Mitomycin C Upregulates IL-8 and MCP-1 Chemokine Expression via Mitogen-Activated Protein Kinases in Corneal Fibroblasts

Chou, San‐Fang; Chang, Shu‐Wen; Chuang, Jia-Ling

doi:10.1167/iovs.06-0835

Cited by 42 publications

(42 citation statements)

References 43 publications

(54 reference statements)

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“…The activation of ERK has been demonstrated following UV, IR, MMC, and cisplatin treatment (12)(13)(14)16). KSR1 is required for maximal ERK activation induced by growth factor stimulation and cisplatin treatment (7, 13).…”

Section: Ksr1 Is Required For Erk Activation Induced By Genotoxicmentioning

confidence: 99%

“…For example, whereas JNK and p38 MAPK are transiently activated at early time points by DNA-damaging agents, biphasic or sustained ERK activation is observed (3,9). MMC has been shown to activate JNK, p38, and ERK in corneal fibroblasts (14). Similar to the response to IR, JNK, and p38 are activated within minutes, whereas ERK is activated several hours following MMC treatment.…”

mentioning

confidence: 99%

“…However, p38 and JNK are primarily activated in response to cellular stress (10,11). In addition to mitogenic stimulation, ERK is also activated in response to multiple types of DNA damage including UV photoproducts induced by UV irradiation (12), DNA interstrand cross-links (ICLs) generated by cisplatin and MMC (13)(14)(15), and double strand breaks (DSBs) introduced by IR, hydroxyurea, and etoposide (16 -18). Depending on the cell type, the stimulus used, and the duration of activation, ERK activation is able to promote a variety of biological responses, such as proliferation, apoptosis, cell cycle arrest, or differentiation (19 -23).…”

mentioning

confidence: 99%

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KSR1 Is Required for Cell Cycle Reinitiation Following DNA Damage

Razidlo¹,

Johnson²,

Stoeger

et al. 2009

Journal of Biological Chemistry

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Section: Ksr1 Is Required For Erk Activation Induced By Genotoxicmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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KSR1 Is Required for Cell Cycle Reinitiation Following DNA Damage

Razidlo¹,

Johnson²,

Stoeger

et al. 2009

Journal of Biological Chemistry

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“…Antibacterial compounds may display cytotoxic effects and trigger immune responses in humans and other animals (44). Increased levels of MCP-1, IL-8, and IL-6 in cells exposed to these compounds are indicative of inflammation (14). Monocyte-chemotactic protein 1 (MCP-1) is a factor specifically attracting monocytes, and IL-8 is a factor used to recruit neutrophils to the site of inflammation.…”

Section: Resultsmentioning

confidence: 99%

The Antibacterial Activity of Ga³⁺Is Influenced by Ligand Complexation as Well as the Bacterial Carbon Source

Rzhepishevska

Ekstrand‐Hammarström

Popp

et al. 2011

Antimicrob Agents Chemother

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Gallium ions have previously been shown to exhibit antibacterial and antibiofilm properties. In this study, we report differential bactericidal activities of two gallium complexes, gallium desferrioxamine B (Ga-DFOB) and gallium citrate (Ga-Cit). Modeling of gallium speciation in growth medium showed that DFOB and citrate both can prevent precipitation of Ga(OH) 3 , but some precipitation can occur above pH 7 with citrate. Despite this, Ga-Cit 90% inhibitory concentrations (IC 90 ) were lower than those of Ga-DFOB for clinical isolates of Pseudomonas aeruginosa and several reference strains of other bacterial species. Treatment with Ga compounds mitigated damage inflicted on murine J774 macrophage-like cells infected with P. aeruginosa PAO1. Again, Ga-Cit showed more potent mitigation than did Ga-DFOB. Ga was also taken up more efficiently by P. aeruginosa in the form of Ga-Cit than in the form of Ga-DFOB. Neither Ga-Cit nor Ga-DFOB was toxic to several human cell lines tested, and no proinflammatory activity was detected in human lung epithelial cells after exposure in vitro. Metabolomic analysis was used to delineate the effects of Ga-Cit on the bacterial cell. Exposure to Ga resulted in lower concentrations of glutamate, a key metabolite for P. aeruginosa, and of many amino acids, indicating that Ga affects various biosynthesis pathways. An altered protein expression profile in the presence of Ga-Cit suggested that some compensatory mechanisms were activated in the bacterium. Furthermore, the antibacterial effect of Ga was shown to vary depending on the carbon source, which has importance in the context of medical applications of gallium.

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“…(66,(70)(71)(72) (Figure 1). 11,32,76,77) (78)(79)(80)(81)(82)(83)(84)(85)(86)(87)(88)(89) and ERK (59,(79)(80)(81)(82) (93,94). Both a JNK-inhibitor (93,(95)(96)(97)(98)(99) as well as a p38-inhibitor (93,(99)(100)(101)(102) are able to reduce gene expression of E-selectin (Figure 1).…”

Section: Induction Of Brain Death Leads To Hemodynamic Changesmentioning

confidence: 99%

Signal Transduction Pathways Involved in Brain Death-Induced Renal Injury

Bouma¹,

Ploeg

Schuurs

2009

American Journal of Transplantation

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Kidneys derived from brain death organ donors show an inferior survival when compared to kidneys derived from living donors. Brain death is known to induce organ injury by evoking an inflammatory response in the donor. Neuronal injury triggers an inflammatory response in the brain, leading to endothelial dysfunction and the release of cytokines in the circulation. Serum levels of interleukin-6, -8, -10, and monocyte chemoattractant protein-1 (MCP-1) are increased after brain death. Binding with cytokine-receptors in kidneys stimulates activation of nuclear factor-kappa B (NF-j B), selectins, adhesion molecules and production of chemokines leading to cellular influx. Mitogenactivated protein kinases (MAP-kinases) mediate inflammatory responses and together with NF-j B they seem to play an important role in brain death induced renal injury. Altering the activation state of MAPkinases could be a promising drug target for early intervention to reduce cerebral injury related donor kidney damage and improve outcome after transplantation.

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Mitomycin C Upregulates IL-8 and MCP-1 Chemokine Expression via Mitogen-Activated Protein Kinases in Corneal Fibroblasts

Abstract: MMC treatment upregulated the expression of IL-8 and MCP-1 mRNA and protein secretion by the activation of mitogen-activated protein kinases (MAPKs) in corneal fibroblasts.

Cited by 42 publications

References 43 publications

KSR1 Is Required for Cell Cycle Reinitiation Following DNA Damage

KSR1 Is Required for Cell Cycle Reinitiation Following DNA Damage

The Antibacterial Activity of Ga³⁺Is Influenced by Ligand Complexation as Well as the Bacterial Carbon Source

Signal Transduction Pathways Involved in Brain Death-Induced Renal Injury

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Mitomycin C Upregulates IL-8 and MCP-1 Chemokine Expression via Mitogen-Activated Protein Kinases in Corneal Fibroblasts

Abstract: MMC treatment upregulated the expression of IL-8 and MCP-1 mRNA and protein secretion by the activation of mitogen-activated protein kinases (MAPKs) in corneal fibroblasts.

Cited by 42 publications

References 43 publications

KSR1 Is Required for Cell Cycle Reinitiation Following DNA Damage

KSR1 Is Required for Cell Cycle Reinitiation Following DNA Damage

The Antibacterial Activity of Ga3+Is Influenced by Ligand Complexation as Well as the Bacterial Carbon Source

Signal Transduction Pathways Involved in Brain Death-Induced Renal Injury

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The Antibacterial Activity of Ga³⁺Is Influenced by Ligand Complexation as Well as the Bacterial Carbon Source