Study of apoptosis in normal skin tissues

Grigaitienė, Jūratė; Marčiukaitienė, Irena Ona; Blažienė, Audra; Chomičienė, Anželika

doi:10.3390/medicina43040037

Cited by 2 publications

(2 citation statements)

References 6 publications

(7 reference statements)

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“…5 A,B). We noted that epidermal cells generally showed a positive staining with the TUNEL assay, which agrees with previous studies [29] , [45] , [46] and reflects physiological DNA fragmentation in the course of keratinocyte cornification. Since the TUNEL assay proved not suitable to analyze IR-induced apoptosis, we next studied the apoptotic response by activated caspase-3 [47] immunofluorescence ( Fig.5C-F ).…”

Section: Resultssupporting

confidence: 92%

Persistent DNA Damage after High Dose In Vivo Gamma Exposure of Minipig Skin

Ahmed

Agay²,

Schrock

et al. 2012

PLoS ONE

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BackgroundExposure to high doses of ionizing radiation (IR) can lead to localized radiation injury of the skin and exposed cells suffer dsDNA breaks that may elicit cell death or stochastic changes. Little is known about the DNA damage response after high-dose exposure of the skin. Here, we investigate the cellular and DNA damage response in acutely irradiated minipig skin.Methods and FindingsIR-induced DNA damage, repair and cellular survival were studied in 15 cm2 of minipig skin exposed in vivo to ∼50 Co-60 γ rays. Skin biopsies of control and 4 h up to 96 days post exposure were investigated for radiation-induced foci (RIF) formation using γ-H2AX, 53BP1, and active ATM-p immunofluorescence. High-dose IR induced massive γ-H2AX phosphorylation and high 53BP1 RIF numbers 4 h, 20 h after IR. As time progressed RIF numbers dropped to a low of <1% of keratinocytes at 28–70 days. The latter contained large RIFs that included ATM-p, indicating the accumulation of complex DNA damage. At 96 days most of the cells with RIFs had disappeared. The frequency of active-caspase-3-positive apoptotic cells was 17-fold increased 3 days after IR and remained >3-fold elevated at all subsequent time points. Replicating basal cells (Ki67+) were reduced 3 days post IR followed by increased proliferation and recovery of epidermal cellularity after 28 days.ConclusionsAcute high dose irradiation of minipig epidermis impaired stem cell replication and induced elevated apoptosis from 3 days onward. DNA repair cleared the high numbers of DBSs in skin cells, while RIFs that persisted in <1% cells marked complex and potentially lethal DNA damage up to several weeks after exposure. An elevated frequency of keratinocytes with persistent RIFs may thus serve as indicator of previous acute radiation exposure, which may be useful in the follow up of nuclear or radiological accident scenarios.

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Section: Resultssupporting

confidence: 92%

Persistent DNA Damage after High Dose In Vivo Gamma Exposure of Minipig Skin

Ahmed

Agay²,

Schrock

et al. 2012

PLoS ONE

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“…Apoptosis is highly important in the renewal of cells and formation of epidermal structure [ 60 ]. Apoptotic cells may not stimulate inflammation if they are ingested by phagocytes before they release their intracellular substances.…”

Section: Discussionmentioning

confidence: 99%

Hataedock Treatment Has Preventive Therapeutic Effects in Atopic Dermatitis‐Induced NC/Nga Mice under High‐Fat Diet Conditions

Cha

Ahn

Cheon

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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This study investigated the preventive therapeutic effects of Hataedock (HTD) treatment on inflammatory regulation and skin protection in AD-induced NC/Nga mice under high-fat diet conditions. Before inducing AD, the extract of Coptidis Rhizoma and Glycyrrhiza uralensis was administered orally to the 3-week-old mice. After that, AD-like skin lesions were induced by applying DNFB. All groups except the control group were fed a high-fat diet freely. We identified the effects of HTD on morphological changes, cytokine release and the induction of apoptosis through histochemistry, immunohistochemistry, and TUNEL assay. HTD downregulated the levels of IL-4 and PKC but increased the levels of LXR. HTD also suppressed the mast cell degranulation and release of MMP-9, Substance P. The levels of TNF-α, p-IκB, iNOS, and COX-2 were also decreased. The upregulation of inflammatory cell's apoptosis is confirmed by our results as increase of apoptotic body and cleaved caspase-3 and decrease of Bcl-2. HTD also reduced edema, angiogenesis, and skin lesion inflammation. Our results indicate HTD suppresses various inflammatory response on AD-induced mice with obesity through the regulation of Th2 differentiation and the protection of lipid barrier. Therefore, HTD could be used as an alternative and preventive therapeutic approach in the management of AD.

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Study of apoptosis in normal skin tissues

Cited by 2 publications

References 6 publications

Persistent DNA Damage after High Dose In Vivo Gamma Exposure of Minipig Skin

Persistent DNA Damage after High Dose In Vivo Gamma Exposure of Minipig Skin

Hataedock Treatment Has Preventive Therapeutic Effects in Atopic Dermatitis‐Induced NC/Nga Mice under High‐Fat Diet Conditions

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