Monocyte chemoattractant protein‐2 can exert its effects through the MCP‐1 receptor (CC CKR2B)

Yamagami, Shinsuke; Tanaka, Hiroko; Endo, Noriaki

doi:10.1016/s0014-5793(96)01411-1

Cited by 25 publications

(12 citation statements)

References 36 publications

(31 reference statements)

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“…Other groups using CCR2-transfected cells have found binding affinities of the four members of the monocyte chemoattractant protein family in the nanomolar range, which are in agreement with our results (34,35) except that we found CCL2 to have an affinity in the subnanomolar range, which probably is due to cell line and assay differences. The finding that CCL8 and CCL13 were unable displace all bound 125 I-CCL2 from CCR2 are known from other binding studies on monocytes and CCR2-transfected cell lines (35)(36)(37)(38), where one group even reported increasing binding of 125 I-CCL2 with increasing concentrations of CCL8 (36), a phenomenon known from other chemokines in binding assays and that probably is due to fact that certain chemokines tend to oligomerize (39). The potencies in chemotaxis for CCL2, CCL7, and CCL13 were in agreement with another study using a CCR2-transfected 300.19 murine pre-B cell line (38).…”

Section: Discussionmentioning

confidence: 70%

A Highly Selective CCR2 Chemokine Agonist Encoded by Human Herpesvirus 6

Lüttichau¹,

Clark‐Lewis²,

Jensen³

et al. 2003

Journal of Biological Chemistry

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The chemokine-like, secreted protein product of the U83 gene from human herpesvirus 6, here named vCCL4, was chemically synthesized to be characterized in a complete library of the 18 known human chemokine receptors expressed individually in stably transfected cell lines. vCCL4 was found to cause calcium mobilization as efficiently as the endogenous chemokine ligand CCL2 through the CCR2 receptor, whereas the virally encoded chemokine did not affect any of the other 17 human chemokine receptors tested. Mutual cross-desensitization between CCL2 and vCCL4 was demonstrated in the CCR2-transfected cells. The affinity of vCCL4 for the CCR2 receptor was 79 nM as determined in competition binding against radioactively labeled CCL2. In the murine pre-B lymphocyte cell line L1.2 stably transfected with the CCR2 receptor, vCCL4 acted as a relatively low potency but highly efficacious chemoattractant being equally or more efficacious in causing cell migration than CCL2 and CCL7 and considerably more efficacious than CCL8 and CCL13. It is concluded that human herpesvirus 6 encodes a highly selective and efficacious CCR2 agonist, which will attract CCR2 expressing cells, for example macrophages and monocytes, conceivably for the virus to infect and to establish latency in. It is suggested that vCCL4 during reactivation of the virus in for example monocyte-derived microglia could perhaps be involved in the pathogenesis of the CCR2-dependent disease, multiple sclerosis.

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Section: Discussionmentioning

confidence: 70%

A Highly Selective CCR2 Chemokine Agonist Encoded by Human Herpesvirus 6

Lüttichau¹,

Clark‐Lewis²,

Jensen³

et al. 2003

Journal of Biological Chemistry

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“…53 This receptor is known as the major functional receptor for MCP-1, although most likely not the only one of biological relevance. 54,55 Using these mice on both the BALB/c and the C57BL/6 background, the importance of the MCP-1-CCR2 pathway in arteriogenesis was impressively demonstrated, and it was shown that this pathway is responsible for the recruitment of monocytes during early phases of arteriogenesis 56 : the data displayed a dramatically reduced recovery of pedal blood flow after femoral artery ligation. This not only correlated with other physiological parameters like the reduction in hemoglobin oxygen saturation in the foot but was also reflected by functional parameters: Because of the reduced blood supply to the distal regions of the leg, the active movement of the limb, assessed in a score, was significantly impaired.…”

Section: Circulating Blood Monocytes Are Critical Mediators Of Arterimentioning

confidence: 99%

Influence of Mechanical, Cellular, and Molecular Factors on Collateral Artery Growth (Arteriogenesis)

Heil

Schäper

2004

Circulation Research

338

306

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Abstract-Growth of collateral blood vessels (arteriogenesis) is potentially able to preserve structure and function of limbs and organs after occlusion of a major artery. The success of the remodeling process depends on the following conditions:(1) existence of an arteriolar network that connects the preocclusive with the postocclusive microcirculation; (2) activation of the arteriolar endothelium by elevated fluid shear stress; (3) invasion (but not incorporation) of bone marrow-derived cells; and (4) proliferation of endothelial and smooth muscle cells. Most organs of most mammals including man can rely on the existence of interconnecting arterioles in most organs and tissues with heart being the exception in rodents and pigs. Arterial occlusion lowers the pressure in the distal vasculature thereby creating a pressure gradient favoring increased flow through preexisting collaterals. This increases fluid shear stress leading to endothelial activation with cellular edema, upregulation of adhesion molecules, mitogenic-, thrombogenic-, and fibrinolytic factors, leading to monocyte invasion with matrix digestion. Smooth muscle cells migrate and proliferate and the vessel enlarges under the influence of increasing circumferential wall stress. Growth factors involved belong to the FGF family and signaling proceeds via the Ras/Raf-and the Rho cascades. Increases in vascular radius and wall thickness restore fluid shear stress and circumferential wall stress to normal levels and growth stops. Although increases in collateral vessel size are very substantial their maximal conductance amounts to only 40% of normal. Key Words: arteriogenesis Ⅲ shear stress Ⅲ monocytes Ⅲ vascular remodeling Ⅲ leukocytes A fter birth, blood vessel growth proceeds mainly by two different processes. Angiogenesis describes the growth of new capillaries by sprouting or intussusception and will be reviewed elsewhere in this issue. The driving force for angiogenesis is ischemia. In contrast, arteriogenesis is based on growth and remodeling of preexisting collateral anastomoses. These arterioarteriolar connections belonging to the arcade-like microvascular blood flow distribution system are recruited to function as collateral vessels after the occlusion of a major artery. The initial triggers of arteriogenesis are physical forces like fluid shear stress. Collateral vessel growth includes attraction and invasion of circulating blood cells, proliferation of vascular wall cells, and remodeling processes with digestion and rearrangement of the extracellular matrix and elastic lamina. This review will focus on the mechanisms involved in arteriogenesis.It has become common knowledge for many years that blood vessels regress when not constantly perfused, that they Original

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“…All chemokines act via seven transmembrane domain, G protein-coupled receptors (3), and five of them, CCR1-CCR5, are known to mediate responses to CC chemokines. The best-characterized ligands are regulated upon activation normal T cells expressed and secreted (RANTES), 1 macrophage inflammatory protein (MIP)-1 ␣ , and monocyte chemotactic protein (MCP)-3 for CCR1 (4-7), MCP-1 and other MCPs for CCR2 (6,8,9), eotaxin, RANTES, and MCP-3 for CCR3 (10)(11)(12), MIP-1 ␣ and RANTES for CCR4 (13), and MIP-1 ␣ , MIP-1 ␤ , and RANTES for CCR5 (14)(15)(16). The expression of CC chemokine receptors differs depending on the type of leukocyte, and influences responsiveness.…”

Section: Introductionmentioning

confidence: 99%

High expression of the chemokine receptor CCR3 in human blood basophils. Role in activation by eotaxin, MCP-4, and other chemokines.

Uguccioni¹,

Mackay²,

et al. 1997

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Eosinophil leukocytes express high numbers of the chemokine receptor CCR3 which binds eotaxin, monocyte chemotactic protein (MCP)-4, and some other CC chemokines. In this paper we show that CCR3 is also highly expressed on human blood basophils, as indicated by Northern blotting and flow cytometry, and mediates mainly chemotaxis. Eotaxin and MCP-4 elicited basophil migration in vitro with similar efficacy as regulated upon activation normal T cells expressed and secreted (RANTES) and MCP-3. They also induced the release of histamine and leukotrienes in IL-3-primed basophils, but their efficacy was lower than that of MCP-1 and MCP-3, which were the most potent stimuli of exocytosis. Pretreatment of the basophils with a CCR3-blocking antibody abrogated the migration induced by eotaxin, RANTES, and by low to optimal concentrations of MCP-4, but decreased only minimally the response to MCP-3. The CCR3-blocking antibody also affected exocytosis: it abrogated histamine and leukotriene release induced by eotaxin, and partially inhibited the response to RANTES and MCP-4. In contrast, the antibody did not affect the responses induced by MCP-1, MCP-3, and macrophage inflammatory protein-1 ␣ , which may depend on CCR1 and CCR2, two additional receptors detected by Northern blotting with basophil RNA. This study demonstrates that CCR3 is the major receptor for eotaxin, RANTES, and MCP-4 in human basophils, and suggests that basophils and eosinophils, which are the characteristic effector cells of allergic inflammation, depend largely on CCR3 for migration towards different chemokines into inflamed tissues. ( J. Clin. Invest. 1997. 100:1137-1143.)

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Monocyte chemoattractant protein‐2 can exert its effects through the MCP‐1 receptor (CC CKR2B)

Cited by 25 publications

References 36 publications

A Highly Selective CCR2 Chemokine Agonist Encoded by Human Herpesvirus 6

A Highly Selective CCR2 Chemokine Agonist Encoded by Human Herpesvirus 6

Influence of Mechanical, Cellular, and Molecular Factors on Collateral Artery Growth (Arteriogenesis)

High expression of the chemokine receptor CCR3 in human blood basophils. Role in activation by eotaxin, MCP-4, and other chemokines.

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