Regulation of Inducible Nitric Oxide Synthase mRNA Levels by Differentiation and Cytokines in Human Keratinocytes

Arany, István; Brysk, Miriam M.; Brysk, Henry; Tyring, Stephen K.

doi:10.1006/bbrc.1996.0452

Cited by 83 publications

(50 citation statements)

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“…In skin tissues, inflammation is likely to be caused by bacterial endotoxin, the wound healing process, various chemokines, and proinflammatory cytokines [11,[21][22][23][24]. As MAPK and PI3K are involved in early intracellular signaling, it is likely that the inhibition of MAPK and PI3K blocks early signaling involved in IFN-g-mediated skin inflammation.…”

Section: Discussionmentioning

confidence: 98%

IFN-gamma regulates the expression of B7-H1 in dermal fibroblast cells

Lee

Seo

Kim

et al. 2005

Journal of Dermatological Science

114

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Section: Discussionmentioning

confidence: 98%

IFN-gamma regulates the expression of B7-H1 in dermal fibroblast cells

Lee

Seo

Kim

et al. 2005

Journal of Dermatological Science

114

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“…IFN-γ stimulates keratinocytes to express various genes, including inflammatory cytokines and chemokines [42,43,44,45], which are also expressed in HAEM lesions [46]. The finding that IFN-γ can also induce/activate SP1 and its target genes supports our previous conclusion that the inflammatory response characteristic of HAEM is multifactorial and includes factors, such as IFN-γ, that are produced by activated virus-specific T cells which infiltrate the HAEM skin in response to Pol expression [6].…”

Section: Discussionmentioning

confidence: 99%

The Herpes Simplex Virus Gene Pol Expressed in Herpes-Associated Erythema Multiforme Lesions Upregulates/Activates SP1 and Inflammatory Cytokines

et al. 2007

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Background/Aims: Herpes-simplex-virus-associated erythema multiforme (HAEM) is characterized by lesional skin expression of the viral protein Pol and localized inflammation. The objective of this study is to examine the mechanism whereby Pol induces localized inflammation. Methods: A431 cells transfected with Pol or an empty vector and lesional skin from HAEM or drug-induced erythema multiforme patients were examined for expression of the transcription factor SP1 and SP1-regulated genes by immunoblotting, immunohistochemistry and immunofluorescence. Results: SP1, TGF-β, p21^waf1 and Hsp27 were upregulated in A431 cells transfected with Pol but not the empty vector. Expression was further increased by exposure to IFN-γ. Pol+ HAEM lesional skin expressed SP1, Hsp27, TGF-β and p21^waf1. Normal skin and drug-induced erythema multiforme lesional skin were negative. Conclusion: The data indicate that Pol activates SP1, causing upregulation of SP1 target genes (notably TGF-β) involved in localized inflammation. Upregulation is potentiated by IFN-γ.

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“…In contrast, iNOS is a calcium-independent enzyme, and releases far greater amounts of NO and exerts cytotoxic and cytostatic effects not only against invading pathogens, but also against healthy cells (6)(7)(8). iNOS is induced in a number of cell types, such as fibroblasts, macrophages, and epithelium of the iris-ciliary body, especially after stimulation by cytokines, such as interleukin-1 (IL-1 ), tumor necrosis factor-(TNF-), and lipopolysaccharides (LPS) (9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

The Role of Nitric Oxide in Ocular Surface Cells

et al. 2002

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The role of nitric oxide (NO) in the ocular surface remains unknown. We investigated the conditions leading to an increase of NO generation in tear and the main sources of NO in ocular surface tissue. We evaluated the dual action (cell survival or cell death) of NO depending on its amount. We measured the concentration of nitrite plus nitrate in the tears of ocular surface diseases and examined the main source of nitric oxide synthase (NOS). When cultured human corneal fibroblast were treated with NO producing donor with or without serum, the viabilities of cells was studied. We found that the main sources of NO in ocular surface tissue were corneal epithelium, fibroblast, endothelium, and inflammatory cells. Three forms of NOS (eNOS, bNOS, and iNOS) were expressed in experimentally induced inflammation. In the fibroblast culture system, the NO donor (SNAP, S-nitroso-N-acetyl-D, L-penicillamine) prevented the death of corneal fibroblast cells caused by serum deprivation in a dose dependent manner up to 500 micrometer SNAP, but a higher dose decreased cell viability. This study suggested that NO might act as a double-edged sword in ocular surface diseases depending on the degree of inflammation related with NO concentration.

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Regulation of Inducible Nitric Oxide Synthase mRNA Levels by Differentiation and Cytokines in Human Keratinocytes

Cited by 83 publications

References 0 publications

IFN-gamma regulates the expression of B7-H1 in dermal fibroblast cells

IFN-gamma regulates the expression of B7-H1 in dermal fibroblast cells

The Herpes Simplex Virus Gene Pol Expressed in Herpes-Associated Erythema Multiforme Lesions Upregulates/Activates SP1 and Inflammatory Cytokines

The Role of Nitric Oxide in Ocular Surface Cells

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