Rat CXC chemokine GRO/CINC‐1 paradoxically stimulates the growth of gastric epithelial cells

Suzuki, Hidekazu; Mori, Masaaki; Seto, Kazuto; Shibata, Futoshi; Nagahashi, Shoichi; Kawaguchi, Chizuko; Suzuki, Masayuki; Matsui, Hirofumi; Watanabe, Kimitsuna; Miura, Soichiro; Ishii, Hiromasa

doi:10.1046/j.1365-2036.2000.014s1094.x

Cited by 20 publications

(22 citation statements)

References 17 publications

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“…Studies by Driscoll et al (16) have demonstrated increased proliferation of rat alveolar epithelial cells in response to stimulation by the CXC chemokines MIP-2 or CINC. Increased proliferation and ERK1/2 signaling has also been observed for the rat gastric epithelial cell line RGM-1 following stimulation by CINC (17). Consistent with these studies, epithelial resurfacing of excisional wounds in CXCR2 knockout mice is significantly delayed compared with wild-type animals (30).…”

Section: Discussionsupporting

confidence: 76%

“…In keeping with this evidence, previous studies have reported that the rat neutrophildirected CXC chemokines MIP-2 and CINC-1 can exert mitogenic effects on alveolar epithelial cells and gastric epithelial cells, respectively (16,17). The CC chemokine MCP-1 has also been reported to induce mitogenic responses in human bronchial epithelial cells (18).…”

Section: Macrophage-inflammatory Protein-3␣ Mediates Epidermal Growthsupporting

confidence: 51%

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Macrophage-Inflammatory Protein-3α Mediates Epidermal Growth Factor Receptor Transactivation and ERK1/2 MAPK Signaling in Caco-2 Colonic Epithelial Cells via Metalloproteinase-Dependent Release of Amphiregulin

Keates

Han

Kelly

et al. 2007

The Journal of Immunology

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Previously, we reported that normal colonocytes produce the memory CD4+ T cell-directed chemokine MIP-3α, and that epithelial MIP-3α levels are elevated in inflammatory bowel disease. Interestingly, the unique receptor for MIP-3α, CCR6, is expressed by a variety of cell types including colonocytes, suggesting that MIP-3α may regulate additional biological activities in the intestine. The aim of this study was to determine whether MIP-3α can induce intestinal epithelial cell proliferation and to examine the signaling mechanisms that mediate this response. We show that nonstimulated Caco-2 and HT-29 colonic epithelial cells express CCR6, and that stimulation of Caco-2 cells by MIP-3α can dose dependently increase cell proliferation as well as activate the epidermal growth factor receptor (EGFR) and ERK1/2 MAPK. MIP-3α-mediated ERK1/2 activation in Caco-2 cells appeared to require metalloproteinase-dependent release of the endogenous EGFR ligand amphiregulin and transactivation of the EGFR. Moreover, blockade of amphiregulin bioactivity using a neutralizing polyclonal Ab significantly reduced MIP-3α-mediated, but not EGF-mediated Caco-2 cell proliferation. Taken together, our findings indicate that MIP-3α can regulate mitogenic signaling in colonic epithelial cells and thus may serve an important homeostatic function in the intestine by regulating tissue turnover and maintenance of the epithelium, in addition to its role in regulating leukocyte recruitment.

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Section: Discussionsupporting

confidence: 76%

Section: Macrophage-inflammatory Protein-3␣ Mediates Epidermal Growthsupporting

confidence: 51%

Macrophage-Inflammatory Protein-3α Mediates Epidermal Growth Factor Receptor Transactivation and ERK1/2 MAPK Signaling in Caco-2 Colonic Epithelial Cells via Metalloproteinase-Dependent Release of Amphiregulin

Keates

Han

Kelly

et al. 2007

The Journal of Immunology

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“…The expected role for expression of these ligands is in the recruitment of leukocytes to sites needed to fight infection and in the homeostasis of the gut epithelium. 23 However, CXCR2 −/− mice remain quite small and do not grow as well as the heterozygous and wildtype mice. A role for CXCR2 in absorption or homeostasis of the gut has not yet been explored.…”

Section: Discussionmentioning

confidence: 99%

Developmental Expression of Two CXC Chemokines, Mip-2 and Kc, and Their Receptors

Luan

Furuta

et al. 2001

Cytokine

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CXC chemokines, macrophage inflammatory protein-2 (MIP-2) and KC, (a cloning designation based on ordinate and abscissa position) as well as the CXC chemokine receptor, CXCR2, are expressed in a variety of cells and tissues in adult mice. Targeted deletion of the gene encoding murine CXCR2 does not result in obvious changes in the development of the organ system of the mouse, though the CXCR2 −/− mouse is compromised with regard to its ability to resist infection, heal wounds, and maintain homeostasis when challenged with microbes and/or chemicals. In an attempt to develop insight into additional possible subtle roles of CXCR2 and its ligands in the development of the mouse, we examined the expression of MIP-2, KC, CXCR2, as well as the Duffy antigen binding protein for chemokines during embryonic (p.c.) days 11.5 through 14.5 in the mouse. We observed strong correlation between the expression of MIP-2 and CXCR2 in the developing brain, cardiovascular system and condensing mesenchyme between 11.5 and 13.5 days. Moreover, the expression of KC was parallel to the expression of the Duffy antigen binding protein for chemokines with regard to temporal pattern and tissue localization. MIP-2 and CXCR2 are highly expressed in the brain, first in the cerebellum and in the head mesenchyme, the meninges and the floor plate, and by 14.5 days are also present in the telencephalon, thalamus and hypothalamus. In the developing brain KC and Duffy were prominently expressed in the neuronal tracts, the forebrain, sympathetic ganglia, and along the periphery of the neural tube. However, KC and Duffy were less prevalent in the developing cardiovascular system, lung and other organs, muscle and bone, than are CXCR2 and MIP-2. These data suggest that the roles for these chemokines and their receptors during development may be more significant than was initially thought based upon the phenotype of the mice with targeted deletion of CXCR2 and Duffy.

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“…Ishiguro et al [8] reported that in a rat model of trinitrobenzene sulfonic acid (TNBS)-induced colitis, CINC-1 enhances the expression of co-stimulatory molecules on dendritic cells in the mesenteric lymph nodes [8]. In addition, Suzuki et al [9] reported the growthstimulatory effects of CINC-1 on rat gastric epithelia cells.…”

Section: Cinc-1 Functionmentioning

confidence: 99%

Rat Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) in Inflammation

Handa¹,

Naito²,

Yoshikawa³

2006

J. Clin. Biochem. Nutr.

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Summary Rat cytokine-induced neutrophil chemoattractant-1 (CINC-1) belongs to the CXCchemokine family and is a counterpart of human growth-related oncogene (GRO) in the interleukin-8 (IL-8) family. In rats, CINC-1 plays a key role in neutrophil-mediated inflammatory diseases by attracting neutrophils to the site of inflammation. Although IL-8 is a well-known chemokine in humans, it remains difficult to investigate human inflammatory diseases in detail. Therefore CINC-1 is expected to be an excellent tool for investigating neutrophil-mediated inflammatory diseases, and it has served extensively as a target chemokine in studies performed to date. However, little is known regarding CINC-1 signaling pathways. In this review, we focused on the signal transduction of CINC-1 production/ expression.

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Rat CXC chemokine GRO/CINC‐1 paradoxically stimulates the growth of gastric epithelial cells

Cited by 20 publications

References 17 publications

Macrophage-Inflammatory Protein-3α Mediates Epidermal Growth Factor Receptor Transactivation and ERK1/2 MAPK Signaling in Caco-2 Colonic Epithelial Cells via Metalloproteinase-Dependent Release of Amphiregulin

Macrophage-Inflammatory Protein-3α Mediates Epidermal Growth Factor Receptor Transactivation and ERK1/2 MAPK Signaling in Caco-2 Colonic Epithelial Cells via Metalloproteinase-Dependent Release of Amphiregulin

Developmental Expression of Two CXC Chemokines, Mip-2 and Kc, and Their Receptors

Rat Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) in Inflammation

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