Kinetics of macrophage subpopulations and expression of monocyte chemoattractant protein-1 (MCP-1) in bleomycin-induced lung injury of rats studied by a novel monoclonal antibody against rat MCP-1

Sakanashi, Yuji; Takeya, Motohiro; Yoshimura, Teizo; Li, Feng; Morioka, Tohru; Takahashi, Kiyoshi

doi:10.1002/jlb.56.6.741

Cited by 66 publications

(43 citation statements)

References 24 publications

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“…MCP-1 was detected in the lesions of various human diseases and animal disease models [22,23], and some of the previous studies suggested that infiltrating PMN might be an important source of MCP-1 in vivo. Infiltrating PMN was one of the main MCP-1-producing cell populations in rat models of bleomycin-induced lung fibrosis [24] and collagen-induced arthritis [25]. The main immunoreactivity for MCP-1 in the early phase of delayed-type hypersensitivity (DTH) reaction induced in the rat skin was associated with infiltrating PMN [26].…”

Section: Introductionmentioning

confidence: 99%

MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression

Yamashiro

Kamohara

Yoshimura

1999

Journal of Leukocyte Biology

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Section: Introductionmentioning

confidence: 99%

MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression

Yamashiro

Kamohara

Yoshimura

1999

Journal of Leukocyte Biology

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“…Five-microgram aliquots of poly(A)ϩ RNA were denatured with formaldehyde and formamide, fractionated by electrophoresis on formaldehyde-agarose gels, transferred to nylon membranes (Hybond N ϩ , Amersham), and immobilized by UV irradiation. The membranes were hybridized overnight with rat MCP-1 cDNA 31 or mouse GAPDH cDNA (American Type Culture Collection, Rockville, Md) and labeled with [ 32 P]dCTP by random priming (Takara Shuzo). The filters were exposed by autoradiography to Kodak XAR5 film for 24 hours at Ϫ70°C with intensifying screens.…”

Section: Northern Blot Analysismentioning

confidence: 99%

“…After avidinbiotin amplification, the slides were incubated with 3Ј,3Ј-diaminobenzidine and counterstained with hematoxylin. To detect MCP-1, the mouse monoclonal antibody clone B4, specific for rat MCP-1, 31 was used, along with the immunohistochemical methods described. 31 Morphometry and cell enumeration were performed by a single observer who was blinded to all treatment protocols.…”

Section: Histopathology and Immunohistochemistrymentioning

confidence: 99%

“…To detect MCP-1, the mouse monoclonal antibody clone B4, specific for rat MCP-1, 31 was used, along with the immunohistochemical methods described. 31 Morphometry and cell enumeration were performed by a single observer who was blinded to all treatment protocols. To quantify the areas affected by inflammatory changes, the hematoxylin-eosinstained whole heart sections (5 per heart) were scanned at ϫ40 magnification by use of a light microscope equipped with a highresolution video camera (Microphoto-FXA, Nikon).…”

Section: Histopathology and Immunohistochemistrymentioning

confidence: 99%

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Inhibition of NO Synthesis Induces Inflammatory Changes and Monocyte Chemoattractant Protein-1 Expression in Rat Hearts and Vessels

Tomita

Egashira

Kubo-Inoue

et al. 1998

ATVB

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107

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Abstract-We recently showed that chronic inhibition of NO synthesis by N -nitro-L-arginine methyl ester (L-NAME) causes coronary vascular remodeling (ie, vascular fibrosis and medial thickening) in rats. To test the hypothesis that the inhibition of NO synthesis induces inflammatory changes in the heart, we characterized the inflammatory lesions that occurred during L-NAME administration and determined whether inflammation involved the induction of monocyte chemoattractant protein-1 (MCP-1) in vivo. During the first week of L-NAME administration to Wistar-Kyoto rats, we observed a marked infiltration of mononuclear leukocytes (ED1-positive macrophages) and fibroblast-like cells (␣-smooth muscle actin-positive myofibroblasts) into the coronary vessels and myocardial interstitial areas. These inflammatory changes were associated with the expression of proliferating cell nuclear antigen and MCP-1 (both mRNA and protein). The areas affected by inflammatory changes, as well as the expression of MCP-1 mRNA, declined after longer (28 days) treatment with L-NAME and were replaced by vascular and myocardial remodeling. Our results support the hypothesis that the inhibition of NO synthesis induces inflammatory changes in coronary vascular and myocardial tissues and involves MCP-1 expression. Results also suggest that the early stages of inflammatory changes are important in the development of later-stage structural changes observed in rat hearts. (Arterioscler Thromb Vasc

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“…A rat MCP-1 cDNA (14) probe and a mouse GAPDH cDNA (American Type Culture Collection, Rockville, MD) probe were used. Relative amount of MCP-1 mRNA was normalized against the amounts of GAPDH mRNA.…”

Section: Histopathology and Immunohistochemistrymentioning

confidence: 99%

Pravastatin Attenuates Cardiovascular Inflammatory and Proliferative Changes in a Rat Model of Chronic Inhibition of Nitric Oxide Synthesis by Its Cholesterol-Lowering Independent Actions.

Egashira

Inoue

et al. 2000

Hypertens Res

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Recent studies suggest that some of the beneficial effects of 3-hydroxyl-3-methylglutaryl (HMG)-CoA reductase inhibitors such as pravastatin may be through their cholesterol-lowering independent effects on the blood vessels. We have recently reported that chronic inhibition of nitric oxide (NO) synthesis with NWnitro-L-arginine methyl ester (L-NAME) increases systolic blood pressure and induces coronary vascular inflammatory changes in rats. We designed this study to investigate whether treatment with pravastatin attenuates such proarteriosclerotic changes through their cholesterol-lowering independent effects.Several groups of Wistar-Kyoto rats were studied: the control group, L group received L-NAME in their drinking water (100 mg/kg per day) and L+Px group received L-NAME plus pravastatin (50, 100 or 250 mg/kg per day). We observed marked increases in monocyte infiltration into the coronary arteries, proliferative cell nuclear antigen-positive cells, and monocyte chemoattractant protein-1 (MCP-1) expression in the heart on day 3 after L-NAME administration began. Treatment with pravastatin did not affect serum cholesterol levels or systolic blood pressure but did reduce the L-NAME induced inflammatory and proliferative changes. Pravastatin also attenuated the MCP-1 gene expression induced by L-NAME. In summary, pravastatin inhibited the inflammatory and proliferative changes in the coronary vessels through their cholesterol-independent effects in this model, which may provide an insight into the mechanisms of antiinflammatory or anti-arteriosclerotic actions of pravastatin. (Hypertens Res 2000; 23: 353-358)

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Kinetics of macrophage subpopulations and expression of monocyte chemoattractant protein-1 (MCP-1) in bleomycin-induced lung injury of rats studied by a novel monoclonal antibody against rat MCP-1

Cited by 66 publications

References 24 publications

MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression

MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression

Inhibition of NO Synthesis Induces Inflammatory Changes and Monocyte Chemoattractant Protein-1 Expression in Rat Hearts and Vessels

Pravastatin Attenuates Cardiovascular Inflammatory and Proliferative Changes in a Rat Model of Chronic Inhibition of Nitric Oxide Synthesis by Its Cholesterol-Lowering Independent Actions.

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