Platelet chemokines and their receptors: what is their relevance to platelet storage and transfusion practice?

Boehlen, Françoise; Clemetson, Kenneth J.

doi:10.1046/j.1365-3148.2001.00340.x

Cited by 139 publications

(131 citation statements)

References 150 publications

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“…RANTES is one of the chemokines produced by cultured human PBMC (Denison et al, 1997). It has also been reported that platelets release RANTES and MIP-1α following activation (Boehlen and Clemetson, 2001). Moreover, we recently demonstrated that PBMC-conditioned medium can promote the invasion of BeWo cells, a trophoblastic cell line (Egawa et al, 2000).…”

Section: Discussionmentioning

confidence: 94%

Trophoblasts acquire a chemokine receptor, CCR1, as they differentiate towards invasive phenotype

et al. 2003

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At the human feto-maternal interface, trophoblasts differentiate towards extravillous trophoblasts (EVTs) and form the cell column. EVTs acquire invasive activity in the distal part of the cell column and begin to migrate into the maternal tissue. We previously reported that dipeptidyl peptidase IV(DPPIV) is expressed on EVTs in the proximal part of cell column and is involved in the inhibition of their migration. Because DPPIV has been shown to degrade several chemokines, we examined possible roles of chemokines in EVT migration.Immunohistochemistry demonstrated that C-C chemokine receptor 1 (CCR1) was hardly detected on cytotrophoblasts and syncytiotrophoblast but was expressed on EVTs in the cell column. In vitro, CCR1 protein was also present on the surface of EVTs that grew out from chorionic villous explants cultured under 20% O2. Chemokines that can bind to CCR1 (CCR1 ligands), such as regulated on activation, normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein-1α (MIP-1α), were confirmed in the decidual tissues by RT-PCR and immunohistochemistry. These CCR1 ligands promoted the migration of the EVTs that were isolated from the explant cultures in vitro. These results indicate that CCR1 is expressed on trophoblasts as they differentiate to EVTs and that CCR1 ligands produced from the decidual tissue induce EVT migration.By contrast, CCR1 was scarcely expressed on EVTs that grew out from villous explants cultured in 1% O2, indicating that a relatively high oxygenic environment is needed to induce CCR1 expression. Moreover, CCR1 expression on the isolated EVTs was significantly reduced in the presence of decidua-conditioned medium. Such regulation of CCR1 by surrounding oxygenic and decidual environments supports a close correlation between EVT invasion and their expression of CCR1.This study demonstrates that trophoblasts acquire CCR1 as they differentiate to an invasive phenotype at the villus-anchoring sites and indicates a novel role for the chemokine-CCR1 system in the initial step of trophoblastic invasion towards the maternal tissue.

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Section: Discussionmentioning

confidence: 94%

Trophoblasts acquire a chemokine receptor, CCR1, as they differentiate towards invasive phenotype

et al. 2003

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“…PF4 is also released from activated T lymphocytes and mast cells (21). It has been shown to influence numerous other biological properties, including inhibiting endothelial cell proliferation, migration, and angiogenesis (22)(23)(24), inhibiting T cell function by down-modulating cell proliferation and cytokine release (25), and supporting the survival of normal hematopoietic precursors and protecting them from the toxicity of chemotherapeutic agents (26).…”

Section: Discussionmentioning

confidence: 99%

Decreased levels of CXC-chemokines in serum of benzene-exposed workers identified by array-based proteomics

Vermeulen¹,

Lan²,

Zhang³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Benzene is an important industrial chemical and environmental contaminant that causes leukemia. To obtain mechanistic insight into benzene's mechanism of action, we examined the impact of benzene on the human serum proteome in a study of exposed healthy shoe-factory workers and unexposed controls. Two sequential studies were performed, each using sera from 10 workers exposed to benzene (overall mean benzene air level >30 ppm) and 10 controls. Serum samples were subjected to anion-exchange fractionation and bound to three types of ProteinChip arrays (Ciphergen Biosystems, Fremont, CA) [hydrophobic (H50), metal affinity (IMAC3-Cu), and cation exchange (WCX2)]. Protein-expression patterns were detected by surface-enhanced laser desorption͞ ionization (SELDI)-TOF MS. Three proteins (4.1, 7.7, and 9.3 kDa) were consistently down-regulated in exposed compared with control subjects in both studies. All proteins were highly inversely correlated with individual estimates of benzene exposure (r > 0.75). The 7.7-and 9.3-kDa proteins were subsequently identified as platelet factor (PF)4 and connective tissue activating peptide (CTAP)-III. Initial proteomic results for PF4 and CTAP-III were subsequently confirmed in a single experiment using a ProteinChiparray-based immunoassay(Ciphergen Biosystems). The altered expression of the platelet-derived CXC-chemokines (40% and 63% for PF4 and CTAP-III, respectively) could not be explained by changes in absolute platelet counts. Thus, SELDI-TOF analysis of a limited number of exposed and unexposed subjects revealed that lowered expression of PF4 and CTAP-III proteins is a potential biomarker of benzene's early biologic effects and may play a role in the immunosuppressive effects of benzene.biomarker ͉ leukemia ͉ mass spectrometry ͉ platelet ͉ molecular epidemiology

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“…In addition, the specific ligands for CCR4, CCL17 (thymus and activation-regulated chemokine) and CCL22 (macrophage-derived chemokine) (19), reportedly induce migration of both Th2 and Th1 cells in vitro (20,21). Finally, the receptor is not limited to T cells because CCR4 mRNA is reportedly expressed by platelets, NK cells, macrophages, and dendritic cells (DCs) (22)(23)(24)(25). In view of these reports, it is clear that the role of CCR4 with regard to T cell function needs better definition.…”

Section: T He Cd4mentioning

confidence: 99%

CCR4 Participation in Th Type 1 (Mycobacterial) and Th Type 2 (Schistosomal) Anamnestic Pulmonary Granulomatous Responses

Freeman

Stolberg

Chiu

et al. 2006

The Journal of Immunology

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CCR4 is purported to be a Th type 2 (Th2) cell-biased receptor but its functional role is unclear. Recent studies suggest that chemokine receptor expression and function are more complex in vivo and raise doubts regarding restricted CCR4 expression by Th2 cells. To address these issues, we analyzed the role of CCR4 in highly polarized models of Th type 1 (Th1) and Th2 cell-mediated pulmonary granulomas, respectively, elicited by i.v. challenge of primed mice with either mycobacterial purified protein derivative or schistosomal egg Ag-coated beads. CCR4 agonists were expressed during both responses, correlating with a shift of CCR4+CD4+ T cells from blood to lungs. CCL22 dominated in draining nodes during the Th1 response. Analysis of CD4+ effector T cells revealed CCR4 expression and CCR4-mediated chemotaxis by both IFN-γ and IL-4 producers. Studies of CCR4 knockout (CCR4−/−) mice showed partial impairment of the local type-2 cytokine response and surprisingly strong impairment of the Th1 response with abrogated IFN-γ production during secondary but not primary challenge. Adoptive transfer indicated CCR4−/−CD4+ Th1 cell function was defective but this could not be reconstituted with wild-type (CCR4+/+) CD4+ T cells indicating involvement of another CCR4+ population. Coculture of CCR4+/+CD4+ T cells and CCR4−/− dendritic cells revealed intact IL-2 but impaired IFN-γ production, pointing to a role for CCR4+ dendritic cells in effector cell expression. Therefore, CCR4 is not Th2-restricted and was required for sustenance and expression of the Th1 effector/memory response to mycobacterial Ags.

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Platelet chemokines and their receptors: what is their relevance to platelet storage and transfusion practice?

Cited by 139 publications

References 150 publications

Trophoblasts acquire a chemokine receptor, CCR1, as they differentiate towards invasive phenotype

Trophoblasts acquire a chemokine receptor, CCR1, as they differentiate towards invasive phenotype

Decreased levels of CXC-chemokines in serum of benzene-exposed workers identified by array-based proteomics

CCR4 Participation in Th Type 1 (Mycobacterial) and Th Type 2 (Schistosomal) Anamnestic Pulmonary Granulomatous Responses

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