Mitogen-Activated Protein Kinase Activation Mediates PDGF- Directed Migration of RPE Cells

Hinton, David R.; He, Shikun; Graf, Kristof; Yang, Dong; Hsueh, Willa A.; Ryan, Stephen J.; Law, Ronald E.

doi:10.1006/excr.1997.3873

Cited by 60 publications

(38 citation statements)

References 14 publications

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“…The PDGF-induced chemotaxis of Rat1 fibroblasts was unaffected by PD98059 treatment (28). In contrast, the chemotactic response to PDGF was dependent on ERK 1/2 in human mesangial cells (29) and retinal pigment epithelial cells (30). Our data support the idea that the PI3-K and ERK pathways both mediate PDGF-stimulated motility responses in neuroblastoma cells.…”

Section: Somatostatin Inhibits Pdgf-induced Rac Activation In Sh-supporting

confidence: 73%

Anti-migratory and Anti-invasive Effect of Somatostatin in Human Neuroblastoma Cells

Pola¹,

Cattaneo²,

Vicentini

2003

Journal of Biological Chemistry

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Cell motility and invasion are crucial events for the spread of cancer and, consequently, the metastatic process. Platelet-derived growth factor (PDGF) is not only capable of stimulating the proliferation of SH-SY5Y human neuroblastoma cells, but also their migration and invasion through an extracellular matrix barrier. Experiments using wortmannin and PD98059, specific inhibitors of the phosphatidylinositol 3-kinase (PI3-K) and of the mitogen-activated protein kinases (ERK 1 and 2) signaling, respectively, show that the activation of both pathways is required for the PDGF-induced cell motility responses. We have previously shown that somatostatin inhibits cell division and ERK 1/2 and Ras activity in SH-SY5Y cells. We report here that it is also capable of potently and effectively inhibiting their PDGF-stimulated migration and invasion. The inhibitory effect of somatostatin is sensitive to pertussis toxin. Although somatostatin does not affect PI3-K, it inhibits ERK 1/2 and the small G-protein Rac activation and ruffle formation induced by PDGF. These results indicate that somatostatin can be considered an anti-migratory and antiinvasive agent that acts by inhibiting ERK 1/2 signaling and the PI3-K pathway via the inhibition of Rac in SH-SY5Y cells.

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Section: Somatostatin Inhibits Pdgf-induced Rac Activation In Sh-supporting

confidence: 73%

Anti-migratory and Anti-invasive Effect of Somatostatin in Human Neuroblastoma Cells

Pola¹,

Cattaneo²,

Vicentini

2003

Journal of Biological Chemistry

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“…26 In brief, 5 Â 10 4 ARPE-19 cells resuspended in 200 ml control medium (1% FBS-DMEM/F12) were seeded onto the upper compartment of the BD Falcon s culture inserts (BD Bioscience, San Jose, CA) with an 8-mm diameter pore size membrane in a 24-well companion plate. The lower chamber was filled with control medium (negative control) and those containing 50, 100, or 200 ng/ml rHMGB1.…”

Section: Migration Assaymentioning

confidence: 99%

Intraocular expression and release of high-mobility group box 1 protein in retinal detachment

Arimura

Kii

Hashiguchi

et al. 2009

Laboratory Investigation

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High-mobility group box 1 (HMGB1) protein is a multifunctional protein, which is mainly present in the nucleus and is released extracellularly by dying cells and/or activated immune cells. Although extracellular HMGB1 is thought to be a typical danger signal of tissue damage and is implicated in diverse diseases, its relevance to ocular diseases is mostly unknown. To determine whether HMGB1 contributes to the pathogenesis of retinal detachment (RD), which involves photoreceptor degeneration, we investigated the expression and release of HMGB1 both in a retinal cell death induced by excessive oxidative stress in vitro and in a rat model of RD-induced photoreceptor degeneration in vivo. In addition, we assessed the vitreous concentrations of HMGB1 and monocyte chemoattractant protein 1 (MCP-1) in human eyes with RD. We also explored the chemotactic activity of recombinant HMGB1 in a human retinal pigment epithelial (RPE) cell line. The results show that the nuclear HMGB1 in the retinal cell is augmented by death stress and upregulation appears to be required for cell survival, whereas extracellular release of HMGB1 is evident not only in retinal cell death in vitro but also in the rat model of RD in vivo. Furthermore, the vitreous level of HMGB1 is significantly increased and is correlated with that of MCP-1 in human eyes with RD. Recombinant HMGB1 induced RPE cell migration through an extracellular signalregulated kinase-dependent mechanism in vitro. Our findings suggest that HMGB1 is a crucial nuclear protein and is released as a danger signal of retinal tissue damage. Extracellular HMGB1 might be an important mediator in RD, potentially acting as a chemotactic factor for RPE cell migration that would lead to an ocular pathological wound-healing response.

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“…Activation of the PI3K and MAPK pathways can be important for cell motility and chemotaxis (18)(19)(20)(21)(22). The products of PI3K regulate the cytoskeleton through Rho family G proteins as well as Akt (23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

ErbB3-Dependent Motility and Intravasation in Breast Cancer Metastasis

Xue¹,

Liang

Mahmood³

et al. 2006

Cancer Research

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A better understanding of how epidermal growth factor receptor family members (ErbBs) contribute to metastasis is important for evaluating ErbB-directed therapies. Activation of ErbB3/ErbB2 heterodimers can affect both proliferation and motility. We find that increasing ErbB3-dependent signaling in orthotopic injection models of breast cancer can enhance intravasation and lung metastasis with no effect on primary tumor growth or microvessel density. Enhanced metastatic ability due to increased expression of ErbB2 or ErbB3 correlated with stronger chemotaxis and invasion responses to heregulin B1. Suppression of ErbB3 expression reduced both intravasation and metastasis. A human breast cancer tumor tissue microarray showed a significant association between ErbB3 and ErbB2 expression and metastasis independent of tumor size. These results indicate that ErbB3-dependent signaling through ErbB3/ErbB2 heterodimers can contribute to metastasis through enhancing tumor cell invasion and intravasation in vivo and that ErbB-directed therapies may be useful for the inhibition of invasion independent of effects on tumor growth.

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Mitogen-Activated Protein Kinase Activation Mediates PDGF- Directed Migration of RPE Cells

Cited by 60 publications

References 14 publications

Anti-migratory and Anti-invasive Effect of Somatostatin in Human Neuroblastoma Cells

Anti-migratory and Anti-invasive Effect of Somatostatin in Human Neuroblastoma Cells

Intraocular expression and release of high-mobility group box 1 protein in retinal detachment

ErbB3-Dependent Motility and Intravasation in Breast Cancer Metastasis

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