242 Human eosinophils (Eos) express RANTES mRNA and store and release biologically active RANTES protein". Journal of Allergy and Clinical Immunology 97, n. 1 (gennaio 1996): 243. http://dx.doi.org/10.1016/s0091-6749(96)80460-x.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

26

Schols, Dominique, Paul Proost, Sofie Struyf, Anja Wuyts, Ingrid De Meester, Simon Scharpé, Jo Van Damme e Erik De Clercq. "CD26-processed RANTES(3–68), but not intact RANTES, has potent anti-HIV-1 activity". Antiviral Research 39, n. 3 (ottobre 1998): 175–87. http://dx.doi.org/10.1016/s0166-3542(98)00039-4.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

27

Westerweel, Peter, Ton Rabelink, Maarten Rookmaaker, Hermann-Josef Gröne e Marianne Verhaar. "RANTES is required for ischaemia-induced angiogenesis, which may hamper RANTES-targeted anti-atherosclerotic therapy". Thrombosis and Haemostasis 99, n. 04 (2008): 794–95. http://dx.doi.org/10.1160/th07-10-0628.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

28

Ying, Sun, Qiu Meng, Luis Taborda-Barata, Christopher J. Corrigan, Julia Barkans, Basil Assoufi, Redwan Moqbel, Stephen R. Durham e A. Barry Kay. "Human eosinophils express messenger RNA encoding RANTES and store and release biologically active RANTES protein". European Journal of Immunology 26, n. 1 (gennaio 1996): 70–76. http://dx.doi.org/10.1002/eji.1830260111.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

29

Koper-Lenkiewicz, Olga M., Joanna Kamińska, Anna Lisowska, Anna Milewska, Tomasz Hirnle e Violetta Dymicka-Piekarska. "Factors Associated with RANTES Concentration in Cardiovascular Disease Patients". BioMed Research International 2019 (18 luglio 2019): 1–11. http://dx.doi.org/10.1155/2019/3026453.

Testo completo

Abstract (sommario):

Objective.The aim of the study was to establish, by means of linear regressions analysis, whether RANTES and CCL2 have a relationship with age, sex, heart rate, ejection fraction, white blood cells count, monocyte count, platelet count, mean platelet volume, hsCRP concentration, creatinine and eGFR value, applied treatments, and coronary risk factors in polish cardiovascular disease patients.Methods.Plasma chemokines concentrations were measured by ELISA method (R&D Systems Europe Ltd., Abingdon, England) in 115 cardiovascular disease patients (83 myocardial infarction/AMI and 32 stable angina/SA) and in the control group (N=25).Results.Univariate linear regression analysis found that (1) for men mean RANTES plasma level is 1.56 times higher as compared to women; (2) if patient’s age increases by 1 year, the mean RANTES concentration value increases by 1.4%; (3) if CCL2 concentration increases by 10 pg/mL, the mean RANTES concentration value increases by 3.3%; (4) if hsCRP concentration increases by 1 mg/L, the mean RANTES concentration value increases by 1.0%. By means of multiple linear regression analysis we found that (1) for men the mean plasma RANTES concentration value increases 1.89 times as compared to women; (2) if CCL2 concentration increases by 10 pg/mL, the mean RANTES concentration value increases by 3.4%; (3) if MPV increases by 1 fL, the mean RANTES concentration value increases by 12%, if other model parameters are fixed. For CCL2 we did not obtain statistically significant linear regression models.Conclusion.Due to high variability of obtained CCL2 concentrations, it seems that RANTES better reflects the presence of the atherosclerotic lesion than CCL2. RANTES as a marker of atherosclerotic process may be an important therapeutic target, and the assessment of RANTES concentration should be interpreted depending on patient’s sex, age, platelet hyperactivity state, hsCRP, and CCL2 concentration.

Gli stili APA, Harvard, Vancouver, ISO e altri

30

Sabbe, Rebecca, Gastón R. Picchio, Cristina Pastore, Olivier Chaloin, Oliver Hartley, Robin Offord e Donald E. Mosier. "Donor- and Ligand-Dependent Differences in C-C Chemokine Receptor 5 Reexpression". Journal of Virology 75, n. 2 (15 gennaio 2001): 661–71. http://dx.doi.org/10.1128/jvi.75.2.661-671.2001.

Testo completo

Abstract (sommario):

ABSTRACT N-terminal modifications of the chemokine RANTES bind to C-C chemokine receptor 5 (CCR5) and block human immunodeficiency virus type 1 (HIV-1) infection with greater efficacy than native RANTES. Modified RANTES compounds induce rapid CCR5 internalization and much slower receptor reexpression than native RANTES, suggesting that receptor sequestration is one mode of anti-HIV activity. The rates of CCR5 internalization and reexpression were compared using the potentn-nonanoyl (NNY)-RANTES derivative and CD4+ T cells derived from donors with different CCR5 gene polymorphisms. NNY-RANTES caused even more rapid receptor internalization and slower reexpression than aminooxypentane (AOP)-RANTES. Polymorphisms in the promoter and coding regions of CCR5 significantly affected the receptor reexpression rate after exposure of cells to NNY-RANTES. These observations may be relevant for understanding the protective effects of different CCR5 genotypes against HIV-1 disease progression.

Gli stili APA, Harvard, Vancouver, ISO e altri

31

Alam, R., S. Stafford, P. Forsythe, R. Harrison, D. Faubion, M. A. Lett-Brown e J. A. Grant. "RANTES is a chemotactic and activating factor for human eosinophils." Journal of Immunology 150, n. 8 (15 aprile 1993): 3442–48. http://dx.doi.org/10.4049/jimmunol.150.8.3442.

Testo completo

Abstract (sommario):

Abstract RANTES is a member of the 8-kDa cytokine family that has been shown to possess chemotactic activity for monocytes and CD4 T cells. In this study, we investigated whether RANTES could affect eosinophil chemotaxis and function. Peripheral blood eosinophils from blood donors were isolated on Percoll gradients to > 98% purity and then used for chemotaxis, flow cytometry, eosinophil cationic protein release assay, and survival assay. We found that RANTES is chemotactic for eosinophils at 10(-9) to 10(-8) M concentrations. RANTES elicited 65% of the chemotactic response to 10(-7) M platelet-activating factor in all experiments. The mechanism of chemotaxis was investigated by studying the expression of adhesion molecules on eosinophils by flow cytometry. We found that RANTES up-regulated the expression of CD11b/CD18 on eosinophils in a dose-dependent manner. In another set of experiments, purified eosinophils incubated with various concentrations of RANTES released eosinophil cationic protein as measured by a RIA. We also investigated the effect of RANTES on eosinophil density. Leukocytes were incubated in the presence or absence of RANTES, and the distribution of eosinophils on discontinuous Percoll gradients was then examined. We found that eosinophils became hypodense (< 1.085) when incubated in RANTES. However, unlike IL-3, RANTES did not affect the survival of eosinophils in a 4-day culture system. Thus, we established that RANTES is a chemotactic and activating factor for eosinophils.

Gli stili APA, Harvard, Vancouver, ISO e altri

32

Casola, Antonella, Allyne Henderson, Tianshuang Liu, Roberto P. Garofalo e Allan R. Brasier. "Regulation of RANTES promoter activation in alveolar epithelial cells after cytokine stimulation". American Journal of Physiology-Lung Cellular and Molecular Physiology 283, n. 6 (1 dicembre 2002): L1280—L1290. http://dx.doi.org/10.1152/ajplung.00162.2002.

Testo completo

Abstract (sommario):

Regulated on activation, normal T cell expressed, and presumably secreted (RANTES) is a member of the CC chemokine family of proteins implicated in a variety of diseases characterized by lung eosinophilia and inflammation, strongly produced by stimulated airway epithelial cells. Because such cytokines as tumor necrosis factor (TNF)-α and interferon-γ (IFN-γ) have been shown to enhance RANTES induction in airway epithelial cells and RANTES gene expression appears to be differentially regulated depending on the cell type and the stimulus applied, in this study we have elucidated mechanisms that operate to control RANTES induction on exposure to TNF-α and/or IFN-γ. Our results indicate that TNF-α and IFN-γ synergistically induce RANTES protein secretion and mRNA expression. RANTES transcription is activated only after stimulation with TNF-α, but not IFN-γ, which affects RANTES mRNA stabilization. Promoter deletion and mutagenesis experiments indicate that the nuclear factor (NF)-κB site is the most important cis-regulatory element controlling TNF-induced RANTES transcription, although NF-interleukin-6 binding site, cAMP responsive element (CRE), and interferon-stimulated responsive element (ISRE) also play a significant role. TNF-α stimulation induces nuclear translocation of interferon regulatory factor (IRF)-3, which in viral infection binds the RANTES ISRE and is necessary for activation of RANTES transcription. However, TNF-induced IRF-3 translocation does not result in IRF-3 binding to the RANTES ISRE. Although viral infection can activate an ISRE-driven promoter, TNF cannot, indicating that RANTES gene enhancers are controlled in a stimulus-specific fashion. Identification of molecular mechanisms involved in RANTES gene expression is fundamental for developing strategies to modulate lung inflammatory responses.

Gli stili APA, Harvard, Vancouver, ISO e altri

33

Pan, Zhong-Zong, Lisa Parkyn, Anuradha Ray e Prabir Ray. "Inducible lung-specific expression of RANTES: preferential recruitment of neutrophils". American Journal of Physiology-Lung Cellular and Molecular Physiology 279, n. 4 (1 ottobre 2000): L658—L666. http://dx.doi.org/10.1152/ajplung.2000.279.4.l658.

Testo completo

Abstract (sommario):

The chemokine regulated on activation normal T cells expressed and secreted (RANTES) has been implicated in eosinophil chemotaxis in asthma and allergic diseases, which are thought to be T helper (Th) type 2-dominated diseases. However, adoptive transfer of Th1 cells in mice upregulates RANTES gene expression in the lung, and increased RANTES expression has been documented in several Th1 cell-dominated conditions that are associated with neutrophilia. The in vivo role of RANTES in the pathogenesis of disease processes is not well understood. To determine the effect of RANTES expression alone in vivo, we generated transgenic mice that overexpress RANTES specifically in the lung in an inducible fashion. The airways of the transgenic mice overexpressing RANTES displayed a significant increase in neutrophil infiltration compared with that in control mice. The increased airway neutrophilia was also evident when the transgenic mice were tested in a murine model of allergic airway inflammation. RANTES expression also induced expression of the chemokine genes macrophage inflammatory protein-2, 10-kDa interferon-γ-inducible protein, and monocyte chemoattractant protein-1 in the lungs of the transgenic mice. Our studies highlight a hitherto unappreciated role for RANTES in neutrophil trafficking during inflammation. Thus increased RANTES expression, as observed during respiratory viral infections, may play an important role in the associated neutrophilia and exacerbations of asthma.

Gli stili APA, Harvard, Vancouver, ISO e altri

34

Baltus, Thomas, Kim S. C. Weber, Zoë Johnson, Amanda E. I. Proudfoot e Christian Weber. "Oligomerization of RANTES is required for CCR1-mediated arrest but not CCR5-mediated transmigration of leukocytes on inflamed endothelium". Blood 102, n. 6 (15 settembre 2003): 1985–88. http://dx.doi.org/10.1182/blood-2003-04-1175.

Testo completo

Abstract (sommario):

Abstract Chemokines control inflammatory leukocyte recruitment. The propensity of chemokines such as CC chemokine ligand 5 (CCL5)/RANTES (regulated on activation, normal T cell expressed and secreted) to bind to glycosaminoglycans and to form higher order oligomers has been shown to be essential for its in vivo activity. However, the specific functional relevance of RANTES oligomerization for distinct steps of leukocyte recruitment on inflamed endothelium mediated by the RANTES receptors CC chemokine receptor 1 (CCR1) and CCR5 remains undefined. We studied RANTES mutants with deficient oligomerization in an assay in which recruitment of monocytes and CD45RO+ CD4+ T cells is triggered by RANTES immobilized on activated endothelium under flow conditions. Notably, the formation of higher order RANTES oligomers was crucial for CCR1-mediated arrest but not for CCR5-mediated spreading/transmigration in flow or transendothelial chemotaxis of leukocytes. Efficient leukocyte arrest in flow but not transmigration may thus require the presentation of RANTES oligomers to bridge surface-bound RANTES and CCR1.

Gli stili APA, Harvard, Vancouver, ISO e altri

35

Turner, L., S. G. Ward e J. Westwick. "RANTES-activated human T lymphocytes. A role for phosphoinositide 3-kinase." Journal of Immunology 155, n. 5 (1 settembre 1995): 2437–44. http://dx.doi.org/10.4049/jimmunol.155.5.2437.

Testo completo

Abstract (sommario):

Abstract RANTES (regulated on activation, normal T cell expressed and secreted), a member of the chemokine family, is a potent chemoattractant for CD4+/CD45RO human T lymphocytes, but the signal-transduction mechanisms utilized by RANTES are poorly defined. In freshly isolated human T lymphocytes loaded with fura-2 acetoxymethyl, the CD3 mAb, UCHT-1, but not RANTES, elicited elevation of intracellular calcium levels. However, RANTES produced a bell-shaped chemotactic response and an increase in polarization of the T lymphocytes. Immunoprecipitates of phosphoinositide (PI) 3-kinase, derived from T lymphocytes stimulated with RANTES, contained increased in vitro PI 3-kinase activity compared with that present in immunoprecipitates derived from vehicle-treated cells. RANTES induction of PI 3-kinase activity was maximal at 10 to 100 ng/ml. Furthermore, the fungal metabolite, wortmannin, which is a potent PI 3-kinase inhibitor, inhibited RANTES-induced T lymphocyte migration, polarization, and increased PI 3-kinase activity. Our results show that RANTES activation of T lymphocytes seems to be independent of detectable elevation of cytosolic-free calcium, but the functional effects of chemotaxis and polarization, induced by RANTES, seem to involve the putative PI 3-kinase signal-transduction pathway.

Gli stili APA, Harvard, Vancouver, ISO e altri

36

Tereshchenko, Irina P., Jana Petrkova, Mikhail I. Voevoda, Milos Taborsky, Zdenka Navratilova, Aida G. Romaschenko, Vladimir N. Maksimov, Frantisek Mrazek e Martin Petrek. "CCL5/RANTES Gene Polymorphisms in Slavonic Patients with Myocardial Infarction". Mediators of Inflammation 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/525691.

Testo completo

Abstract (sommario):

Coronary artery inflammation is a critical process in the pathogenesis of myocardial infarction (MI). The chemokine CCL5/RANTES (regulated upon activation, normal T cells expressed and secreted) is expressed in advanced atherosclerotic lesions. Functional polymorphisms of the RANTES gene can, therefore, be involved in the pathogenesis of coronary artery disease. We examined the association of polymorphisms in the RANTES gene with myocardial infarction in Slavonic populations of Czech and Russian origin. A total of 467 post-MI patients and 337 control subjects were genotyped for RANTES promoter G-403A (rs2107538) and intron 1.1 T/C (rs2280789) variants by PCR-SSP. Both RANTES genotypes and allele frequencies did not differ between case and control groups. Haplotype-based analysis also failed to reveal an association between MI and investigated markers. Strong linkage disequilibrium was detected between particular RANTES alleles. The data do not support an association between RANTES G-403A polymorphism and MI, as reported previously.

Gli stili APA, Harvard, Vancouver, ISO e altri

37

Nelson, P. J., H. T. Kim, W. C. Manning, T. J. Goralski e A. M. Krensky. "Genomic organization and transcriptional regulation of the RANTES chemokine gene." Journal of Immunology 151, n. 5 (1 settembre 1993): 2601–12. http://dx.doi.org/10.4049/jimmunol.151.5.2601.

Testo completo

Abstract (sommario):

Abstract RANTES is a member of a large supergene family of pro-inflammatory cytokines called CC chemokines that appear to play a fundamental role in inflammatory processes. The RANTES protein causes release of histamine from basophils and is a chemoattractant for CD45RO/CD4+ "memory" T lymphocytes, monocytes, and eosinophils. Although expression of RANTES was first thought to be limited to activated T cells, recent data have shown that it is produced by a variety of tissue types in response to specific stimuli. RANTES mRNA is expressed late (3 to 5 days) after activation of resting T cells whereas in fibroblasts, renal epithelial and mesangial cells, RANTES mRNA is quickly up-regulated by TNF-alpha stimulation. In order to gain a better understanding of the molecular mechanisms that regulate expression of the RANTES locus, we have characterized the RANTES gene and determined a putative promoter region. The RANTES gene spans approximately 7.1 kb and is composed of three exons of 133, 112 and 1075 bases and two introns of approximately 1.4 and 4.4 kb with the position of intron/exon boundaries conserved relative to the other CC chemokine family members. Approximately 1 kb of DNA from the immediate 5' upstream region of RANTES was sequenced and found to contain a large number of potential consensus elements for specific T cell/hemopoietic, myeloid, muscle, and ubiquitously expressed DNA-binding factors. RANTES-promoter-luciferase gene fusion assays demonstrate high levels of reporter gene activity in a "mature" T cell line Hut78, the erythroleukemic cell line HEL, and the rhabdomyosarcoma cell line RD, with little or no activity in the "early" T cell line Jurkat, the gamma delta T cell line PEER, the thymic tumor Molt4, or the pre-erythroid cell line K562. Deletion analysis of the promoter region indicates that different transcriptional mechanisms control expression of RANTES in the various tissues studied.

Gli stili APA, Harvard, Vancouver, ISO e altri

38

Oran, Paul E., Nisha D. Sherma, Chad R. Borges, Jason W. Jarvis e Randall W. Nelson. "Intrapersonal and Populational Heterogeneity of the Chemokine RANTES". Clinical Chemistry 56, n. 9 (1 settembre 2010): 1432–41. http://dx.doi.org/10.1373/clinchem.2010.147884.

Testo completo

Abstract (sommario):

BACKGROUND Current immunoassays for the chemokine RANTES (regulated on activation, normal T-cell expressed and secreted) are not tailored for specific isoforms that exist endogenously, despite the fact that variants with modified activity are known to exist. This is surprising in view of this protein’s ubiquitous increased presence in many diseases and that the 2 established isoforms are truncated by enzymes also correlated to disease. An in-depth population survey of RANTES heterogeneity in the context of multiple diseases via a mass spectrometric immunoassay (MSIA) may resolve this issue. METHODS We developed an MSIA for RANTES and endogenous variants apparent in human plasma. Samples from multiple cohorts of individuals (type 2 diabetes, congestive heart failure, history of myocardial infarction, and cancer patients) were run in parallel with samples from healthy individuals (239 people total). We used 230 μL of plasma per individual and tabulated relative percent abundance (RPA) values for identified isoforms. RESULTS We detected at least 19 variants, including the dipeptidyl peptidase IV (DPP-IV)–truncated variant. The majority of variants were unreported in the literature. Identifiable modifications included N- and/or C-terminal truncations, oxidation, glycation, and glycosylation. We observed statistically significant differences in RPA values for multiple variants between disease cohorts and recognized prospective disease-specific protein profiles for RANTES. CONCLUSIONS Because of widespread interest in the clinical value of RANTES, the protein diversity established here may aid in the design of future, fully quantitative assays. Equally important, an inclusive qualitative understanding of RANTES heterogeneity may present new insights into the relationship between RANTES and disease.

Gli stili APA, Harvard, Vancouver, ISO e altri

39

Terada, N., K. Maesako, N. Hamano, G. Houki, T. Ikeda, M. Sai, T. Yamashita et al. "Eosinophil adhesion regulates RANTES production in nasal epithelial cells." Journal of Immunology 158, n. 11 (1 giugno 1997): 5464–70. http://dx.doi.org/10.4049/jimmunol.158.11.5464.

Testo completo

Abstract (sommario):

Abstract Among the many known chemotactic factors for eosinophils, the proinflammatory chemokine RANTES is particularly important, because it is potently and selectively chemotactic for eosinophils. Throughout the process of the migration of eosinophils from the blood vessels into the nasal cavity, eosinophil functions are assumed to be regulated by surface adhesion molecules. Conversely, the messages conferred by the eosinophils to the endothelial and epithelial cells are also of great interest. In the present study, we showed that eosinophil adhesion to human nasal epithelial cells (HNECs) inhibits RANTES production in HNECs. Eosinophils were isolated from peripheral blood obtained from patients with allergic rhinitis. Human mucosal microvascular endothelial cells and HNECs were isolated from human nasal mucosa specimens. After stimulation of the HNECs in the presence of eosinophils, the secretion of RANTES, induced by a combination of TNF-alpha and IFN-gamma, appeared to have decreased. The amount of the decrease was a function of the number of involved eosinophils. On the other hand, the presence of eosinophils did not affect RANTES production by the endothelial cells. After pretreatment of the eosinophils with anti-CD18 mAb or coculture with HNECs in Transwell culture inserts, these cells did not inhibit the TNF-alpha- and IFN-gamma-induced RANTES production. These results were virtually identical with those observed on RANTES mRNA expression. The adhesion of eosinophils to HNECs plays a key role in the inhibition of RANTES production. Our data indicate that a certain established system causes the signal transfer from eosinophils to HNECs to inhibit RANTES production, thus decreasing the eosinophil infiltration.

Gli stili APA, Harvard, Vancouver, ISO e altri

40

Wei, Jin-Hua, Xiao Feng, Zhi-Jian Sun, Pang Cheng, Bin-Fang Ma, Jie Zhao, Yu-Hang Dong, Yuan-Qiang Zhang e Zhen Li. "Different locations of RANTES and its receptors on mouse epididymal spermatozoa". Reproduction, Fertility and Development 28, n. 10 (2016): 1509. http://dx.doi.org/10.1071/rd14231.

Testo completo

Abstract (sommario):

Our previous study showed that the chemokine regulated upon activation normal T-cell expressed and secreted (RANTES) originating from the mouse epididymis bound to the midpiece of luminal spermatozoa. The present study was undertaken to investigate the association between RANTES and epididymal spermatozoa and to determine whether the association is mediated by the RANTES receptors CCR1, CCR3 or CCR5. The use of reverse transcription polymerase chain reaction (RT-PCR), immunohistochemical staining and immunofluorescent staining demonstrated that RANTES secreted by apical and narrow cells of mouse epididymal ducts was associated with luminal spermatozoa. Flow cytometric analysis and immunofluorescent labelling revealed that the association between RANTES and spermatozoa of different regions weakened gradually as the spermatozoa moved along the epididymis. Moreover, CCR1, CCR3 and CCR5 were expressed in epididymal spermatozoa and located on the head of epididymal spermatozoa, while RANTES was generally located at the midpiece. In conclusion, RANTES and its receptors were not in the same sperm location, suggesting that RANTES binding to mouse epididymal spermatozoa is independent of CCR1, CCR3 and CCR5.

Gli stili APA, Harvard, Vancouver, ISO e altri

41

Hariharan, Deepa, Wenzhe Ho, Joann Cutilli, Donald E. Campbell e Steven D. Douglas. "C-C chemokine profile of cord blood mononuclear cells: selective defect in RANTES production". Blood 95, n. 2 (15 gennaio 2000): 715–18. http://dx.doi.org/10.1182/blood.v95.2.715.

Testo completo

Abstract (sommario):

Three C-C chemokines inhibit human immunodeficiency virus (HIV) entry into macrophages: macrophage inflammatory protein-1 (MIP-1), MIP-1β, and regulated-upon activation, normal T-cell expressed and secreted (RANTES). We studied the ability of placental cord blood mononuclear cells (CBMC) to secrete these C-C chemokines in comparison to adult blood mononuclear cells (ABMC). CBMC had diminished ability to secrete RANTES, as determined by enzyme-linked immunosorbent assay. Secretion of MIP-1 and MIP-1β were similar in CBMC and ABMC. Whereas MIP-1 and MIP-1β secretion were comparable in monocytes and lymphocytes, RANTES was secreted primarily by lymphocytes. Flow cytometric analysis of RANTES expression showed diminished intracellular RANTES expression in cord blood lymphocytes (CBL) compared to adult (peripheral) blood lymphocytes (ABL). A subset analysis of RANTES-producing CBL and ABL demonstrated that RANTES was produced predominantly by CD8+/CD45RO+ cells. CBL had a reduced proportion of CD8+/CD45RO+ cells compared with ABL, which may account for the diminished RANTES secretion by CBMC. These results may be relevant to the pathogenesis of perinatal HIV infection.

Gli stili APA, Harvard, Vancouver, ISO e altri

42

Levy, Jay A. "The Unexpected Pleiotropic Activities of RANTES". Journal of Immunology 182, n. 7 (19 marzo 2009): 3945–46. http://dx.doi.org/10.4049/jimmunol.0990015.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

43

Lechner, Johann, e Volker von Baehr. "Entzündungssignal RANTES / CCL5 aus dem Kieferknochen". Zeitschrift für Komplementärmedizin 10, n. 01 (febbraio 2018): 52–57. http://dx.doi.org/10.1055/s-0044-101566.

Testo completo

Abstract (sommario):

Summary Hintergrund: Diese Studie behandelt die Frage, ob allgemeine und weit verbreitete zahnärztliche Eingriffe, wie Zahnextraktionen und operative Entfernung von Weisheitszähnen, zu chronischer Kieferknochenentzündung führen. Eine mangelhafte Wundheilung im Kieferknochen kann über Entzündungsmediatoren eine versteckte Ursache chronischer Erkrankungen sein. Materialien und Methoden: Mittels Mutliplexanalyse untersuchen wir fettig-degenerativ osteonekrotisch / osteolytisch veränderten Kieferknochen (FDOK) in zwei Gruppen auf sieben Zytokine: 16 FDOK-Präparate postoperativ in Bereichen der retromolaren Weisheitszahngebiete und 19 Präparate von gesundem Kieferknochen. Ergebnisse: Alle FDOK-Proben zeigen RANTES / CCL5 (R / C) und den Fibroblastenwachstumsfaktor (FGF)-2 als einzige stark überexprimierte Botenstoffe. Die FDOK-Proben zeigen im Mittel einen 30-fachen Überschuss von R / C und einen 20-fachen Überschuss von FGF-2 im Vergleich zu gesunden Kontrollgruppen. Schlussfolgerungen: Da R / C in der Literatur als wichtiger Treiber von entzündlichen Erkrankungen diskutiert wird und onkogene Wirkung haben kann, verfolgen wir die Hypothese, dass FDOK infolge mangelhafter oder unvollständiger Wundheilung im Kieferknochen eine Quelle hyperaktivierter Signalwege ist. Dabei wirkt das FDOK-Areal als unentdeckter Herd einer „stillen Entzündung“. Aufgrund der R / C-Beteiligungen bei vielen Immunerkrankungen kann die chirurgische Beseitigung einer FDOK potenzielle Entwicklungen von entzündlich systemischen Erkrankungen positiv beeinflussen.

Gli stili APA, Harvard, Vancouver, ISO e altri

44

Stura, Enrico A., Loïc Martin, Hugues Lortat-Jacob, Romain Vivès e Claudio Vita. "Heparin-aggregated RANTES can be crystallised". Acta Crystallographica Section D Biological Crystallography 58, n. 10 (26 settembre 2002): 1670–73. http://dx.doi.org/10.1107/s0907444902012817.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

45

Whyte, Anthony, e RichardM Binns. "RANTES and chemokines in rheumatoid arthritis". Lancet 343, n. 8908 (maggio 1994): 1291–92. http://dx.doi.org/10.1016/s0140-6736(94)92181-4.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

46

Shaw, Jeffrey P., Zoë Johnson, Frédéric Borlat, Catherine Zwahlen, Andreas Kungl, Karen Roulin, Axel Harrenga, Timothy N. C. Wells e Amanda E. I. Proudfoot. "The X-Ray Structure of RANTES". Structure 12, n. 11 (novembre 2004): 2081–93. http://dx.doi.org/10.1016/j.str.2004.08.014.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

47

Appay, Victor, e Sarah L. Rowland-Jones. "RANTES: a versatile and controversial chemokine". Trends in Immunology 22, n. 2 (febbraio 2001): 83–87. http://dx.doi.org/10.1016/s1471-4906(00)01812-3.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

48

Xie, Chun, Kui Liu, Yuyang Fu, Xiangmei Qin, Geetha Jonnala, Tao Wang, Hong W. Wang, Michael Maldonado, Xin J. Zhou e Chandra Mohan. "RANTES Deficiency Attenuates Autoantibody-Induced Glomerulonephritis". Journal of Clinical Immunology 31, n. 1 (1 ottobre 2010): 128–35. http://dx.doi.org/10.1007/s10875-010-9470-x.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

49

Chihara, Junichi, Tomokazu Kakazu, Ikkou Higashimoto, Norihiro Saito, Kohei Honda, Akira Tsuda, Hiroyuki Kayaba, Yumiko Kamada, Hajime Oyamada e Osamu Urayama. "RANTES Augments Eosinophil Lucigenin-Dependent Chemiluminescence". International Archives of Allergy and Immunology 117, n. 1 (1998): 40–43. http://dx.doi.org/10.1159/000053569.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

50

SCHRöDER, JENS-MICHAEL, YOSHIKAZU KAMEYOSHI e ENNO CHRISTOPHERS. "RANTES, A Novel Eosinophil-Chemotactic Cytokine". Annals of the New York Academy of Sciences 725, n. 1 (luglio 1994): 91–103. http://dx.doi.org/10.1111/j.1749-6632.1994.tb39793.x.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

Articoli di riviste sul tema "RANTES"

Cita una fonte nei formati APA, MLA, Chicago, Harvard e in molti altri stili