Synergistic induction of monocyte chemoattractant protein‐1 (MCP‐1) by platelet‐derived growth factor and interleukin‐1

doi:10.1016/0014-5793(95)01155-8

Cited by 34 publications

(3 citation statements)

References 22 publications

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“…Very few cells (< 0.1%) from normal arteries expressed MCP-1 mRNA [5]. Expression of MCP-1 is regulated by various growth factors, such as platelet-derived growth factor, interleukin-8, tumor necrosis factor-α, thrombin and interferon-γ, and also by mildly oxidized low-density lipoprotein in mesangial cells and VSMCs [9, 11, 31, 32, 33]. …”

Section: Discussionmentioning

confidence: 99%

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Monocyte Chemotactic Protein 1 Amplifies Serotonin-Induced Vascular Smooth Muscle Cell Proliferation

et al. 2001

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Monocyte chemotactic protein 1 (MCP-1), which is synthesized by vascular cells, is a chemoattractant for monocytes and has been implicated in a wide range of acute and chronic inflammatory processes characterized by monocyte infiltration, including atherosclerosis. However, it is unclear whether MCP-1 is able to modulate vascular smooth muscle cell (VSMC) proliferation. We assessed the effect of MCP-1 on VSMC proliferation and its interaction with serotonin (5-HT), a mitogen for VSMCs. Growth-arrested VSMCs were stimulated with different concentrations of MCP-1 (25–200 ng/ml) and 5-HT (5 and 50 µM) in serum-free medium. DNA synthesis in VSMCs was measured by [³H]thymidine incorporation. 5-HT at concentrations of 5 and 50 µM significantly stimulated DNA synthesis by 1.8- and 2.1-fold over the control value, respectively (p < 0.0001). However, MCP-1 at the concentrations tested did not have any significant effect on DNA synthesis. Even though MCP-1 (50 ng/ml) by itself is not mitogenic, when added to 5-HT, it significantly amplified the mitogenic effect of 5-HT compared with that of 5-HT alone (p < 0.0001). The 5-HT_2A receptor antagonist sarpogrelate (10 µM) and its major metabolite M-1 (0.1 µM), pertussis toxin (10 ng/ml), Src family protein tyrosine kinase (PTK) inhibitor PP2 (1 µM), protein kinase C (PKC) inhibitor Ro31-8220 (0.1 µM) and mitogen-activated protein kinase (MAPK) kinase inhibitor PD098059 (10 µM) significantly inhibited the mitogenic effect of 5-HT and its interaction with MCP-1. Anti-MCP-1 antibody (2 µg/ml) and the Janus kinase 2 (JAK2) inhibitor AG490 (10 µM) significantly inhibited the interaction of MCP-1 with 5-HT. Further, the amplified mitogenic effect of 5-HT with MCP-1 was completely reversed by the combined use of sarpogrelate with anti-MCP-1 antibody. Our results suggest that MCP-1 amplifies the mitogenic effect of 5-HT on VSMCs. The mitogenic effect of 5-HT may be mediated by the G protein-Src family PTK-PKC-MAPK pathway. The activation of the JAK2/signal transducer and activator of transcription 3 pathway by MCP-1 in addition to the MAPK pathway by 5-HT may explain the potentiating effect of MCP-1 on 5-HT-induced mitogenesis.

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Section: Discussionmentioning

confidence: 99%

“…Conti et al [10]demonstrated that MCP-1 stimulates the release of serotonin (5-HT) from rat peritoneal mast cells. Goppelt-Struebe and Stroebel [11]have shown that 5-HT induces MCP-1 RNA expression in rat mesangial cells. However, there have been no studies testing the direct interaction between MCP-1 and 5-HT.…”

Section: Introductionmentioning

confidence: 99%

Monocyte Chemotactic Protein 1 Amplifies Serotonin-Induced Vascular Smooth Muscle Cell Proliferation

et al. 2001

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“…We hypothesized that the lack of statistical significance for the latter two cytokines (TNF-α and IL-1β) relative to the former two cytokines (TGF-β and CCL2) may be due differences in the timescales of their secretion and their relative stability or consumption after secretion in cell culture and during processing; for example, the half-life of TNF-α is on the order of minutes, whereas the half-life of secreted latent TGF-β is on the order of hours and is then activated into TGF-β1. 68–70 To circumvent these potential sources of variability at the protein level and quantitatively confirm phenotypic trends, we looked at the gene-level quantifying the expression of both M1 (IL-1β) and M2 (CD206) markers using RT-qPCR and found that stiff hydrogels significantly downregulated IL-1β gene expression while upregulating CD206 gene expression. 71 Furthermore, our studies explain that the M2 macrophage phenotype, commonly observed in fibrosis, is regulated by multiple fibrotic stimuli working both parallel and in tandem synergistically.…”

Section: Discussionmentioning

confidence: 99%

Destructive fibrotic teamwork: how both microenvironment stiffness and profibrotic interleukin 13 impair alveolar macrophage phenotype and function

et al. 2022

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Tooth eruption molecules enhance MCP-1 gene expression in the dental follicle of the rat

Que

Wise

1998

Dev. Dyn.

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Synergistic induction of monocyte chemoattractant protein‐1 (MCP‐1) by platelet‐derived growth factor and interleukin‐1

Cited by 34 publications

References 22 publications

Monocyte Chemotactic Protein 1 Amplifies Serotonin-Induced Vascular Smooth Muscle Cell Proliferation

Monocyte Chemotactic Protein 1 Amplifies Serotonin-Induced Vascular Smooth Muscle Cell Proliferation

Destructive fibrotic teamwork: how both microenvironment stiffness and profibrotic interleukin 13 impair alveolar macrophage phenotype and function

Tooth eruption molecules enhance MCP-1 gene expression in the dental follicle of the rat

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