Reduced Nrf2 activation in PI3K phosphorylation‐impaired vitiliginous keratinocytes increases susceptibility to ROS‐generating chemical‐induced apoptosis
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Summary
Results showed that 4‐TBP or HQ treatment increased apoptosis and the expression levels of TNF, IL‐1ɑ, and ROS in PI3K‐knockdown keratinocytes which reduced Nrf2 nuclear translocation compared to control keratinocyte which was significantly recovered by an antioxidant treatment.
- Type
- article
- Published
- 2017-08-24
- Cited by
- 19
- References
- 34
- OpenAlex
- https://openalex.org/W2745626651
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:21833685
Keywords
Vitiligo, PI3K/AKT/mTOR pathway, Oxidative stress, Apoptosis, Viability assay
References
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- The Mechanism of Melanocytes-Specific Cytotoxicity Induced by Phenol Compounds Having a Prooxidant Effect, relating to the Appearance of Leukoderma
- A role for tyrosinase-related protein 1 in 4-tert-butylphenol-induced toxicity in melanocytes: Implications for vitiligo.
- A cloned, immortal line of murine melanoblasts inducible to differentiate to melanocytes.
- Protease-activated receptor-2 activates NQO-1 via Nrf2 stabilization in keratinocytes.
- Increased tumor necrosis factor alpha (TNF-alpha) and interleukin 1 alpha (IL1-alpha) levels in the lesional skin of patients with nonsegmental vitiligo.
- The living skin equivalent as a model in vitro for ranking the toxic potential of dermal irritants.
- Keratinocytes in the depigmented epidermis of vitiligo are more vulnerable to trauma (suction) than keratinocytes in the normally pigmented epidermis, resulting in their apoptosis
- Ellagic acid protects human keratinocyte (HaCaT) cells against UVA-induced oxidative stress and apoptosis through the upregulation of the HO-1 and Nrf-2 antioxidant genes.
- Low catalase levels in the epidermis of patients with vitiligo.
- Redox cycling of phenol induces oxidative stress in human epidermal keratinocytes.
- Monobenzyl ether of hydroquinone and 4-tertiary butyl phenol activate markedly different physiological responses in melanocytes: relevance to skin depigmentation.
- Role of keratinocyte-derived factors involved in regulating the proliferation and differentiation of mammalian epidermal melanocytes.
- Impaired PI3K/Akt activation-mediated NF-kappaB inactivation under elevated TNF-alpha is more vulnerable to apoptosis in vitiliginous keratinocytes.
- Impaired activation of the Nrf2-ARE signaling pathway undermines H2O2-induced oxidative stress response: a possible mechanism for melanocyte degeneration in vitiligo.
- Intradermal concentration of hydroquinone after application of hydroquinone ointments is higher than its cytotoxic concentration.
- Ultrastructural and functional alterations of mitochondria in perilesional vitiligo skin.
- Less keratinocyte-derived factors related to more keratinocyte apoptosis in depigmented than normally pigmented suction-blistered epidermis may cause passive melanocyte death in vitiligo.
Cited by
- The convergence theory for vitiligo: A reappraisal
- Involvement of non‐melanocytic skin cells in vitiligo
- Therapeutic Potential of Patient iPSC-Derived iMelanocytes in Autologous Transplantation.
- Hydroquinone exposure alters the morphology of lymphoid organs in vaccinated C57Bl/6 mice.
- Functional Role of p53 in the Regulation of Chemical-Induced Oxidative Stress
- Vitexin protects melanocytes from oxidative stress via activating MAPK-Nrf2/ARE pathway
- Mechanisms of melanocyte death in vitiligo
- Skin Pigmentation Abnormalities and Their Possible Relationship with Skin Aging
- The PI3K/Akt Pathway: Emerging Roles in Skin Homeostasis and a Group of Non-Malignant Skin Disorders
- Ginsenoside Rk1 protects human melanocytes from H2O2-induced oxidative injury via regulation of the PI3K/AKT/Nrf2/HO-1 pathway
- Association between celiac disease and vitiligo: A review of the literature
- [[Translated article]]Nuclear Factor Erythroid 2-Related Factor 2 in Vitiligo
- Abnormal nuclear expression of aquaporin‐3 in lesional and perilesional skin of vitiligo patients: A novel immunohistochemical finding
- Hsa_circ_0001944 regulates apoptosis by regulating the binding of PARP1 and HuR in leukemia and malignant transformed cells induced by hydroquinone
- Nano-selenium protects grass carp hepatocytes against 4-tert-butylphenol-induced mitochondrial apoptosis and necroptosis via suppressing ROS-PARP1 axis.
- Aquaporin-3 Downregulation in Vitiligo Keratinocytes Increases Oxidative Stress of Melanocytes
- Investigating the molecular mechanism of purslane‑based vitiligo treatment using network pharmacology, molecular docking and in vitro analyses
- Restoration of Stressed Melanocytes Functions: Role of Keratinocytes Derived Exosomes
- Protective effects of Qinglongyi-Buguzhi herb pair against H 2 O 2 ‑induced oxidative injury in B16F10 mouse melanoma cells via PI3K/Akt/Nrf2 signaling pathway
- Therapeutic Potential of P atient iPSC-Derived iMelanocytes in Autologous Transplantation Graphical
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