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At least 19 recordsLinked to original sources
PubMed1983

Replacement of irradiated epidermis by migration of non-irradiated epidermis in the newt limb: the necessity of healthy epidermis for regeneration.

An X-irradiated newt limb is able to regenerate if non-irradiated skin as well as non-irradiated muscle is transplanted to the stump. Non-irradiated epidermis is brought to the stump with a skin graft but not with a muscle graft. In order to know whether limb regeneration required healthy epidermis or not, a triploid skin cuff was set at the most proximal level of an irradiated limb and muscle was transplanted to the level of the midforearm. The forearm was then amputated through the muscle graft. A cytophotometrical analysis of DNA content of the epidermis cell nuclei sampled from the skin of the regenerate was undertaken to detect a migration of triploid epidermal cells. The result was a complete replacement of diploid irradiated epidermis by triploid epidermis, during the six weeks necessary for regeneration. Another investigation consisted of detecting a possible migration of non-irradiated triploid epidermis along an irradiated limb which had not been amputated. Healthy epidermis was found to migrate distally and replace irradiated epidermis in three weeks. Previous experiments involving transplantation of a non-irradiated skin cuff or muscle to an irradiated limb stump were carried out again but on animals which had been entirely irradiated to prevent any extra healthy epidermis cells from contaminating the regenerating limb epidermis. A regenerate developed from the skin graft but not from muscle graft. It is concluded that healthy epidermis must be present on the limb stump to permit the blastema to develop.

Animals↗
PubMed2002

Comparison of gene expression profiles in human keratinocyte mono-layer cultures, reconstituted epidermis and normal human skin; transcriptional effects of retinoid treatments in reconstituted human epidermis.

In order to validate a model for predictive screening of dermatological drugs, we used a customized cDNA macro-array system containing 475 skin-related genes to analyze the gene expression patterns in human keratinocytes from different origins: (1) normal human epidermal keratinocyte mono-layer cultures, (2) the commercially available SkinEthic reconstituted human epidermis model, and (3) biopsies of normal human epidermis. Few markers of those that were detected significantly in keratinocyte mono-layers or in reconstituted epidermis were undetected or detected at very low level in the normal epidermis biopsies. A comparative expression of more than 100 markers could be evidenced in both normal epidermis and reconstituted epidermis samples; however, only 90% of these were detected in keratinocyte mono-layers: expression of several terminal differentiation markers, such as filaggrin, loricrin, and corneodesmosin were strongly detected in normal epidermis and reconstituted epidermis, but were not significantly expressed in keratinocyte mono-layers. Under the experimental conditions described herein, the reconstituted human epidermis model was found to significantly reproduce the gene expression profile of normal human epidermis. Using the same methodology, we then investigated the effects of all-trans retinoic acid, 9-cis retinoic acid, all-trans retinol and a commercialized tretinoin-containing cream (Retacnyl) on the gene expression profiles of reconstituted human epidermis. According to the nature and the length of the treatments, more than 40 genes were found significantly modified. Among the genes whose expression was decreased, we found cytokeratins 1, 10, 2E, and 6B, several cornified envelope precursors, integrins alpha 3, alpha 6, beta 1, beta 4, some components of desmosomes, of hemi-desmosomes and of the epidermal basement membrane. Transcriptional upregulation was observed for keratins 18 and 19, autocrine and paracrine growth factors such as HB-EGF, IGF 1, PDGF-A, calgranulins A and B, interleukin-1 alpha and the other IL-1-related markers, type II IL-1 receptor and type I IL-1-receptor antagonist. Our results confirm most of the known effects of retinoids on human epidermis, but also give new insights into their complex pharmacological activity on skin. The reconstituted human epidermis used proves to be a highly predictive model for efficacy evaluation of skin-targeted compounds, such as retinoids.

Administration, Topical↗
PubMed1985

Characterization and activity of phospholipase A2 in normal human epidermis and in lesion-free epidermis of patients with psoriasis or eczema.

The kinetic properties of phospholipase A2 isolated from single large specimens of normal human epidermis and 'uninvolved' (lesion-free) psoriatic epidermis were determined. The enzymes from the two sources behaved identically with respect to changes in protein concentration, Ca2+ concentration and pH, but the enzymes responded differently to changes in substrate concentration. Furthermore, the specific activity of the enzyme derived from lesion-free psoriatic epidermis was higher than that from normal epidermis under all conditions used. Increased specific activity of the enzyme in the lesion-free epidermis was also found when biopsy specimens taken from thirty-five patients with psoriasis vulgaris at varying severity were compared with biopsies of normal epidermis from thirty-one control volunteers (P less than 0.001). Mixing experiments, in which homogenates of lesion-free psoriatic epidermis and control epidermis were combined, suggested that the relatively low activity of the enzyme in normal epidermis was due to the presence of an inhibitor. As the activity of the enzyme was not elevated in the lesion-free epidermis from twelve cases of eczema, which is also an inflammatory condition of the epidermis and superficial dermis, it is suggested that the raised phospholipase A2 activity demonstrated in the lesion-free epidermis of psoriasis may play an important role in the pathogenesis of the disease.

Adolescent↗
PubMed2004

Keratinocytes in the depigmented epidermis of vitiligo are more vulnerable to trauma (suction) than keratinocytes in the normally pigmented epidermis, resulting in their apoptosis.

BACKGROUND: Vitiligo may develop following minor physical trauma. However, in autologous epidermal grafting, depigmentation of the donor (normally pigmented) site from a suction blister is rare, even in cases displaying failure of repigmentation at the recipient (depigmented) site. OBJECTIVES: To examine whether the suction procedure is more likely to damage keratinocytes in the depigmented than in the normally pigmented epidermis of vitiligo, and to determine what kind of damage occurs to the keratinocytes. METHODS: Paired roofs of suction blisters from five patients with generalized vitiligo, five with localized and seven with segmental type, were used for the study. Multiple new lesions developed in two of the five patients with the generalized type. Apoptosis of keratinocytes in the epidermis was determined by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-digoxigenin nick end labelling (TUNEL) staining, with immunohistochemistry for Bax and active caspase 3. Expression of Bcl-2, Bax, FLIP and p53, activation of caspases 3, 8 and 9, and cleavage of poly(adenosine diphosphate ribose) polymerase (PARP) in the epidermis were analysed by Western blotting in four patients with each type. RESULTS: Apoptotic keratinocytes, which stained with TUNEL and anti-Bax and antiactive caspase 3 antibodies, were scattered in the blistered epidermis, mainly in the lower portions. The depigmented epidermis displayed significantly more apoptotic keratinocytes than the normally pigmented epidermis. The numerical difference between the paired epidermides was related to the disease activity and not to the type of lesions. The number of apoptotic keratinocytes in the normally pigmented epidermis was as high as that in the depigmented epidermis in the two patients with active generalized type vitiligo. Expression of Bax and p53 in the depigmented epidermis was higher than in the normally pigmented epidermis, whereas expression of FLIP was lower. In addition, the activation of caspases 3, 8 and 9, and cleavage of PARP, were increased in the depigmented compared with the normally pigmented epidermis. The degree of difference in expression and activation was parallel to the results of the TUNEL assay. CONCLUSIONS: The keratinocytes in the depigmented compared with the normally pigmented epidermis of vitiligo may become apoptotic more easily after suction.

Adolescent↗
PubMed1995

Frequent p53 accumulation in the chronically sun-exposed epidermis and clonal expansion of p53 mutant cells in the epidermis adjacent to basal cell carcinoma.

p53 expression was studied immunohistochemically to identify a precursor lesion of basal cell carcinoma (BCC) in the epidermis adjacent to BCC. With two different anti-p53 antibodies of CM1 and DO7, p53 expression was frequently detected in the epidermis adjacent to BCCs arising on the face and in the normal epidermis with usual sun exposure. In the epidermis adjacent to BCC, stained cells were occasionally clustered in a small area, but no cluster was found in the normal epidermis with usual sun exposure. The expression was less frequent in the normal epidermis with rare sun exposure. Ten cases of normal skin with usual sun exposure, showing CM1 staining in the epidermis, were screened for p53 gene mutations with polymerase chain reaction-single-strand conformation polymorphism analysis using DNAs obtained from the epidermis. No mutation was detected in exons 2 to 10 of the p53 gene in these 10 cases. The epidermis flanking three BCCs that was stained with CM1, on the other hand, carried a missense mutation of C to G transversion at a dipyrimidine site of codon 249. This alteration replaced arginine with threonine. The mutation of codon 249 was not detected in the three BCCs. Our results first suggest that ultraviolet light irradiating the skin in a daily life induces p53 accumulation in the epidermis and secondly that the frequent clonal expansion of p53 mutant cells occurs in the epidermis adjacent to BCCs. This clonal expansion of mutant p53 may provide a molecular basis for high risk of developing subsequent new skin cancers in patients with BCC.

Adolescent↗
PubMed2002

Functional expression of AQP3 in human skin epidermis and reconstructed epidermis.

The purpose of this study was to examine the presence of aquaporin water channels in human skin and to assess their functional role. On western blots of human epidermis obtained from plastic surgery, a strong signal was obtained with polyclonal anti-aquaporin-3 antibodies. By indirect immunofluorescence on 5 microm cryosections, anti-aquaporin-3 antibodies strongly stained keratinocyte plasma membranes in human epidermis, whereas no staining was observed in the dermis or the stratum corneum or when anti-aquaporin-3 antibodies were preabsorbed with the peptide used for immunization. Similarly, a strong signal with anti-aquaporin-3 antibodies was observed in keratinocyte plasma membranes of reconstructed human epidermis in culture at the air-liquid interface for up to 3 wk. The keratinocyte plasma membrane localization of aquaporin-3 was confirmed at the electron microscope level in prickle cells. In addition an intracellular localization of aquaporin-3 was also detected in epidermis basal cells. Osmotically induced transepidermal water permeability was measured on stripped human skin and on reconstructed epidermis. Water transport across both stripped human skin and 2-3 wk reconstructed epidermis was comparable, inhibited by > 50% by 1 mM HgCl2 and fully inhibited by acid pH. By stopped-flow light scattering, keratinocyte plasma membranes, where aquaporin-3 is localized, exhibited a high, pH-sensitive, water permeability. Although human skin is highly impermeable to water, this is primarily accounted for by the stratum corneum, where a steep water content gradient was demonstrated. In contrast, the water content of viable strata of the epidermis is remarkably constant. Our results suggest that the human epidermis, below the stratum corneum, exhibits a high, aquaporin-3-mediated, water permeability. We propose that the role of aquaporin-3 is to water-clamp viable layers of the epidermis in order to improve the hydration of the epidermis below the stratum corneum.

Antibodies↗
PubMed1990

mRNA for tissue-type plasminogen activator is present in lesional epidermis from patients with psoriasis, pemphigus, or bullous pemphigoid, but is not detected in normal epidermis.

Plasminogen activator (PA), which catalyzes the conversion of plasminogen to the proteinase plasmin, has been implicated in a variety of cutaneous disorders. Lesional epidermis from patients with psoriasis, pemphigus, bullous pemphigoid, and Hailey-Hailey disease contains elevated levels of tissue-type PA (tPA) activity compared to non-lesional epidermis or to epidermis from normal individuals. In the present study, we have used Northern blot analysis to demonstrate that mRNA for tPA is detectable in lesions from patients with psoriasis, pemphigus, and bullous pemphigoid, but is not detectable in normal epidermis. These data strongly suggest that the tPA enzymatic activity present in lesional epidermis results from enhanced synthesis of the enzyme in situ, secondary to elevated steady-state levels of tPA mRNA. Cultured keratinocytes likewise are shown to contain tPA mRNA. Previous investigators have suggested that the phenotypes of keratinocytes in culture, psoriatic epidermis, and epidermis in the process of wound reepithelialization are comparable. Our findings, combined with those of other investigators, suggest that elevated tPA expression may be another common feature of epidermis under these circumstances.

Biopsy↗
PubMed1976

The synthesis of specific proteins in adult mouse epidermis during phases of proliferation and differentiation induced by the tumor promoter TPA, and in basal and differentiating layers of neonatal mouse epidermis.

Mouse epidermis can be induced to undergo sequential waves of proliferation and keratinization by treatment with the tumor promoter TPA (12-O-tetradecanoyl-phorbol-13-acetate). This model system offers a unique possibility to study the synthesis of differentiation-specific proteins in the epidermis. During these studies it could be shown by sodium dodecyl sulfate-polyacrylamide gel electrophoresis that several previously undetected proteins appear in the epidermis during the phase of differentiation. These have been fractionated according to solubility in 1 M phosphate buffer, pH 7.0, or 0.1 M sodium citrate buffer, pH 2.6. Of the soluble proteins, a band of approximate molecular weight 13,500 (band 1) appears early during the differentiative phase (24 hr after treatment with TPA). Another previously undetected protein of approximate molecular weight 27,000 (band 2) appears in the soluble fraction after 48 hr, at a time when many of the typical manifestations of increased keratinization can be observed. Both of these soluble proteins, although not detectable in normal adult mouse epidermis, are shown to be present in newborn mouse epidermis, which demonstrates histologically a well-developed layer of keratinizing and cornified cells. In addition, by separation of neonatal and TPA-treated adult mouse epidermis into "basal" and "cornified" layers, it could be demonstrated that these two proteins are localized exclusively in the upper layer of the epidermis.

Animals↗
PubMed1983

5-Methylchrysene metabolism in mouse epidermis in vivo, diol epoxide--DNA adduct persistence, and diol epoxide reactivity with DNA as potential factors influencing the predominance of 5-methylchrysene-1,2-diol-3,4-epoxide--DNA adducts in mouse epidermis.

5-Methylchrysene (5-MeC) can form two bay region dihydrodiol epoxides: 1,2-dihydroxy-3,4-epoxy-1,2,3,4-tetrahydro-5-methylchrysene (DE-I) which has the methyl group and the epoxide ring in the same bay region, and 7,8-dihydroxy-9,10-epoxy-7,8,10-tetrahydro-5-methylchrysene (DE-II). In a previous study, we observed that the ratio of DE-I:DNA adducts to DE-II:DNA adducts in mouse epidermis, 24 h after application of [3H]5-MeC metabolites was 2.7 to 1. To investigate the basis for this observation we have now studies: (i) the formation of [3H]5-MeC in mouse epidermis in vivo at various time intervals from 0.33 to 24 h; (ii) the persistence of DE-I:DNA adducts and DE-II:DNA adducts in mouse epidermis at 4-48 h after application of [3H]5-MeC; and (iii) the reactions of DE-I and DE-II with calf thymus DNA in vitro. In contrast to results obtained with mouse liver 9000 grams supernatant, the dihydrodiol precursors of DE-I and DE-II were present in equivalent quantities in mouse epidermis in vivo at every time point studied. The ratio of DE-I:DNA adducts to DE-II:DNA adducts in mouse epidermis was constant throughout the time period studied. However, the extent of formation of DE-I:DNA adducts was greater than that of DE-II:DNA adducts upon reaction of DE-I or DE-II with calf thymus DNA in vitro. These results suggest that differences in reactivity with DNA of DE-I and DE-II may bw responsible for the higher levels in mouse epidermis of DE-I:DNA adducts compared with DE-II:DNA adducts and provide a possible basis for the observed enhancing effect of a bay region methyl group on the carcinogenicity of polynuclear aromatic hydrocarbons.

Animals↗
PubMed1992

"HepG2/erythroid/brain" type glucose transporter (GLUT1) is highly expressed in human epidermis: keratinocyte differentiation affects GLUT1 levels in reconstituted epidermis.

In mature animals, the "HepG2/erythroid/brain" glucose transporter isoform (GLUT1) appears to be expressed at the highest levels at blood tissue barriers; however, these levels may still be lower than the levels of expression seen in fetal tissues. Also, glucose transporters might serve as water channels. Therefore, we decided to investigate GLUT1 expression in human epidermis, a very active tissue, in terms of metabolism, even if not directly vascularized. We found GLUT1 transcripts in human skin and demonstrated, by immunohistochemistry, that GLUT1 protein is highly expressed in the basal layer and, to a lower extent, in the immediately suprabasal layer of the epidermis. This distribution pattern suggested that GLUT1 expression is affected by keratinocyte differentiation. To investigate this possibility, we used human epidermis reconstituted in culture. Our culture system allows the reconstruction of a stratified squamous epithelium which has been successfully grafted onto patients presenting large skin defects. Human keratinocytes have been cultured under conditions which allow a modulation of cellular differentiation and stratification. We observed that (i) GLUT1 expression is 4-6-fold higher in "stem-like" basal cells than in large, differentiated keratinocytes; (ii) culture conditions causing cell differentiation reduce GLUT1 expression, while conditions which minimize either differentiation or stratification of keratinocytes enhance GLUT1 expression. Finally, we found that IGF-1 and insulin, probably acting through the IGF-1 receptor, increase GLUT1 expression and stimulate glucose transport activity in epidermis reconstituted in culture. In conclusion, our data demonstrate that GLUT1 is highly expressed in the basal layers of human epidermis and that its expression is modulated by keratinocyte differentiation.

Brain↗
PubMed1984

Glycogen metabolism in psoriatic epidermis and in regenerating epidermis.

The observation that the glycogen content of epidermis from psoriatic lesions and from regenerating wound epithelium is increased has been confirmed by quantitative estimation. In epidermis from psoriatic lesions, although the proportion of glycogen synthase in the I form is only about 5% of the total and similar to control values, total glycogen synthase activity is increased approximately 4-fold and hence glycogen synthase I activity is increased to the same extent. In contrast, total phosphorylase activity is only slightly increased and, since the proportion of the enzyme in the a form is reduced, phosphorylase a activity is similar to control values. In epidermis from psoriatic lesions, the concentration of UDP-glucose is approximately doubled, and the concentrations of fructose 1,6-bisphosphate and of 6-phosphogluconate are increased approximately 5-fold. It is concluded that rates of glycogen synthesis, of glycolysis and of the pentose phosphate pathway are all enhanced in vivo and in consequence the rate of glucose uptake by psoriatic epidermis must be increased. In the non-involved epidermis of psoriatic patients the glycogen content is within normal limits, and although total glycogen synthase activity is increased the ratio of glycogen synthase I to phosphorylase a is maintained at normal levels by the appropriate phosphorylation of both enzymes. In regenerating wound epithelium in the pig, the changes in enzyme activity and in metabolite concentration closely resemble those found in epithelium from psoriatic lesions except that in wound epithelium the proportion of phosphorylase in the a form is increased relative to normal epithelium.

Animals↗
PubMed1996

Coexpression of p21Waf1/Cip1 and p53 in sun-exposed normal epidermis, but not in neoplastic epidermis.

Wild-type p53 accumulation induced by DNA damaging agents such as ultraviolet (UV) radiation, gamma-irradiation and drugs, may arrest the cell cycle until DNA damage is repaired. p21Waf1/Cip1 is a cyclin-dependent kinase (CDK) inhibitor induced by wild-type p53. CDK is activated by cyclin and progresses the cell cycle. On the other hand, CDK inhibitors inhibit CDK activity to arrest the cell cycle. Thus, p21Waf1/Cip1 is thought to mediate the signal of p53 induced by DNA damaging agents to arrest the cell cycle. p21Waf1/Cip1 is induced by wild-type, but not mutant p53. To investigate p21Waf1/Cip1 regulation by p53 in epidermis in vivo, immunohistochemical staining of p21Waf1/Cip1 and p53 were conducted in chronically sun-exposed normal epidermis and in neoplastic epidermis, p21Waf1/Cip1 expression was found to be coincident with the p53-positive regions or not coincident with the p53-positive regions in chronically sun-exposed normal epidermis, whereas there was only low or undetectable p21Waf1/Cip1 expression in any regions including the p53-positive regions of solar keratosis and squamous cell carcinoma of the skin. This suggests that wild-type p53 and p21Waf1/Cip1 may play a part in chronically sun-exposed normal epidermis response to UV exposure, whereas p21Waf1/Cip1 cannot be induced by mutated p53 in solar keratosis and squamous cell carcinoma of the skin.

Aged↗
PubMed1985

Comparison of differentiation patterns in 12-O-tetradecanoylphorbol-13-acetate-treated epidermis and fetal epidermis.

12-O-Tetradecanoylphorbol-13-acetate (TPA)-treated adult epidermis as well as untreated fetal and adult epidermis were investigated to elucidate the effect of TPA in terms of cell differentiation using techniques of ultrastructural stereology. Twenty-four hours after a single application of TPA, the treated epidermis was characterized by involutional changes, i.e., increased volume density of intercellular spaces and of mitochondria, vacuoles, and cytoplasmic ground substance in the basal layer. However, 48 h after application, the TPA-treated epidermis was very similar to fetal epidermis, i.e., high volume density of nuclei ribosomes, rough endoplasmic reticulum, membrane-coating granules, and keratohyalin granules, and low volume density of bundled filaments in the upper layers. These stereological data indicate that the changes observed 48 h after TPA treatment were related not only to increased cell proliferation but also to inhibition of cell differentiation expressed as a reversion of the adult differentiation patterns and the acquisition of fetal characteristics in all epidermal layers.

Animals↗
PubMed1989

Unusual patterns of keratin expression in the overlying epidermis of patients with dermatofibromas: biochemical alterations in the epidermis as a consequence of dermal tumors.

Dermatofibromas are frequently associated with acanthosis of the overlying epidermis. Using monospecific antisera and cRNA probes, we have examined the pattern of expression of keratin and keratin mRNA in the affected epidermis of patients with these dermal tumors. Our studies reveal several abnormalities in keratin expression within the thickened areas of overlying epidermis. In two of 15 patients, we detected K6 and K16, keratins which are frequently associated with epidermal diseases of hyperproliferation but are not present in normal epidermis. In both cases, K6 and K16 were found in suprabasal layers, similar to that seen for psoriasis and squamous cell carcinomas. Expression of K6 and K16 in skin samples from patients with dermatofibromas seemed to be dependent upon how near was the tumor to the overlying epidermis, and possibly upon the degree of cellularity within the tumor mass. A second aberration in keratin expression, and one which did not appear to be linked to K6/K16 expression, was the altered expression of the basal epidermal keratin K14. Expression of this keratin and its mRNA was variable, often extending into multiple suprabasal layers and including both basal-like and squamous-like cells. In contrast to the expression of K6/K16, aberrant expression of K14 was a relatively frequent event, occurring in greater than 70% of the dermatofibroma skin samples examined. These observations provide the first biochemical evidence in support of previous morphologic studies, indicating that alterations in epidermal differentiation can occur as a consequence of dermal skin tumors.

Fibroma↗
PubMedDate not supplied

A dual role for involucrin in the epidermis-ultrastructural localization in epidermis and hair follicle in humans and transgenic mice.

Transgenic mice expressing human involucrin (hINV) have an abnormal hair coat appearance. To understand this phenotype, we used immunoelectron microscopy to examine hINV distribution in the hair follicle and epidermis. In human epidermis, hINV is first observed in the cytoplasm of spinous and granular layer cells. In transition cells, it is equally distributed between the cytoplasm and the nascent cornified envelope, while in the corneocytes it is largely cornified envelope-associated. In transgenic mice, the pattern of expression is similar except that much more antigen appears to be present. An important finding is the presence of hINV in hair follicle structures--low levels in the hair and high levels in the inner root sheath (IRS). The distribution of hINV is comparable in human and transgenic mouse follicles; however, much higher levels are observed in the mice. In contrast, hINV is not detected in cells of the outer root sheath (ORS). Thus, hINV is differentially expressed in two related and contiguous tissues, the epidermis and the ORS. Based on these results we conclude that hINV is a specific product of differentiated IRS cells that is localized at the cell envelope, suggesting a function as a cross-linked constituent of IRS cell envelope. These results suggest that hINV may have a dual role in epidermis, as a cross-linked structural protein in the epidermal corneocyte and the hair follicle IRS.

Animals↗
PubMed1978

Epidermotropically metastatic malignant melanoma. Differentiating malignant melanoma metastatic to the epidermis from malignant melanoma primary in the epidermis.

In four instances, metastases to epidermis from primary cutaneous malignant melanomas at different sites showed histological features similar to those of cutaneous malignant melanoma primary in the epidermis. In these metastases, atypical melanocytes were present within the epidermis and in the upper part of the dermis much as in primary cutaneous malignant melanoma. Therefore, the presence of atypical melanocytes within the epidermis is not in itself an absolute criterion of malignant melanoma primary in skin. Nor does that finding absolutely deny malignant melanoma metastastic to the skin. Features that may enable histologic differentiation of epidermotropically metastatic malignant melanoma from primary cutaneous malignant melanoma are emphasized.

Adult↗
PubMed2006

Human skin responses to UV radiation: pigment in the upper epidermis protects against DNA damage in the lower epidermis and facilitates apoptosis.

Melanin plays an important role in protecting the skin against UV radiation, and melanomas and basal/squamous cell carcinomas occur more frequently in individuals with fair/light skin. We previously reported that levels of melanin correlate inversely with amounts of DNA damage induced by UV in normal human skin of different racial/ethnic groups. We have now separately examined DNA damage in the upper and lower epidermal layers in various types of skin before and after exposure to UV and have measured subsequent apoptosis and phosphorylation of p53. The results show that two major mechanisms underlie the increased photocarcinogenesis in fair/light skin. First, UV-induced DNA damage in the lower epidermis (including keratinocyte stem cells and melanocytes) is more effectively prevented in darker skin, suggesting that the pigmented epidermis is an efficient UV filter. Second, UV-induced apoptosis is significantly greater in darker skin, which suggests that UV-damaged cells may be removed more efficiently in pigmented epidermis. The combination of decreased DNA damage and more efficient removal of UV-damaged cells may play a critical role in the decreased photocarcinogenesis seen in individuals with darker skin.

Adult↗