nach oben

Journal of Cutaneous Medicine and Surgery

Erschienen in:

01.12.2005

Molecular Aspects of Ultraviolet Radiation-induced Apoptosis in the Skin

verfasst von: Jeffrey Chow, Victor A. Tron

Erschienen in: Journal of Cutaneous Medicine and Surgery | Ausgabe 6/2005

Einloggen, um Zugang zu erhalten

Abstract

Background

Apoptosis, or programmed cell death, is an essential physiological process that controls cell numbers during physiological processes, and eliminates abnormal cells that can potentially harm an organism.

Objective

This review summarizes our current state of knowledge of apoptosis induction in skin by UV radiation.

Methods

A review of the literature was undertaken focusing on cell death in the skin secondary to UV radiation.

Results

It is evident that a number of apoptotic pathways, both intrinsic and extrinsic, are induced following exposure to damaging UV radiation.

Conclusion

Although our understanding of the apoptotic processes is gradually increasing, many important aspects remain obscure. These include interconnections between pathways, wavelength-specific differences and cell type differences.

Kerr JF, Wyllie AH, Currie AR. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer 1972; 26:239–257PubMed

Savill J, Gregory C, Haslett C. Cell biology. Eat me or die. Science 2003; 302:1516–1517PubMedCrossRef

Ziegler U, Groscurth P. Morphological features of cell death. News Physiol Sci 2004; 19:124–128PubMedCrossRef

Zuzarte-Luis V, Hurle JM. Programmed cell death in the developing limb. Int J Dev Biol 2002; 46:871–876PubMed

Vaux DL, Korsmeyer SJ. Cell death in development. Cell 1999; 96:245–254PubMedCrossRef

Rathmell JC, Thompson CB. Pathways of apoptosis in lymphocyte development, homeostasis, and disease. Cell 2002; 109 Suppl:S97–107PubMedCrossRef

Fadeel B, Orrenius S, Zhivotovsky B. Apoptosis in human disease: a new skin for the old ceremony? Biochem Biophys Res Commun 1999; 266:699–717PubMedCrossRef

de Laat A, van der Leun JC, Gruijl FR. Carcinogenesis induced by UVA (365-nm) radiation: the dose-time dependence of tumor formation in hairless mice. Carcinogenesis 1997; 18:1013–1020PubMedCrossRef

Slee EA, Keogh SA, Martin SJ. Cleavage of BID during cytotoxic drug and UV radiation-induced apoptosis occurs downstream of the point of Bcl-2 action and is catalysed by caspase-3: a potential feedback loop for amplification of apoptosis-associated mitochondrial cytochrome c release. Cell Death Differ 2000; 7:556–565PubMedCrossRef

10.

Ziegler A, Jonason AS, Leffell DJ, et al. Sunburn and p53 in the onset of skin cancer. Nature 1994; 372:773–776PubMedCrossRef

11.

Cleaver JE, Bootsma D. Xeroderma pigmentosum: biochemical and genetic characteristics. Annu Rev Genet 1975; 9:19–38PubMedCrossRef

12.

Kraemer KH, Lee MM, Scotto J. Xeroderma pigmentosum. Cutaneous, ocular, and neurologic abnormalities in 830 published cases. Arch Dermatol 1987; 123:241–250PubMedCrossRef

13.

Kahn HS, Tatham LM, Patel AV, et al. Increased cancer mortality following a history of nonmelanoma skin cancer. Jama 1998; 280:910–912PubMedCrossRef

14.

Ichihashi M, Ueda M, Budiyanto A, et al. UV-induced skin damage. Toxicology 2003; 189:21–39PubMedCrossRef

15.

Kulms D, Schwarz T. Independent contribution of three different pathways to ultraviolet-B-induced apoptosis. Biochem Pharmacol 2002; 64:837–841PubMedCrossRef

16.

Guzman E, Langowski JL, Owen-Schaub L. Mad dogs, Englishmen and apoptosis: the role of cell death in UV-induced skin cancer. Apoptosis 2003; 8:315–325PubMedCrossRef

17.

Campbell C, Quinn AG, Ro YS, et al. p53 mutations are common and early events that precede tumor invasion in squamous cell neoplasia of the skin. J Invest Dermatol 1993; 100:746–748PubMedCrossRef

18.

Deng C, Zhang P, Harper JW, et al. Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control. Cell 1995; 82:675–684PubMedCrossRef

19.

Tron VA, Trotter MJ, Tang L, et al. p53-regulated apoptosis is differentiation dependent in ultraviolet B-irradiated mouse keratinocytes. Am J Pathol 1998; 153:579–585PubMed

20.

Chaturvedi V, Sitailo LA, Qin JZ, et al. Knockdown of p53 levels in human keratinocytes accelerates Mcl-1 and Bcl-x(L) reduction thereby enhancing UV-light induced apoptosis. Oncogene 2005 Jun 6; [Epub ahead of print].

21.

Li G, Mitchell DL, Ho VC, et al. Decreased DNA repair but normal apoptosis in ultraviolet-irradiated skin of p53-transgenic mice. Am J Pathol 1996;148:1113–1123PubMed

22.

Chresta CM, Hickman JA. Oddball p53 in testicular tumors. Nat Med 1996; 2:745–746PubMedCrossRef

23.

Ford JM, Hanawalt PC. Expression of wild-type p53 is required for efficient global genomic nucleotide excision repair in UV-irradiated human fibroblasts. J Biol Chem 1997; 272:28073–28080PubMedCrossRef

24.

Smith ML, Fornace AJ Jr. p53-mediated protective responses to UV irradiation. Proc Natl Acad Sci USA 1997; 94:12255–12257PubMedCrossRef

25.

Young LC, Peters AC, Maeda T, et al. DNA mismatch repair protein Msh6 is required for optimal levels of ultraviolet-B-induced apoptosis in primary mouse fibroblasts. J Invest Dermatol 2003; 121:876–880PubMedCrossRef

26.

Peters AC, Young LC, Maeda T, et al. Mammalian DNA mismatch repair protects cells from UVB-induced DNA damage by facilitating apoptosis and p53 activation. DNA Repair (Amst) 2003; 2:427–435CrossRef

27.

Young LC, Hays JB, Tron VA, et al. DNA mismatch repair proteins: potential guardians against genomic instability and tumorigenesis induced by ultraviolet photoproducts. J Invest Dermatol 2003; 121:435–440PubMedCrossRef

28.

Maeda T, Chua PP, Chong MT, et al. Nucleotide excision repair genes are upregulated by low-dose artificial ultraviolet B: evidence of a photoprotective SOS response? J Invest Dermatol 2001; 117:1490–1497PubMedCrossRef

29.

Hildesheim J, Bulavin DV, Anver MR, et al. Gadd45a protects against UV irradiation-induced skin tumors, and promotes apoptosis and stress signaling via MAPK and p53. Cancer Res 2002; 62:7305–7315PubMed

30.

Maeda T, Hanna AN, Sim AB, et al. GADD45 regulates G2/M arrest, DNA repair, and cell death in keratinocytes following ultraviolet exposure. J Invest Dermatol 2002; 119:22–26PubMedCrossRef

31.

Smith ML, Ford JM, Hollander MC, et al. p53-mediated DNA repair responses to UV radiation: studies of mouse cells lacking p53, p21, and/or gadd45 genes. Mol Cell Biol 2000; 20:3705–3714PubMedCrossRef

32.

Takekawa M, Saito H. A family of stress-inducible GADD45-like proteins mediate activation of the stress-responsive MTK1/MEKK4 MAPKKK. Cell 1998; 95:521–530PubMedCrossRef

33.

Jin S, Mazzacurati L, Zhu X, et al. Gadd45a contributes to p53 stabilization in response to DNA damage. Oncogene 2003; 22:8536–8540PubMedCrossRef

34.

Menon EL, Perera R, Kuhn RJ, et al. Reactive oxygen species formation by UV-A irradiation of urocanic acid and the role of trace metals in this chemistry. Photochem Photobiol 2003; 78:567–575PubMedCrossRef

35.

Ichiki H, Sakurada H, Kamo N, et al. Generation of active oxygens, cell deformation and membrane potential changes upon UV-B irradiation in human blood cells. Biol Pharm Bull 1994; 17:1065–1069PubMed

36.

Reid TM, Loeb LA. Tandem double CC–>TT mutations are produced by reactive oxygen species. Proc Natl Acad Sci USA 1993; 90:3904–3907PubMedCrossRef

37.

Zhang X, Rosenstein BS, Wang Y, et al. Identification of possible reactive oxygen species involved in ultraviolet radiation-induced oxidative DNA damage. Free Radic Biol Med 1997; 23:980–985PubMedCrossRef

38.

Renzing J, Hansen S, Lane DP. Oxidative stress is involved in the UV activation of p53. J Cell Sci 1996; 109 (Pt 5):1105–1112PubMed

39.

Vile GF. Active oxygen species mediate the solar ultraviolet radiation-dependent increase in the tumour suppressor protein p53 in human skin fibroblasts. FEBS Lett 1997; 412:70–74PubMedCrossRef

40.

Devary Y, Gottlieb RA, Smeal T, et al. The mammalian ultraviolet response is triggered by activation of Src tyrosine kinases. Cell 1992; 71:1081–1091PubMedCrossRef

41.

Farber JL. Mechanisms of cell injury by activated oxygen species. Environ Health Perspect 1994; 102 Suppl 10:17–24PubMed

42.

Thorburn A. Death receptor-induced cell killing. Cell Signal 2004; 16:139–144PubMedCrossRef

43.

Gutierrez-Steil C, Wrone-Smith T, Sun X, et al. Sunlight-induced basal cell carcinoma tumor cells and ultraviolet-B-irradiated psoriatic plaques express Fas ligand (CD95L). J Clin Invest 1998; 101:33–39PubMed

44.

Hill LL, Ouhtit A, Loughlin SM, et al. Fas ligand: a sensor for DNA damage critical in skin cancer etiology. Science 1999; 285:898–900PubMedCrossRef

45.

Leverkus M, Yaar M, Gilchrest BA. Fas/Fas ligand interaction contributes to UV-induced apoptosis in human keratinocytes. Exp Cell Res 1997; 232:255–262PubMedCrossRef

46.

Faris M, Latinis KM, Kempiak SJ, et al. Stress-induced Fas ligand expression in T cells is mediated through a MEK kinase 1-regulated response element in the Fas ligand promoter. Mol Cell Biol 1998; 18:5414–5424PubMed

47.

Faris M, Kokot N, Latinis K, et al. The c-Jun N-terminal kinase cascade plays a role in stress-induced apoptosis in Jurkat cells by up-regulating Fas ligand expression. J Immunol 1998; 160:134–144PubMed

48.

Kasibhatla S, Brunner T, Genestier L, et al. DNA damaging agents induce expression of Fas ligand and subsequent apoptosis in T lymphocytes via the activation of NF-kappa B and AP-1. Mol Cell 1998; 1:543–551PubMedCrossRef

49.

Muller M, Wilder S, Bannasch D, et al. p53 activates the CD95 (APO-1/Fas) gene in response to DNA damage by anticancer drugs. J Exp Med 1998; 188:2033–2045PubMedCrossRef

50.

Zhuang S, Kochevar IE. Ultraviolet A radiation induces rapid apoptosis of human leukemia cells by Fas ligand-independent activation of the Fas death pathways. Photochem Photobiol 2003; 78:61–67PubMedCrossRef

51.

Aragane Y, Kulms D, Metze D, et al. Ultraviolet light induces apoptosis via direct activation of CD95 (Fas/APO-1) independently of its ligand CD95L. J Cell Biol 1998; 140:171–182PubMedCrossRef

52.

Lewis M, Tartaglia LA, Lee A, et al. Cloning and expression of cDNAs for two distinct murine tumor necrosis factor receptors demonstrate one receptor is species specific. Proc Natl Acad Sci USA 1991; 88:2830–2834PubMedCrossRef

53.

Zhuang L, Wang B, Shinder GA, et al. TNF receptor p55 plays a pivotal role in murine keratinocyte apoptosis induced by ultraviolet B irradiation. J Immunol 1999; 162:1440–1447PubMed

54.

Kock A, Schwarz T, Kirnbauer R, et al. Human keratinocytes are a source for tumor necrosis factor alpha: evidence for synthesis and release upon stimulation with endotoxin or ultraviolet light. J Exp Med 1990; 172:1609–1614PubMedCrossRef

55.

Bazzoni F, Kruys V, Shakhov A, et al. Analysis of tumor necrosis factor promoter responses to ultraviolet light. J Clin Invest 1994; 93:56–62PubMedCrossRef

56.

Corsini E, Bruccoleri A, Marinovich M, et al. In vitro mechanism(s) of ultraviolet-induced tumor necrosis factor-alpha release in a human keratinocyte cell line. Photodermatol Photoimmunol Photomed 1995; 11:112–118PubMed

57.

Kibitel J, Hejmadi V, Alas L, et al. UV-DNA damage in mouse and human cells induces the expression of tumor necrosis factor alpha. Photochem Photobiol 1998; 67:541–546PubMedCrossRef

58.

Leverkus M, Yaar M, Eller MS, et al. Post-transcriptional regulation of UV induced TNF-alpha expression. J Invest Dermatol 1998; 110:353–357PubMedCrossRef

59.

de Kossodo S, Cruz PD Jr, Dougherty I, et al. Expression of the tumor necrosis factor gene by dermal fibroblasts in response to ultraviolet irradiation or lipopolysaccharide. J Invest Dermatol 1995; 104:318–322PubMedCrossRef

60.

Clingen PH, Berneburg M, Petit-Frere C, et al. Contrasting effects of an ultraviolet B and an ultraviolet A tanning lamp on interleukin-6, tumour necrosis factor-alpha and intercellular adhesion molecule-1 expression. Br J Dermatol 2001; 145:54–62PubMedCrossRef

61.

Avalos-Diaz E, Alvarado-Flores E, Herrera-Esparza R. UV-A irradiation induces transcription of IL-6 and TNF alpha genes in human keratinocytes and dermal fibroblasts. Rev Rhum Engl Ed 1999; 66:13–19PubMed

62.

Sheikh MS, Antinore MJ, Huang Y et al. Ultraviolet-irradiation-induced apoptosis is mediated via ligand independent activation of tumor necrosis factor receptor 1. Oncogene 1998; 17:2555–2563PubMedCrossRef

63.

Pan G, O’Rourke K, Chinnaiyan AM, et al. The receptor for the cytotoxic ligand TRAIL. Science 1997; 276:111–113PubMedCrossRef

64.

Sheridan JP, Marsters SA, Pitti RM, et al. Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors. Science 1997; 277:818–821PubMedCrossRef

65.

MacFarlane M, Ahmad M, Srinivasula SM, et al. Identification and molecular cloning of two novel receptors for the cytotoxic ligand TRAIL. J Biol Chem 1997; 272:25417–25420PubMedCrossRef

66.

Walczak H, Degli-Esposti MA, Johnson RS, et al. TRAIL-R2: a novel apoptosis-mediating receptor for TRAIL. Embo J 1997; 16:5386–5397PubMedCrossRef

67.

Wiley SR, Schooley K, Smolak PJ, et al. Identification and characterization of a new member of the TNF family that induces apoptosis. Immunity 1995; 3:673–682PubMedCrossRef

68.

Ravi R, Bedi GC, Engstrom LW, et al. Regulation of death receptor expression and TRAIL/Apo2L-induced apoptosis by NF-kappaB. Nat Cell Biol 2001; 3:409–416PubMedCrossRef

69.

Sheikh MS, Burns TF, Huang Y, et al. p53-dependent and -independent regulation of the death receptor KILLER/DR5 gene expression in response to genotoxic stress and tumor necrosis factor alpha. Cancer Res 1998; 58:1593–1598PubMed

70.

Guan B, Yue P, Clayman GL, et al. Evidence that the death receptor DR4 is a DNA damage-inducible, p53-regulated gene. J Cell Physiol 2001; 188:98–105PubMedCrossRef

71.

Godar DE, Lucas AD. Spectral dependence of UV-induced immediate and delayed apoptosis: the role of membrane and DNA damage. Photochem Photobiol 1995; 62:108–113PubMed

72.

Godar DE. Preprogrammed and programmed cell death mechanisms of apoptosis: UV-induced immediate and delayed apoptosis. Photochem Photobiol 1996; 63:825–830PubMed

73.

Nishigaki R, Mitani H, Tsuchida N, et al. Effect of cyclobutane pyrimidine dimers on apoptosis induced by different wavelengths of UV. Photochem Photobiol 1999; 70:228–235PubMedCrossRef

Titel: Molecular Aspects of Ultraviolet Radiation-induced Apoptosis in the Skin
verfasst von: Jeffrey Chow
Victor A. Tron
Publikationsdatum: 01.12.2005
Verlag: Springer-Verlag
Erschienen in: Journal of Cutaneous Medicine and Surgery / Ausgabe 6/2005
Print ISSN: 1203-4754
Elektronische ISSN: 1615-7109
DOI: https://doi.org/10.1007/s10227-005-0109-0

Leitlinien kompakt für die Dermatologie

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Neu im Fachgebiet Dermatologie

22.04.2024 | DGIM 2024 | Nachrichten

Update Dermatologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Springer Medizin

Molecular Aspects of Ultraviolet Radiation-induced Apoptosis in the Skin

Abstract

Background

Objective

Methods

Results

Conclusion

Leitlinien kompakt für die Dermatologie

Neu im Fachgebiet Dermatologie

Auf diese Krankheiten bei Geflüchteten sollten Sie vorbereitet sein

Kein Abstrich bei chronischen Wunden ohne Entzündungszeichen!

„Nur wer sich gut aufgehoben fühlt, kann auch für Patientensicherheit sorgen“

Vitiligo: Prävalenz steigt und viele Erkrankte werden spät behandelt

Update Dermatologie

Springer Medizin

Abstract

Background

Objective

Methods

Results

Conclusion

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 6/2005

Imipramine-Induced Facial Pigmentation: Case Report and Literature Review

Safety and Efficacy of a Milk-derived Extract in the Treatment of Plaque Psoriasis:An Open-label Study

Safe Psoriasis Control: A New Outcome Measure for the Composite Assessment of the Efficacy and Safety of Psoriasis Treatment

Multiple Cutaneous and Uterine Leiomyomas Associated with Gastric Gist

The Cochrane Skin Group: Promoting the Best Evidence

Misnomers in Dermatology

Leitlinien kompakt für die Dermatologie

Neu im Fachgebiet Dermatologie

Auf diese Krankheiten bei Geflüchteten sollten Sie vorbereitet sein

Kein Abstrich bei chronischen Wunden ohne Entzündungszeichen!

„Nur wer sich gut aufgehoben fühlt, kann auch für Patientensicherheit sorgen“

Vitiligo: Prävalenz steigt und viele Erkrankte werden spät behandelt

Update Dermatologie