Retinoic acid and hydroquinone induce inverse expression patterns on cornified envelope-associated proteins: Implication in skin irritation

Cheong, Kwang Ho; Kim, Ha Jung; Kim, Jiyoung; Kim, Chang‐Hyun; Lim, Won-Suk; Noh, Minsoo; Lee, Ai-Young

doi:10.1016/j.jdermsci.2014.08.003

Cited by 14 publications

(10 citation statements)

References 28 publications

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“…In general, normal HFKs increase secretion of epithelial differentiation markers including A100A7, filaggrin, and keratin 10 upon retinoic acid treatment in order to strengthen skin barrier function, whereas this differentiation-induced protection is impaired by highly reactive chemicals such as hydroquinone and formaldehyde (Cheong et al ., 2014; Lee et al ., 2016). Especially, enhanced production of inflammatory cytokines in normal HFKs by formaldehyde was well characterized.…”

Section: Resultsmentioning

confidence: 99%

“…Retinoic acid was shown to induce the keratinocyte differentiation by increasing expression of epidermal differentiation maker proteins such as S100A7, filaggrin, and keratin 10 (Cheong et al ., 2014). Based on this, we tried to test induction of these epidermal differentiation maker proteins in immortalized HFK7-E6E7 cells by treatment of 0.1 and 1 mM retinoic acid.…”

Section: Discussionmentioning

confidence: 99%

“…Experiments to test responsiveness of immortalized HKFs to retinotic acid, hydroquinone, and formaldehyde were conducted as previously described (Cheong et al ., 2014; Lee et al ., 2016). Briefly, immortalized HKFs were incubated with designated compounds for 24 hr.…”

Section: Methodsmentioning

confidence: 99%

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Establishment of Immortalized Primary Human Foreskin Keratinocytes and Their Application to Toxicity Assessment and Three Dimensional Skin Culture Construction

Choi

Park

Lee

et al. 2017

Biomolecules & Therapeutics

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In spite of frequent usage of primary human foreskin keratinocytes (HFKs) in the study of skin biology, senescence-induced blockage of in vitro proliferation has been a big hurdle for their effective utilization. In order to overcome this passage limitation, we first isolated ten HFK lines from circumcision patients and successfully immortalized four of them via a retroviral transduction of high-risk human papillomavirus (HPV) E6 and E7 oncogenes. We confirmed expression of a keratinocyte marker protein, keratin 14 and two viral oncoproteins in these immortalized HFKs. We also observed their robust responsiveness to various exogenous stimuli, which was evidenced by increased mRNA expression of epithelial differentiation markers and pro-inflammatory genes in response to three reactive chemicals. In addition, their applicability to cytotoxicity assessment turned out to be comparable to that of HaCaT cells. Finally, we confirmed their differentiation capacity by construction of well-stratified three dimensional skin cultures. These newly established immortalized HFKs will be valuable tools not only for generation of in vitro skin disease models but also for prediction of potential toxicities of various cosmetic chemicals.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Establishment of Immortalized Primary Human Foreskin Keratinocytes and Their Application to Toxicity Assessment and Three Dimensional Skin Culture Construction

Choi

Park

Lee

et al. 2017

Biomolecules & Therapeutics

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“…Retinoic acid has been frequently used to induce dryness and scaling in the applied skin [50]. It can reduce levels of loricrin and SPRRs in human keratinocytes and mice skin in a dose-dependent manner [51]. Different from these results on atopic dermatitis, ichthyoses, and retinoic acid applications, expression levels of several CE proteins have been found to be increased in epidermal barrier disruption of human skin by tape stripping and in skin irritation by sodium dodecyl sulfate application [52].…”

Section: Cornified Envelopesmentioning

confidence: 99%

Molecular Mechanism of Epidermal Barrier Dysfunction as Primary Abnormalities

Lee

2020

IJMS

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Epidermal barrier integrity could be influenced by various factors involved in epidermal cell differentiation and proliferation, cell-cell adhesion, and skin lipids. Dysfunction of this barrier can cause skin disorders, including eczema. Inversely, eczema can also damage the epidermal barrier. These interactions through vicious cycles make the mechanism complicated in connection with other mechanisms, particularly immunologic responses. In this article, the molecular mechanisms concerning epidermal barrier abnormalities are reviewed in terms of the following categories: epidermal calcium gradients, filaggrin, cornified envelopes, desquamation, and skin lipids. Mechanisms linked to ichthyoses, atopic dermatitis without exacerbation or lesion, and early time of experimental irritation were included. On the other hand, the mechanism associated with epidermal barrier abnormalities resulting from preceding skin disorders was excluded. The molecular mechanism involved in epidermal barrier dysfunction has been mostly episodic. Some mechanisms have been identified in cultured cells or animal models. Nonetheless, research into the relationship between the causative molecules has been gradually increasing. Further evidence-based systematic data of target molecules and their interactions would probably be helpful for a better understanding of the molecular mechanism underlying the dysfunction of the epidermal barrier.may not be the primary events in lesional skin. However, they can play a role in part as primary abnormalities because abnormalities in the epidermal barrier are already present in non-lesional skin of atopic dermatitis [1]. Epidermal trauma from tape stripping or irritant application also leads to initial disruption of the barrier, although the result at certain time points may be combined with compensatory reactions followed by trauma.Causative mechanisms involved in primary epidermal barrier dysfunction might be more valuable for the prevention of skin diseases induced by barrier abnormalities. However, the underlying mechanism has been discussed mainly in connection with immunologic responses, including cytokine production [1,9,10]. Accordingly, this review covers molecular mechanisms of epidermal barrier dysfunction as primary abnormalities by focusing on the causative factors of skin diseases (atopic dermatitis and ichthyoses) and experimental skin conditions (tape stripping and irritant application) associated with skin barrier abnormalities. Molecular Mechanisms Related to Epidermal Barrier DysfunctionFormation and maintenance of skin barrier integrity could be influenced by genetic and environmental factors involved in epidermal cell differentiation and proliferation, cell-cell adhesion, and skin lipids. Mechanisms related to epidermal barrier dysfunction at molecular levels have commonly illustrated filaggrin mutations [3,11]. Regarding the mechanism behind skin barrier integrity, the role of epidermal calcium gradients could be considered based on their influence on keratinocyte proliferation and dif...

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“…In fact, skin irritation is one of the frequent adverse reactions in RA. We have previously reported that RA could reduce the thickness of stratum corneum [3]. Stratum Corneum thickness is determined by the generation and desquamation of corneocytes.…”

Section: Introductionmentioning

confidence: 99%

Complementary effect of hydroquinone and retinoic acid on corneocyte desquamation with their combination use

Cheong

Lee

2017

Journal of Dermatological Science

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Retinoic acid and hydroquinone induce inverse expression patterns on cornified envelope-associated proteins: Implication in skin irritation

Cited by 14 publications

References 28 publications

Establishment of Immortalized Primary Human Foreskin Keratinocytes and Their Application to Toxicity Assessment and Three Dimensional Skin Culture Construction

Establishment of Immortalized Primary Human Foreskin Keratinocytes and Their Application to Toxicity Assessment and Three Dimensional Skin Culture Construction

Molecular Mechanism of Epidermal Barrier Dysfunction as Primary Abnormalities

Complementary effect of hydroquinone and retinoic acid on corneocyte desquamation with their combination use

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