Monocyte chemoattractant protein-1–induced angiogenesis is mediated by vascular endothelial growth factor-A

Hong, Ki Hwan; Ryu, Jewon; Han, Ki Hoon

doi:10.1182/blood-2004-08-3178

Cited by 336 publications

(255 citation statements)

References 18 publications

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“…Moreover, data from studies of animal models suggest that MCP-1 is involved in the pathogenesis of RA (36)(37)(38), and MCP-1 was recently reported to be a sensitive marker of disease activity in patients with juvenile RA (39). MCP-1 attracts memory T lymphocytes and natural killer cells, which are major contributors to the pathogenesis of RA (40). In addition, MCP-1 mediates angiogenesis via VEGF (41).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐124a is a key regulator of proliferation and monocyte chemoattractant protein 1 secretion in fibroblast‐like synoviocytes from patients with rheumatoid arthritis

Nakamachi¹,

Kawano²,

Takenokuchi³

et al. 2009

Arthritis & Rheumatism

301

209

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Objective. To elucidate the role of microRNA (miRNA) in the pathogenesis of rheumatoid arthritis (RA), we analyzed synoviocytes from RA patients for their miRNA expression.Methods. Synoviocytes derived from surgical specimens obtained from RA patients were compared with those obtained from osteoarthritis (OA) patients for their expression of a panel of 156 miRNA with quantitative stem-loop reverse transcription-polymerase chain reaction. The miRNA whose expression decreased or increased in RA synoviocytes as compared with OA synoviocytes were identified, and their target genes were predicted by computer analysis. We used an in vitro system of enhancing the expression of specific miRNA by transfection of precursors into synoviocytes, and then we performed proliferation, cell cycle, and apoptosis assays, as well as enzyme-linked immunosorbent assays for cytokine production. The effects of transfection on predicted target protein and messenger RNA (mRNA) were then examined by Western blot analysis and luciferase reporter assay.Results. We found that miR-124a levels significantly decreased in RA synoviocytes as compared with OA synoviocytes. Transfection of precursor miR-124a into RA synoviocytes significantly suppressed their proliferation and arrested the cell cycle at the G 1 phase. We identified a putative consensus site for miR-124a binding in the 3 -untranslated region of cyclin-dependent kinase 2 (CDK-2) and monocyte chemoattractant protein 1 (MCP-1) mRNA. Induction of miR-124a in RA synoviocytes significantly suppressed the production of the CDK-2 and MCP-1 proteins. Luciferase reporter assay demonstrated that miR-124a specifically suppressed the reporter activity driven by the 3 -untranslated regions of CDK-2 and MCP-1 mRNA.Conclusion. The results of this study suggest that miR-124a is a key miRNA in the posttranscriptional regulatory mechanisms of RA synoviocytes.MicroRNA (miRNA) are a well-established class of small (ϳ22 nucleotides) endogenous noncoding RNAs that influence the stability and translation of messenger RNA (mRNA) (1). Using various computational and experimental approaches, hundreds of miRNA have been identified in numerous animal species. The miRNA genes are transcribed by RNA polymerase II as primary miRNA (pri-miRNA) (2,3). The RNase III enzyme Drosha then processes the nuclear pri-miRNA, yielding a ϳ70-nucleotide molecule known as precursor miRNA (pre-miRNA) (4), which is exported from the nucleus. Maturation of the pre-miRNA into miRNA is then mediated by the cytoplasmic enzyme Dicer (5), after which the mature miRNA is loaded into the RNA-induced silencing complex (RISC)

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐124a is a key regulator of proliferation and monocyte chemoattractant protein 1 secretion in fibroblast‐like synoviocytes from patients with rheumatoid arthritis

Nakamachi¹,

Kawano²,

Takenokuchi³

et al. 2009

Arthritis & Rheumatism

301

209

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“…Thus, APBA3 is a possible target for metastasis suppression by targeting monocyte/macrophage-specific machineries. CCL2 functions not only as a chemoattractant, as it has also been reported to induce VEGFA expression by regulating VEGFA mRNA transcription and stability (42,43). Thus, CCL2 produced by tumor and stromal cells might contribute to VEGFA expression in IMs.…”

Section: Discussionmentioning

confidence: 99%

Control of metastatic niche formation by targeting APBA3/Mint3 in inflammatory monocytes

Hara

Nakaoka

Hayashi

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Cancer metastasis is intricately orchestrated by both cancer and normal cells, such as endothelial cells and macrophages. Monocytes/macrophages, which are often co-opted by cancer cells and promote tumor malignancy, acquire more than half of their energy from glycolysis even during normoxic conditions. This glycolytic activity is maintained during normoxia by the functions of hypoxia inducible factor 1 (HIF-1) and its activator APBA3. The mechanism by which APBA3 inhibition partially suppresses macrophage function and affects cancer metastasis is of interest in view of avoidance of the adverse effects of complete suppression of macrophage function during therapy. Here, we report that APBA3-deficient mice show reduced metastasis, with no apparent effect on primary tumor growth. APBA3 deficiency in inflammatory monocytes, which strongly express the chemokine receptor CCR2 and are recruited toward chemokine CCL2 from metastatic sites, hampers glycolysis-dependent chemotaxis of cells toward metastatic sites and inhibits VEGFA expression, similar to the effects observed with HIF-1 deficiency. Host APBA3 induces VEGFA-mediated E-selectin expression in the endothelial cells of target organs, thereby promoting extravasation of cancer cells and micrometastasis formation. Administration of E-selectin-neutralizing antibody also abolished host APBA3-mediated metastatic formation. Thus, targeting APBA3 is useful for controlling metastatic niche formation by inflammatory monocytes.APBA3/Mint3 | macrophage | metastasis C ancer metastasis comprises multiple processes of neoplastic progression, termed the "invasion-metastasis cascade" (1, 2). Thousands of circulating tumor cells (CTCs) can be released from invasive primary tumors; however, most patients develop only a few metastases, suggesting that metastatic initiation processes (such as extravasation and colonization at distant organs) are quite inefficient but key for controlling metastatic cancer diseases. Unlike at primary sites, single or small groups of disseminated CTCs encounter large numbers of normal cells in their new environments, which determines their survival and metastatic efficiency, as shown by studies with genetically engineered mouse models (3-5).Macrophages are myeloid cells that are co-opted essentially to foster tumor progression and metastasis. The functions of tumorassociated macrophages include angiogenesis, suppression of antitumor immune responses, chemoresistance, and metastasis; these are considered novel targets for cancer therapy (6-10). Monocytes (i.e., macrophage precursors) are characterized by the surface molecules CD11b and CD115, and comprise at least two subsets: Gr-1 + (Ly-6C high )CCR2 + CX3CR1 low inflammatory monocytes (IMs) and Gr-1 low (Ly-6C low )CCR2 low CX3CR1 high resident monocytes (RMs) (11). Their recruitment from the bone marrow (BM) to peripheral tissues is mediated mainly by chemokine-chemokine receptor complexes such as the CCL2/CCR2 system (12, 13). Even in metastatic cascades, the CCL2-CCR2 axis is a key pathway for IM ...

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“…ICAM-1 and MCP-1 (Hong et al, 2005;Lu et al, 1999;Melder et al, 1996). The role of VEGF in causing inflammation during diabetic retinopathy has also been demonstrated by studies showing that increases in VEGF expression are correlated with increased levels of ICAM-1 immunoreactivity and leukostasis in the retinas of diabetic animals (Hammes et al, 1998;Joussen et al, 2001;Joussen et al, 2002;Miyamoto et al, 1999;Murata et al, 1996;Qaum et al, 2001).…”

Section: Vegf and Vascular Inflammation-vegf Is A Potent Inducer Of Vmentioning

confidence: 96%

Vascular endothelial growth factor in eye disease

Penn

Madan

Caldwell

et al. 2008

Progress in Retinal and Eye Research

615

527

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Collectively, angiogenic ocular conditions represent the leading cause of irreversible vision loss in developed countries. In the U.S., for example, retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration are the principal causes of blindness in the infant, working age and elderly populations, respectively. Evidence suggests that vascular endothelial growth factor (VEGF), a 40 kDa dimeric glycoprotein, promotes angiogenesis in each of these conditions, making it a highly significant therapeutic target. However, VEGF is pleiotropic, affecting a broad spectrum of endothelial, neuronal and glial behaviors, and confounding the validity of anti-VEGF strategies, particularly under chronic disease conditions. In fact, among other functions VEGF can influence cell proliferation, cell migration, proteolysis, cell survival and vessel permeability in a wide variety of biological contexts. This article will describe the roles played by VEGF in the pathogenesis of retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. The potential disadvantages of inhibiting VEGF will be discussed, as will the rationales for targeting other VEGF-related modulators of angiogenesis.

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Monocyte chemoattractant protein-1–induced angiogenesis is mediated by vascular endothelial growth factor-A

Abstract: Monocyte chemoattractant protein-1 (MCP-1) has been recognized as an angiogenic chemokine. In the present study, we investigated the detailed mechanism by which MCP-1 induces angiogenesis.

Cited by 336 publications

References 18 publications

MicroRNA‐124a is a key regulator of proliferation and monocyte chemoattractant protein 1 secretion in fibroblast‐like synoviocytes from patients with rheumatoid arthritis

MicroRNA‐124a is a key regulator of proliferation and monocyte chemoattractant protein 1 secretion in fibroblast‐like synoviocytes from patients with rheumatoid arthritis

Control of metastatic niche formation by targeting APBA3/Mint3 in inflammatory monocytes

Vascular endothelial growth factor in eye disease

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