Synergistic phototoxic effects of glycolic acid in a human keratinocyte cell line (HaCaT)

Lai, Wan Wen; Hsiao, Yu Ping; Chung, Jing Gung; Wei, Yau Huei; Cheng, Ya Wen; Yang, Jen‐Hung

doi:10.1016/j.jdermsci.2011.09.001

Cited by 24 publications

(20 citation statements)

References 19 publications

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“…Our results, based on cells obtained directly from smokers, showed no significant difference with cells from nonsmokers. Among nonsmokers, only 11% of the cells were in the S/G2/M phases -much lower than predicted by other authors who had examined oral keratinocytes [19,28,29] and epidermal keratinocytes [19,43]. This higher percentage of cells in the S/G2/M phases is probably due to the fact that most of these observations were carried out on cultured cell lines, and not on cells obtained directly from patients.…”

Section: Discussionmentioning

confidence: 63%

Tobacco smoking alters the number of oral epithelial cells with apoptotic features

Michcik

Cichorek

Daca

et al. 2014

Folia Histochem Cytobiol.

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Tobacco smoking is a global problem associated with the occurrence of many systemic diseases and tumors. Oral cavity tumors are common tobacco-related cancers, and of all the anatomical structures that are exposed to the effects of smoking, the oral cavity remains the least-explored area. Changes that occur in the biology of oral epithelial keratinocytes under the influence of the components of tobacco smoke often go unnoticed, if they are asymptomatic. The proper functioning of the oral epithelium is determined by the proliferation and differentiation of the cells in keratinization -the process of programmed cell death, which extends through to the mechanisms of apoptosis. Due to incomplete knowledge of the impact of tobacco smoke on the biology of keratinocytes, an evaluation of the cell cycle was conducted and the apoptosis of oral epithelial keratinocytes was analyzed. The study involved 77 patients divided into four groups according to their intensity of smoking, ranging from 0 to 27 pack-years. There were no differences in the cell count between nonsmokers and smokers in the proper cell-cycle phases. The percentage of proliferating cells in the oral epithelium is about 11%. A reduction in the number of early-apoptotic cells (caspase positive/propidium iodide negative) and an increase in the number of late-apoptotic cells (caspase positive/annexin V positive/propidium iodide positive) were observed to occur with increasing pack-years. The present study demonstrates that smoking does not affect the oral keratinocyte cell cycle, but does modify the number of cells with early and late apoptotic features. An intensification of the impact of tobacco smoke components on the biology of the oral keratinocytes is clearly noticeable at approximately 6 pack-years. This indicates that the biology of the first organ exposed to tobacco smoke -the oral epithelium -is altered by tobacco smoking.

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Section: Discussionmentioning

confidence: 63%

Tobacco smoking alters the number of oral epithelial cells with apoptotic features

Michcik

Cichorek

Daca

et al. 2014

Folia Histochem Cytobiol.

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“…Free radical scavengers, such as vitamins C and E, carotenoids and glutathione are also localized on the skin to prevent the damaging effects of ROS [50]. It has been documented that large-scale deletions of mitochondrial DNA (mtDNA) are present in sun-exposed skin tissues [51,52]. In one of our previous studies, we showed that a high proportion of mtDNA deletion rendered human cells more susceptible to UV-induced apoptosis through enhanced release of cytochrome c [53].…”

Section: Uv-induced Apoptosis Of Keratinocytesmentioning

confidence: 99%

Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy

Lee

Wu²,

Hong

et al. 2013

IJMS

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196

164

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The human skin is an integral system that acts as a physical and immunological barrier to outside pathogens, toxicants, and harmful irradiations. Environmental ultraviolet rays (UV) from the sun might potentially play a more active role in regulating several important biological responses in the context of global warming. UV rays first encounter the uppermost epidermal keratinocytes causing apoptosis. The molecular mechanisms of UV-induced apoptosis of keratinocytes include direct DNA damage (intrinsic), clustering of death receptors on the cell surface (extrinsic), and generation of ROS. When apoptotic keratinocytes are processed by adjacent immature Langerhans cells (LCs), the inappropriately activated Langerhans cells could result in immunosuppression. Furthermore, UV can deplete LCs in the epidermis and impair their migratory capacity, leading to their accumulation in the dermis. Intriguingly, receptor activator of NF-κB (RANK) activation of LCs by UV can induce the pro-survival and anti-apoptotic signals due to the upregulation of Bcl-xL, leading to the generation of regulatory T cells. Meanwhile, a physiological dosage of UV can also enhance melanocyte survival and melanogenesis. Analogous to its effect in keratinocytes, a therapeutic dosage of UV can induce cell cycle arrest, activate antioxidant and DNA repair enzymes, and induce apoptosis through translocation of the Bcl-2 family proteins in melanocytes to ensure genomic integrity and survival of melanocytes. Furthermore, UV can elicit the synthesis of vitamin D, an important molecule in calcium homeostasis of various types of skin cells contributing to DNA repair and immunomodulation. Taken together, the above-mentioned effects of UV on apoptosis and its related biological effects such as proliferation inhibition, melanin synthesis, and immunomodulations on skin residential cells have provided an integrated biochemical and molecular biological basis for phototherapy that has been widely used in the treatment of many dermatological diseases.

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“…GA has various biological activities such as antioxidant anti-inflammatory effects. Furthermore, GA not only exists in all whole fruits but also acts as an antioxidant, which protects keratinocytes from the ROS-mediated damage induced by UVB irradiation [24].…”

Section: Introductionmentioning

confidence: 99%

Topical application of glycolic acid suppresses the UVB induced IL-6, IL-8, MCP-1 and COX-2 inflammation by modulating NF-κB signaling pathway in keratinocytes and mice skin

Tang

Liao

Hung

et al. 2017

Journal of Dermatological Science

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Synergistic phototoxic effects of glycolic acid in a human keratinocyte cell line (HaCaT)

Cited by 24 publications

References 19 publications

Tobacco smoking alters the number of oral epithelial cells with apoptotic features

Tobacco smoking alters the number of oral epithelial cells with apoptotic features

Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy

Topical application of glycolic acid suppresses the UVB induced IL-6, IL-8, MCP-1 and COX-2 inflammation by modulating NF-κB signaling pathway in keratinocytes and mice skin

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