UV-DNA Damage in Mouse and Human Cells Induces the Expression of Tumor Necrosis Factor α

Kibitel, Jeannie; Hejmadit, Vidya; Alas, Lori; O’Connor, Adrienne; Sutherland, Betsy M.; Yarosh, Daniel B.

doi:10.1111/j.1751-1097.1998.tb09452.x

Cited by 56 publications

(34 citation statements)

References 30 publications

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“…CsA and ascomycin increase UVB-induced TNF-a production DNA damage has been shown to be a signal that induces the production of TNF-a (Kibitel et al 1998 Fig. 4 Calcineurin inhibitors, but not immunosuppressive steroids, decrease CPD repair in NHEK cells.…”

Section: Topical Immunosuppressants Inhibit Cpd Repair In Artificial mentioning

confidence: 98%

Calcineurin inhibitors reduce nuclear localization of transcription factor NFAT in UV-irradiated keratinocytes and reduce DNA repair

et al. 2006

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Calcineurin inhibitors are drugs used to suppress the immune system by blocking the nuclear localization of the NFAT transcription factor. Systemic use of these drugs is essential to organ transplantation, but comes at the cost of elevated rates of skin cancer. They have been used topically in atopic dermatitis and other skin diseases on the assumption that they avoid the cancer risk by localized use. The results here show that in skin cells and artificial models of human skin, calcineurin inhibitors block UV-induced nuclear localization of NFAT, and significantly reduce repair of cyclobutane pyrimidine dimers induced in DNA. In addition they inhibit apoptosis of UV-irradiated cells. The effect of blocking nuclear localization of NFAT and inhibiting DNA repair should be considered in judging the risk of topical use of calcineurin inhibitors.

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Section: Topical Immunosuppressants Inhibit Cpd Repair In Artificial mentioning

confidence: 98%

Calcineurin inhibitors reduce nuclear localization of transcription factor NFAT in UV-irradiated keratinocytes and reduce DNA repair

et al. 2006

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“…Moreover, the MAP kinase family, including ERK, JNK and p38 MAPKs, has been implicated in mammalian melanogenesis (4)(5)(6). Some herbal extracts have been reported to exert anti-melanogenic influence by modulating MAPK signalling (7,8).…”

Section: Conflict Of Interestmentioning

confidence: 99%

Skin organ culture as a model to study oxidative stress, inflammation and structural alterations associated with UVB‐induced photodamage

Portugal-Cohen

Soroka

Frušić-Zlotkin

et al. 2011

Experimental Dermatology

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“…Among a number of chromophores (porphyrins, aromatic amino acids, urocanic acid), DNA is regarded as the most important for several reasons. (a) The wavelength dependency of some UVB effects is similar to that for DNA absorption (Petit-Frere et al, 1998), (b) Acceleration of DNA repair inhibits particular biological UVB effects (Kibitel et al, 1998;Kripke et al, 1992 ;Nishigori et al, 1996;Petit-Frere et al, 1998;Wolf et al, 1995), (c) Lower UVB doses achieve the same biological effects in DNA repair deficient compared to proficient cells (Krutmann et al, 1994). Thus, these data favour the concept that DNA is the most important molecular target for UVB.…”

Section: Introductionmentioning

confidence: 79%

UVB-Induced Murine Bone Marrow Derived Macrophages and Apoptosis

Srivastava

Larrea

2008

Immunological Investigations

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A major part of the mutagenic and carcinogenic properties of sunlight has been attributed to UV rays. UV radiation in the middle-wavelength range between 290 and 320 nm (UVB) represents one of the most relevant environmental dangers because of its hazardous effects. Like other adverse agents (alkylating chemicals, oxidants), UVB induces apoptosis in mammalian cells. Elucidation of the underlying molecular mechanisms is of primary importance for the understanding of how UVB can damage cells. To exert its biological effects, UVB must be first absorbed by a cellular chromophore, which transfers the energy into a biochemical signal. DNA damage is regarded as an important reservoir for transferring the biochemical signals of UVB. We have examined the signal mechanism of UVB induced apoptosis in bone marrow derived macrophages. Macrophages exposed to 50 mJ/cm(2) doses and above of UVB irradiation showed the morphological characteristics of apoptotic cells, and electrophoresis of DNA isolated from these cells showed characteristic fragmentation. The DNA fragmentation induced in macrophages with 50 mJ/cm(2) UVB exposure appeared to be sufficient for activating p53, Bax, Caspase-3 and PARP cleavage. This study provides evidence that UVB can cause the apoptosis in bone marrow derived macrophages induced by DNA damage providing an useful experimental model for research and investigational purposes.

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UV-DNA Damage in Mouse and Human Cells Induces the Expression of Tumor Necrosis Factor α

Cited by 56 publications

References 30 publications

Calcineurin inhibitors reduce nuclear localization of transcription factor NFAT in UV-irradiated keratinocytes and reduce DNA repair

Calcineurin inhibitors reduce nuclear localization of transcription factor NFAT in UV-irradiated keratinocytes and reduce DNA repair

Skin organ culture as a model to study oxidative stress, inflammation and structural alterations associated with UVB‐induced photodamage

UVB-Induced Murine Bone Marrow Derived Macrophages and Apoptosis

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