The effect of X-ray irradiation upon the epithelial melanin unit of the hair bulb in hooded rat

Kostanecki, W; Radwan, I.; Mroczkowski, Tomasz

doi:10.1007/bf00572496

Cited by 6 publications

(3 citation statements)

References 6 publications

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“…damage (29), carotid artery stenosis (31), and coronary artery disease (32)(33)(34)(35). Irradiation also affects viability and proliferation of host cells (36). For instance, it has been demonstrated that local low-dose irradiation delays wound healing in a dose-dependent manner by inhibiting cell proliferation and inducing apoptotic cell death (37).…”

Section: Discussionmentioning

confidence: 99%

Circulating progenitor cells contribute to neointimal formation in nonirradiated chimeric mice

Tanaka¹,

Sata²,

Natori³

et al. 2007

FASEB j.

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Recent evidence suggests that bone marrow-derived cells may contribute to repair and lesion formation following vascular injury. In most studies, bone marrow-derived cells were tracked by transplanting exogenous cells into bone marrow that had been compromised by irradiation. It remains to be determined whether endogenous circulating progenitors actually contribute to arterial remodeling under physiological conditions. Here, we established a parabiotic model in which two mice were conjoined subcutaneously without any vascular anastomosis. When wild-type mice were joined with transgenic mice that expressed green fluorescent protein (GFP) in all tissues, GFP-positive cells were detected not only in the peripheral blood but also in the bone marrow of the wild-type mice. The femoral arteries of the wild-type mice were mechanically injured by insertion of a large wire. At 4 wk, there was neointima hyperplasia that mainly consisted of alpha-smooth muscle actin-positive cells. GFP-positive cells were readily detected in the neointima (14.8+/-4.5%) and media (31.1+/-8.8%) of the injured artery. Some GFP-positive cells expressed alpha-smooth muscle actin or an endothelial cell marker. These results indicate that circulating progenitors contribute to re-endothelialization and neointimal formation after mechanical vascular injury even in nonirradiated mice.

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Section: Discussionmentioning

confidence: 99%

Circulating progenitor cells contribute to neointimal formation in nonirradiated chimeric mice

Tanaka¹,

Sata²,

Natori³

et al. 2007

FASEB j.

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“…Parental WM35 cells expressing wild-type p53 (p53 wt ) and cells transfected with dominant-negative p53 (p53 DN ) were supplemented with 100 mM pTpT. Cells were collected at time 0, 24, and 72 h after pTpT addition and total RNA was processed for northern blot analysis (A) as detailed in tyrosinase activity and melanin content of skin increase 3±5 d after suf®cient sun exposure (Kostanecki et al, 1976), a phenomenon termed delayed tanning. Of note, X-irradiation and certain DNAdamaging chemotherapeutic agents also induce tanning-like hyperpigmentation (Gilchrest and Eller, 1999).…”

Section: Discussionmentioning

confidence: 99%

Tyrosinase Gene Expression is Regulated by p53

Khlgatian

Hadshiew

Asawanonda

et al. 2002

Journal of Investigative Dermatology

105

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Tyrosinase, the rate-limiting enzyme for melanin synthesis, is induced after ultraviolet irradiation as part of the tanning response, the major recognized photoprotective response of human skin. Other DNA-damaging agents and DNA fragments such as thymidine dinucleotides also induce tyrosinase gene expression. Moreover, like ultraviolet light they also activate p53. To determine whether p53 activation is required for this increased tyrosinase expression, we employed two experimental systems: (i) a human melanoma line (WM35) known to express wild-type p53 versus WM35 cells engineered to express a transcriptionally inactive dominant-negative p53 (WM35-p53DN) or the empty vector alone (WM35-pCMV7) and (ii) mice with wild-type p53 versus p53 knockout mice. In WM35-p53DN cells, the baseline p53 protein level was higher than in WM35 or WM35-pCMV7 cells, and tyrosinase transcripts were lower. After ultraviolet irradiation, in all cell lines the p53 protein level increased within the first 24 h, as expected; and at 24 h tyrosinase mRNA levels were decreased. Consistent with the literature, these data in combination suggest that increased p53 protein level downregulates tyrosinase mRNA. In WM35 and WM35-pCMV7 cells at 48 and 72 h, however, whereas p53 levels remained elevated, tyrosinase mRNA levels compared to pre-irradiation levels tripled, whereas in WM35-p53DN cells levels remained below baseline. In thymidine-dinucleotide-treated WM35 and WM35-pCMV7 cells there was a comparable upregulation of tyrosinase mRNA within 24 h that persisted through 72 h, but there was no upregulation of tyrosinase mRNA in WM35-p53DN cells any time after ultraviolet irradiation or thymidine dinucleotide treatment. In ear skin of p53 wild-type mice, topical application of thymidine dinucleotide induced a 4-5-fold increase in epidermal melanin content after 3 wk, but in p53 knockout mice thymidine dinucleotide application caused no detectable increase in melanin. Together, these data demonstrate that p53 activation increases tyrosinase mRNA level and subsequently pigmentation. The data further suggest that tanning is part of a p53-mediated adaptive response of mammalian skin to DNA damage from ultraviolet irradiation.

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“…Although the histopathology of irradiated hair folhcles has been described previously (Geary 1952, Montagna & Chase 1956, Van Scott & Reinertson 1957 and many studies on the radiation response of the follicle and hair shaft melanin-content have been reported (Moshman & Upton 1954, Potten 1968, Potten & Forbes 1972, Kostanecki et al 1976) no scanning electron-microscopic analyses of these irradiated structures have, to our knowledge, been published.…”

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confidence: 92%

Surface Architecture of X‐lrradiated Hair Follicles

Klein‐Szanto

Rey

1978

J Cutan Pathol

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The combined use of scanning electron-microscopy and chemical separation of epidermis permitted the study of the irradiated and normal hair follicle surface characteristics. Irradiation reduced the length and density of the hair follicles, producing at the same time marked alterations and deformities of the individual follicles. As most of these changes were dose- and time-dependent, these structures, studied by these techniques, provide an interesting model as biological indicators of radiation dose.

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The effect of X-ray irradiation upon the epithelial melanin unit of the hair bulb in hooded rat

Cited by 6 publications

References 6 publications

Circulating progenitor cells contribute to neointimal formation in nonirradiated chimeric mice

Circulating progenitor cells contribute to neointimal formation in nonirradiated chimeric mice

Tyrosinase Gene Expression is Regulated by p53

Surface Architecture of X‐lrradiated Hair Follicles

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