Localization of Liposomes Containing a DNA Repair Enzyme in Murine Skin

Yarosh, Daniel B.; Bucana, Corazon D.; Cox, Pat; Alas, Lori; Kibitel, Jeannie; Kripke, Margaret L.

doi:10.1111/1523-1747.ep12395551

Cited by 131 publications

(70 citation statements)

References 12 publications

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“…Other studies have reported that UVBmediated DNA damage can be reduced by the application of exogenous DNA repair enzymes. The bacterial DNA repair enzyme T4 endonuclease V (T4N5) can be delivered into cells by liposomes (37). Topically applied T4N5 liposomes penetrate the skin, increase the removal of CPDs, and reduce the incidence of skin cancer (14,15).…”

Section: Discussionmentioning

confidence: 99%

(−)-Epigallocatechin-3-Gallate Prevents Photocarcinogenesis in Mice through Interleukin-12–Dependent DNA Repair

et al. 2006

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We have shown previously that topical application of (À)-epigallocatechin-3-gallate (EGCG), the major polyphenol of green tea, prevents photocarcinogenesis in mice. EGCG prevents UVB-induced immunosuppression by inducing interleukin-12 (IL-12). As immunosuppression is a risk factor for photocarcinogenesis, we investigated the possibility that EGCG also prevents UVB-induced photocarcinogenesis through an IL-12-dependent DNA repair mechanism. To investigate this possibility, we determined the effects of EGCG on photocarcinogenesis in IL-12 knockout (KO) mice using the formation of cyclobutane pyrimidine dimers (CPD) as an indicator of the extent of UVB-induced DNA damage. Topical application of EGCG (1 mg/cm 2 skin) prevented photocarcinogenesis in wild-type (C3H/HeN) mice in terms of tumor incidence and tumor multiplicity but did not prevent photocarcinogenesis in IL-12 KO mice. UVB-induced DNA damage, as determined by the formation of CPDs and the number of sunburn cells, was resolved more rapidly in the skin of wild-type mice treated with EGCG than untreated control mice. In contrast, the extent of UVB-induced DNA damage and the numbers of sunburn cells were not significantly different in the EGCG-treated IL-12 KO mice and untreated control mice. In addition, treatment of XPAproficient human fibroblast cells with EGCG promoted repair of UVB-induced CPDs in a dose-dependent manner but not in an XPA-deficient cells, indicating that the nucleotide excision repair mechanism is involved in EGCG-mediated DNA repair. Taken together, these results indicate for the first time that EGCG can prevent photocarcinogenesis through an EGCGinduced IL-12-dependent DNA repair mechanism.

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Section: Discussionmentioning

confidence: 99%

(−)-Epigallocatechin-3-Gallate Prevents Photocarcinogenesis in Mice through Interleukin-12–Dependent DNA Repair

et al. 2006

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“…The ring observed around the larger vesicles is generally detected when observing liposomes using this TEM technique (Wertz et al, 1986;Lasic, 1993a;Yarosh et al, 1994;Zeidel et al, 1994;Memoli et al, 1995;Kulkarni et al, 1995;Son & Alkan, 1989;Polozova et al, 1995). The fact that this ring was much larger in the steps near to vesicle disintegration has also been reported by our research group for solubilization of PC liposomes with different surfactants (de la Maza & Parra, 1994a,b, 1995.…”

Section: Tem Observations Quasielastic and Static Light-scattering Vsupporting

confidence: 72%

“…It has been previously demonstrated that the TEM technique applied to negatively stained liposomes constituted an appropriate technique to study the formation and morphology of different liposome structures and their interaction with biological tissues (Wertz et al, 1986;Lasic, 1993a;Yarosh et al, 1994;Zeidel et al, 1994;Kulkarni et al, 1995;Memoli et al, 1995). This technique has been demonstrated to be very convenient in the characterization of the aggregates (vesicles and mixed micelles) formed during the interaction of different amphiphilic compounds with liposomes (Beigel et al, 1988;Son & Alkan, 1989;Lasic, 1993b;Polozova et al, 1995;de la Maza & Parra, 1994a,b, 1995.…”

Section: Transmission Electron Microscopy (Tem)mentioning

confidence: 99%

Intermediate aggregates resulting in the interaction of bile salt with liposomes studied by transmission electron microscopy and light scattering techniques

Maza

Manich

Parra

1997

Journal of Microscopy

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SummaryThe interaction of sodium cholate (SC) with phosphatidylcholine liposomes was studied by means of transmission electron microscopy (TEM), changes in the mean particle size (quasielastic light scattering, QELS) and in the static light scattering (SLS) of the system during liposome solubilization. A good correlation was found between the TEM diameter of particles and the mean hydrodynamic diameter (HD) determined by QELS. The intermediate aggregates resulting in this interaction were dependent on the SC concentration in the system. Thus, an initial vesicle growth occurred when the SC concentration in the system was 13 . 79 mol%. Additional SC amounts (41 . 17 mol% SC) led to the formation of the largest vesicles (HD 410 nm). Increasing SC amounts led to a slight fall in the vesicle diameter and in the SLS of the system. Thus, for 47 . 08 mol% SC, TEM images still showed the presence of vesicles albeit with traces of smaller structures and signs of vesicle fusion. When SC concentration exceeded 48 mol% an abrupt decrease in SLS occurred, the size curve starting to show a bimodal distribution. Thus, for 50 mol% SC a sharp distribution curve appeared at 52 nm indicating the formation of small particles and TEM images showed clear signs of vesicle disintegration with formation of tubular structures. The subsequent self organization of these tubular structures (54 mol% SC) led to the formation of open multilayered structures in coexistence with small particles. A gradual increase in the number of these small particles (mixed micelles) led to the complete solubilization of liposomes.

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“…Progress in this area may come from the field of photocarcinogenesis. Studies employing a liposome-encapsulated repair enzyme called photolyase, derived from the algae Anacystis nidulans, demonstrated that when applied to human skin, photolyase reached the lower levels of the skin and removed DNA damage in the cells (47). Furthermore, removal of the pre-existing DNA damage led to physiological effects.…”

Section: Photoprotectionmentioning

confidence: 99%

Photoaging of human skin

Berneburg

Plettenberg

Krutmann

2000

Photoderm Photoimm Photomed

341

271

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Chronic sun exposure causes photoaging of human skin, a process that is characterized by clinical, histological and biochemical changes which differ from alterations in chronologically aged but sun-protected skin. Within recent years, substantial progress has been made in unraveling the underlying mechanisms of photoaging. Induction of matrix metalloproteinases as a consequence of activator protein (AP)-1 and nuclear factor (NF)-kB activation as well as mutations of mitochondrial DNA have been identified recently.T he term photoaging describes distinct clinical, histological and functional features of chronically sunexposed skin. It has evolved from a variety of terms such as heliodermatosis, actinic dermatosis, and accelerated skin aging. Photoaged, chronically sun-exposed skin has characteristics in common with sun-protected, chronologically aged skin. However, there are features which are found exclusively in photoaged skin, making it an independent entity with its own pathophysiology.Extended life-span, more spare time and excessive exposure to ultraviolet (UV) radiation from natural sunlight or tanning devices, especially in the western population, has resulted in an ever increasing demand to protect human skin against the detrimental effects of UV-exposure of the skin to ultraviolet light. Therefore, photoaging will be of increasing concern in the future.The clinical and histological characteristics of photoaged skin have been known for some time (1); however, not until recently have the underlying molecular mechanisms responsible for the specific macro-and microAbbreviations: EGF, epidermal growth factor; ERK, extracellular signal-regulated kinase; GAG, glycosaminoglycans; JNK, c-Jun amino terminal kinase; mt, mitochondrial; MAP, mitogen-activated protein; MMP, matrix metalloproteinase; MED, minimal erythema dose; NF-kB, Nuclear factor kB; nm, nanometer; OXPHOS, oxidative phosphorylation; RA, retinoic acid; ROS, reactive oxygen species; TIMP, tissue specific inhibitor of matrix metalloproteinases. 239This has increased our understanding of photoaging significantly and has led to new prophylactic and therapeutic strategies aimed at the prevention and repair of the detrimental effects of chronic sun-exposure on the skin.Key words: antioxidants; mitochondrial DNA; photoaging; reactive oxygen species; repetitive sun exposure; retinoic acid; sunscreens; ultraviolet light.scopic alterations been discovered. The role of selected transcription factors (AP-1, NF-kB) in photoaging has been demonstrated and it has been found that mutations of mitochondrial DNA may also be involved. The elucidation of these pathophysiological mechanisms provides the basis for evaluating the efficacy of photo(aging)protective substances and might help in the development of new strategies which will provide protection and repair of photoaged human skin. Previous reviews on this topic have described the different aspects of photoaging (2 -4). Hence, this review will only briefly summarize the clinical and histological features of photoa...

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Localization of Liposomes Containing a DNA Repair Enzyme in Murine Skin

Cited by 131 publications

References 12 publications

(−)-Epigallocatechin-3-Gallate Prevents Photocarcinogenesis in Mice through Interleukin-12–Dependent DNA Repair

(−)-Epigallocatechin-3-Gallate Prevents Photocarcinogenesis in Mice through Interleukin-12–Dependent DNA Repair

Intermediate aggregates resulting in the interaction of bile salt with liposomes studied by transmission electron microscopy and light scattering techniques

Photoaging of human skin

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