Chemokines in renal diseases

Wada, Takashi; Yokoyama, Hitoshi; Matsushima, Kouji; Kobayashi, Ken

doi:10.1016/s1567-5769(01)00004-2

Cited by 26 publications

(16 citation statements)

References 59 publications

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“…Cells were harvested and total RNA was isolated at 4,8,16, and 24 h. Northern blot analysis revealed that IL-1␤ significantly stimulated MCP-1 mRNA expression from 4 to 24 h and BMP-7 inhibited IL-1␤-induced MCP-1 mRNA expression in a time-dependent manner from 4 to 24 h. The peak inhibition was seen at 16 h. BMP-7 also inhibited constitutive expression of MCP-1 mRNA (Fig. 3A).…”

Section: Bmp-7 Inhibits Constitutive and Il-1␤-induced Mcp-1 Mrna Expmentioning

confidence: 92%

“…3 is an important mediator for monocyte/macrophage infiltration in acute and chronic inflammatory renal diseases (1)(2)(3)(4). A critical role for MCP-1 in the pathogenesis of renal inflammation was established by renal parenchymal cell culture studies as well as by blocking MCP-1 activity with neutralizing Abs in animal models of inflammatory renal disease (3)(4)(5)(6).…”

Section: Onocyte Chemoattractant Protein-1 (Mcp-1)mentioning

confidence: 99%

“…A critical role for MCP-1 in the pathogenesis of renal inflammation was established by renal parenchymal cell culture studies as well as by blocking MCP-1 activity with neutralizing Abs in animal models of inflammatory renal disease (3)(4)(5)(6). Therefore, clinically applicable anti-MCP-1 agents have been sought that inhibit local MCP-1 production by renal cells, neutralize MCP-1 activity, or block receptors for MCP-1.…”

Section: Onocyte Chemoattractant Protein-1 (Mcp-1)mentioning

confidence: 99%

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Bone Morphogenetic Protein-7 Inhibits Constitutive and Interleukin-1β-Induced Monocyte Chemoattractant Protein-1 Expression in Human Mesangial Cells: Role for JNK/AP-1 Pathway

Lee

Yang

Jin

et al. 2003

The Journal of Immunology

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Bone morphogenetic protein-7 (BMP-7), which belongs to the TGF-β superfamily, has been shown to reduce macrophage infiltration and tissue injury in animal models of inflammatory renal disease. To explore the mechanism involved in the anti-inflammatory effect, we investigated the effect of BMP-7 on monocyte chemoattractant protein-1 (MCP-1) expression in cultured human mesangial cells. BMP- 7 significantly inhibited constitutive and IL-1β-induced MCP-1 protein production and MCP-1 mRNA expression by mesangial cells in a time- and concentration-dependent manner. BMP-7 also inhibited IL-1β-induced monocyte chemotactic activity released from the mesangial cells. We examined the role of transcription factors NF-κB and AP-1 in BMP-7 inhibition of IL-1β-induced MCP-1 expression. IL-1β increased NF-κB and AP-1 activity and both transcription factors mediated IL-1β-induced MCP-1 expression in mesangial cells. BMP-7 inhibited IL-1β-induced AP-1 activity in a concentration-dependent manner. In contrast, IL-1β-induced NF-κB activity and IκBα degradation were not affected by BMP-7. Furthermore, IL-1β-induced phosphorylation of c-Jun N-terminal kinase was inhibited by BMP-7. These data suggest that BMP-7 inhibits constitutive and IL-1β-induced MCP-1 expression in human mesangial cells partly by inhibiting c-Jun N-terminal kinase activity and subsequent AP-1 activity, and provide new insight into the therapeutic potential of BMP-7 in the inflammatory renal diseases.

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Section: Bmp-7 Inhibits Constitutive and Il-1␤-induced Mcp-1 Mrna Expmentioning

confidence: 92%

Section: Onocyte Chemoattractant Protein-1 (Mcp-1)mentioning

confidence: 99%

Section: Onocyte Chemoattractant Protein-1 (Mcp-1)mentioning

confidence: 99%

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Bone Morphogenetic Protein-7 Inhibits Constitutive and Interleukin-1β-Induced Monocyte Chemoattractant Protein-1 Expression in Human Mesangial Cells: Role for JNK/AP-1 Pathway

Lee

Yang

Jin

et al. 2003

The Journal of Immunology

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“…53 As in AKI, urinary IL-8/ CXCL8 levels are increased early, but elevated urinary MCP-1 levels associate with progressive renal injury. 54,55 In addition, enhanced expression of glomerular MCP-1/CCL2 and ligands of CCR5 (including RANTES/CCL5, MIP-1␣/CCL3, and MIP-1ß/CCL4) are detected in patients with various forms of glomerulonephritis.…”

Section: Role Of CCL and Cx3cl Chemokines In Chronic Kidney Diseasementioning

confidence: 97%

Chemokines in Renal Injury

Chung

Lan

2011

Journal of the American Society of Nephrology

240

181

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Renal inflammation underlies many chronic kidney diseases and the infiltration of leukocytes mediates much of the nephritogenic inflammatory response. As several recent reviews have dealt with the basic biology, mouse models, and blockade studies of chemokines in renal diseases, [1][2][3][4][5][6][7][8][9][10][11] we focus here on recent developments in pathophysiology of that chemokine effect. CHEMOKINES AND CHEMOKINE RECEPTORSChemokines are a group of chemotactic cytokines (approximately 8 to 17 kD) with the ability to bind G-proteincoupled receptors and act as potent attractants for leukocytes in acute and chronic inflammation. There are four subfamilies of chemokines, including CCL, CXCL, CX3CL, and CL (Figure 1). 7,6 At present, 19 receptors are known ( Figure 1). 6,7 The large CC chemokine family has the first two cysteine residues adjacent to each other, whereas the CXC family has a single amino acid residue in between the first two cysteines. Fractalkine (CX3CL1) is the only member of the CX3C chemokine family where three amino acid residues separate the first two cysteines. Finally, two related chemokines absent the two cysteine residues that bind the XCR1 receptor belong to the XC family. As shown in Figure 1, many chemokines bind multiple receptors and most receptors bind multiple chemokines. However, CC chemokine receptors exclusively bind CC chemokines and CXC receptors bind only CXC chemokines.Chemokines and their corresponding receptors are expressed in different cell types (Figure 2). 7,12 Generally speaking, monocytes are mostly attracted by CCL chemokines acting through CCR1, CCR2, andCCR5receptors,whereasneutrophilsare the target of CXCL chemokines through REGULATION OF CHEMOKINE EXPRESSIONOn the basis of their regulation and production, chemokines can be classified broadly as homeostatic/lymphoid or inflammatory chemokines. The former is responsible for leukocyte homing and ABSTRACTThe main function of chemokines is to guide inflammatory cells in their migration to sites of inflammation. During the last 2 decades, an expanding number of chemokines and their receptors have driven broad inquiry into how inflammatory cells are recruited in a variety of diseases. Although this review focuses on chemokines and their receptors in renal injury, proinflammatory IL-17, TGF␤, and TWEAK signaling pathways also play a critical role in their expression. Recent studies in transgenic mice as well as blockade of chemokine signaling by neutralizing ligands or receptor antagonists now allow direct interrogation of chemokine action. The emerging role of regulatory T cells and Th17 cells during renal injury also forges tight relationships between chemokines and T cell infiltration in the development of kidney disease. As chemokine receptor blockade inches toward clinical use, the field remains an attractive area with potential for unexpected opportunity in the future.

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“…5,6 Recent studies have established an important role of chemokines and their specific receptors in the regulation of leukocyte migration in renal inflammatory disease. [7][8][9][10][11] However, the precise molecular basis for the directional migration of effector T cells in glomerulonephritis is not defined.…”

mentioning

confidence: 99%

Chemokine Receptor CXCR3 Mediates T Cell Recruitment and Tissue Injury in Nephrotoxic Nephritis in Mice

Panzer¹,

Steinmetz²,

Paust³

et al. 2007

Journal of the American Society of Nephrology

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The chemokine receptor CXCR3 is highly expressed on Th1 polarized T cells and has been predicted to play an important role in T cell recruitment and immune response in a number of inflammatory and autoimmune diseases. For testing whether CXCR3 plays a role in renal inflammation, CXCR3-deficient mice were generated and nephrotoxic nephritis was induced in C57BL/6 CXCR3 Ϫ/Ϫ and C57BL/6wild-type mice. Induction of the nephrotoxic nephritis leads to an increased renal mRNA expression of IP-10/CXCL10 (8.6-fold), Mig/CXCL9 (2.3-fold), and I-TAC/CXCL11 (4.9-fold) during the autologous phase at days 7 and 14. This increased chemokine expression was paralleled by the renal infiltration of T cells, followed by renal tissue injury, albuminuria, and loss of renal function. Compared with wild-type mice, CXCR3-deficient mice had significantly reduced renal T cell infiltrates. Moreover, CXCR3 Ϫ/Ϫ mice developed less severe nephritis, with significantly lower albuminuria, better renal function, and a reduced frequency of glomerular crescent formation. Nephritic wild-type and CXCR3 Ϫ/Ϫ mice both elicited an efficient systemic nephritogenic immune response in terms of antigen-specific IgG production and IFN-␥ expression by splenocytes in response to the nephritogenic antigen. These findings indicate that the ameliorated nephritis in CXCR3-deficient mice is due to impaired renal trafficking of effector T cells rather than their inability to mount an efficient humoral or cellular immune response. The neutralization of CXCR3 might be a promising therapeutic strategy for Th1-dependent inflammatory renal disease.

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Chemokines in renal diseases

Cited by 26 publications

References 59 publications

Bone Morphogenetic Protein-7 Inhibits Constitutive and Interleukin-1β-Induced Monocyte Chemoattractant Protein-1 Expression in Human Mesangial Cells: Role for JNK/AP-1 Pathway

Bone Morphogenetic Protein-7 Inhibits Constitutive and Interleukin-1β-Induced Monocyte Chemoattractant Protein-1 Expression in Human Mesangial Cells: Role for JNK/AP-1 Pathway

Chemokines in Renal Injury

Chemokine Receptor CXCR3 Mediates T Cell Recruitment and Tissue Injury in Nephrotoxic Nephritis in Mice

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