Inhibition of the angiogenesis by the MCP‐1 (monocyte chemoattractant protein‐1) binding peptide

Kim, Mee Young; Byeon, Cheol Woo; Hong, Ki Hwan; Han, Ki Hoon; Jeong, Sunjoo

doi:10.1016/j.febslet.2005.01.070

Cited by 40 publications

(27 citation statements)

References 32 publications

(35 reference statements)

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“…According to our observations, MCP-1 is not associated with tumour mass, and this chemokine does not promote production of inflammatory proteins. MCP-1 is the first CC chemokine reported to play a direct role in tumour angiogenesis [23], and some studies describe possible mechanisms by which this chemokine induces angiogenesis [24,25]. Results of our immunohistochemical analysis are in accordance with this observation, since microvessel density and macrophage level were higher in high-grade than in low-grade lymphomas as observed in previous studies [26].…”

Section: Discussionsupporting

confidence: 95%

Macrophage chemotactic protein-1 mRNA levels in non-Hodgkin lymphoma

et al. 2010

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Non-Hodgkin lymphoma (NHL) is one of the most common malignancies whose incidence increases, and the treatment results are not satisfactory. The aim of this study was to determine the capacity of NHL to produce MCP-1, chemokine that induces chemotaxis of macrophages and lymphoid cells. The mRNA expression and protein MCP-1 expression were determined in the samples of 20 patients with NHL and 8 reactive tonsils. MCP-1 mRNA was detected in 8/8 tonsils and in 19/20 patients with NHL by real-time PCR analysis. In addition, the amount of detected MCP-1 cDNA was significantly higher in patients with limited stage, good IPI, normal level of fibrinogen and LDH. Finally, in patients with aggressive NHL, the level of MCP-1 cDNA was higher than in indolent tumours. Immunohistochemical analysis revealed that majority of stromal elements such as macrophages, endothelial and smooth muscle cells in reactive as well as in neoplastic lymphoid tissue showed strong cytoplasmic MCP-1 expression. Moderate cytoplasmic MCP-1 expression was also observed in reactive lymphocytes, while tumour cells of indolent NHL were mostly pale in comparison with aggressive lymphomas which predominantly demonstrated intense MCP-1 staining. These intriguing preliminary results emphasize the need for further investigations that must be conducted on the representative sample with concordant measurement of serum MCP-1 level.

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Section: Discussionsupporting

confidence: 95%

Macrophage chemotactic protein-1 mRNA levels in non-Hodgkin lymphoma

et al. 2010

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“…Gharaee-Kermani et al [28] showed that MCP-1 promotes collagen expression by fibroblasts in a transforming growth factor b-dependent manner. Recently, MCP-1 has been recognized as an angiogenic chemokine [29][30][31]. Salcedo et al [30] showed that the angiogenic effect of MCP-1 does not require inflammatory leukocytes.…”

Section: Discussionmentioning

confidence: 99%

Chemokines in proliferative diabetic retinopathy and proliferative vitreoretinopathy

Asrar

Struyf

Kangave

et al. 2008

Acta Ophthalmologica

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“…Furthermore, ongoing studies have also determined that imposition of a chronic exercise regimen can have the beneficial impact of blunting the severity of this inflammatory condition and can include reductions in the levels of C-reactive peptide, IL-1␤, tumor necrosis factor-␣, and IL-6 (18,42,48). To investigate the correlation between the genesis of the metabolic syndrome and the regulation of skeletal muscle microvessel density in response to chronic exercise, we determined levels of inflammatory cytokines associated with angiogenesis within the setting of cancerous tumor progression [IL-13 (16,33,34), MCP-1 (25,27,28,33), and IL-1␤ (9, 41, 54)]. As presented in Fig.…”

Section: Discussionmentioning

confidence: 99%

Exercise training blunts microvascular rarefaction in the metabolic syndrome

Frisbee¹,

Samora²,

Peterson³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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son, and Randall Bryner. Exercise training blunts microvascular rarefaction in the metabolic syndrome. Am J Physiol Heart Circ Physiol 291: H2483-H2492, 2006. First published June 23, 2006 doi:10.1152/ajpheart.00566.2006.-Reduced skeletal muscle microvessel density (MVD) in the obese Zucker rat (OZR) model of the metabolic syndrome is a function of a chronic reduction in vascular nitric oxide (NO) bioavailability. Previous studies suggest that exercise can improve NO bioavailability and reduce chronic inflammation and that low vascular NO bioavailability may be associated with impaired angiogenic responses via increased matrix metalloproteinase (MMP)-2 and MMP-9 activity. As such, we hypothesized that chronic exercise (EX) would increase NO bioavailability in OZR and blunt microvascular rarefaction through reduced MMP activity, and potentially via altered plasma cytokine levels. Ten weeks of treadmill exercise (1 h/day, 5 days/wk, 22 m/min) reduced body mass and fasting insulin and triglyceride levels in EX-OZR vs. sedentary (SED) OZR. In EX-OZR, gastrocnemius muscle MVD was improved by 19 Ϯ 4%, whereas skeletal muscle arteriolar dilation and conduit arterial methacholine-induced NO release were increased. In EX-OZR, functional hyperemia was improved vs. SED-OZR, and minimum vascular resistance within perfused gastrocnemius muscle was reduced, although no change in arteriolar stiffness was identified. Western blotting and gelatin zymography demonstrated that neither expression nor activity of MMP-2 or MMP-9 was altered in skeletal muscle of EX vs. SED animals. Plasma markers of inflammation associated with angiogenesis, monocyte chemoattractant protein-1 and IL-1␤, were increased in SED-OZR and were reduced with training, whereas IL-13 was reduced in SED-OZR and increased with exercise. These data suggest that exercise-induced improvements in skeletal muscle MVD in OZR are associated with increased NO bioavailability and may stem from altered inflammatory profiles rather than MMP function. skeletal muscle microcirculation; regulation of skeletal muscle perfusion; microvessel density; vascular remodeling; vascular resistance THE OBESE ZUCKER RAT (OZR) is a model of the metabolic syndrome based on chronic hyperphagia (5, 21). As such, this animal model rapidly becomes obese and develops profound insulin resistance and hypertriglyceridemia, with a clinically relevant hypertension and the genesis of a prothrombotic and proinflammatory state (2,17,24,51). We have previously demonstrated that, with evolution of the metabolic syndrome in the OZR, a progressive reduction in skeletal muscle microvessel density develops that can result in 25% reduction in the total number of microvessels within this tissue compared with levels determined in control animals (14). This rarefaction of the vascular network contributes to an elevation in peripheral vascular resistance in OZR (12, 14, 15) and appears to be largely independent of any developing increase in mean arterial pressure (13). In contrast, ongoing studies in our laborat...

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Inhibition of the angiogenesis by the MCP‐1 (monocyte chemoattractant protein‐1) binding peptide

Cited by 40 publications

References 32 publications

Macrophage chemotactic protein-1 mRNA levels in non-Hodgkin lymphoma

Macrophage chemotactic protein-1 mRNA levels in non-Hodgkin lymphoma

Chemokines in proliferative diabetic retinopathy and proliferative vitreoretinopathy

Exercise training blunts microvascular rarefaction in the metabolic syndrome

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