In vivo and in vitro evidence for epidermal H2O2‐mediated oxidative stress in piebaldism

Vafaee, Tayyebeh; Rokos, Hartmut; Salem, Mohamed M. A. E. L.; Schallreuter, Karin U.

doi:10.1111/j.1600-0625.2009.00966.x

Cited by 8 publications

(6 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Finally, we investigated the transcription of two crucial ROS scavenging enzymes of human skin in cultured human ORS keratinocytes, catalase and SOD2 (Chelikani et al, 2004;Halliwell and Gutteridge, 2007;Marionnet et al, 2011;Silva et al, 2005;Vafaee et al, 2010) which are expressed in human HFs and whose activity likely impacts on HF aging and greying (Slominski et al, 2005;Wood et al, 2009). Interestingly, catalase transcription was significantly upregulated in all test groups treated with HPT-axis hormones, and TSH and T 4 also enhanced SOD2 mRNA steady-state levels in ORS keratinocytes (Figure 6b and c).…”

Section: Hpt-axis Hormones Up-regulate the Expression Of Ros Scavenging Enzymes By Human Hf Keratinocytesmentioning

confidence: 98%

Hypothalamic–Pituitary–Thyroid Axis Hormones Stimulate Mitochondrial Function and Biogenesis in Human Hair Follicles

Vidali

Knuever

Lerchner

et al. 2014

Journal of Investigative Dermatology

View full text Add to dashboard Cite

Thyroid hormones regulate mitochondrial function. As other hypothalamic-pituitary-thyroid (HPT) axis hormones, i.e., thyrotropin-releasing hormone (TRH) and thyrotropin (TSH), are expressed in human hair follicles (HFs) and regulate mitochondrial function in human epidermis, we investigated in organ-cultured human scalp HFs whether TRH (30 nM), TSH (10 mU ml(-1)), thyroxine (T4) (100 nM), and triiodothyronine (T3) (100 pM) alter intrafollicular mitochondrial energy metabolism. All HPT-axis members increased gene and protein expression of mitochondrial-encoded subunit 1 of cytochrome c oxidase (MTCO1), a subunit of respiratory chain complex IV, mitochondrial transcription factor A (TFAM), and Porin. All hormones also stimulated intrafollicular complex I/IV activity and mitochondrial biogenesis. The TSH effects on MTCO1, TFAM, and porin could be abolished by K1-70, a TSH-receptor antagonist, suggesting a TSH receptor-mediated action. Notably, as measured by calorimetry, T3 and TSH increased follicular heat production, whereas T3/T4 and TRH stimulated ATP production in cultured HF keratinocytes. HPT-axis hormones did not increase reactive oxygen species (ROS) production. Rather, T3 and T4 reduced ROS formation, and all tested HPT-axis hormones increased the transcription of ROS scavengers (catalase, superoxide dismutase 2) in HF keratinocytes. Thus, mitochondrial biology, energy metabolism, and redox state of human HFs are subject to profound (neuro-)endocrine regulation by HPT-axis hormones. The neuroendocrine control of mitochondrial biology in a complex human mini-organ revealed here may be therapeutically exploitable.

show abstract

Section: Hpt-axis Hormones Up-regulate the Expression Of Ros Scavenging Enzymes By Human Hf Keratinocytesmentioning

confidence: 98%

Hypothalamic–Pituitary–Thyroid Axis Hormones Stimulate Mitochondrial Function and Biogenesis in Human Hair Follicles

Vidali

Knuever

Lerchner

et al. 2014

Journal of Investigative Dermatology

View full text Add to dashboard Cite

show abstract

“…In active vitiligo, ROS and H 2 O 2 were found in excess, and these molecules can affect biological processes. Additionally, excess H 2 O 2 levels impair tyrosinase activity through the oxidation of methionine residues in this key melanogenic enzyme [59]. Processes that are involved in oxidative damage repair can be damaged by H 2 O 2 as well [60], and numerous proteins and peptides, in addition to tyrosinase, are affected during oxidative stress.…”

Section: Ros and Vitiligo Pathogenesismentioning

confidence: 99%

Reactive Oxygen Species in Skin Repair, Regeneration, Aging, and Inflammation

Xu¹,

Zheng²,

Liu³

et al. 2018

Reactive Oxygen Species (ROS) in Living Cells

View full text Add to dashboard Cite

As the most important and largest surface barrier, the skin provides a necessary protection to the organism from the external factors, including chemical, biological, and physical irritation, injury, and others. External environmental irritants or their metabolites are inherent oxidants and/or directly or indirectly drive the production of various reactive oxidants, reactive oxygen species (ROSs), owing to the redox imbalances. ROSs, the most common free oxygen radicals, participate in a series of physiological and pathological skin processes. Here, we discussed the role of oxidative events in injury, repair, photoaging, and cutaneous disease development. Intrinsic and extrinsic factors lead to the skin barrier damage, which leads to the disequilibrium in oxidant and antioxidant balance and induces excessive ROS production. The underlying mechanisms include DNA damage, MAPK/AP-1, NF-κB, and JAK/STAT-signaling pathways, apoptosis and autophagy, and autoimmune reaction of melanocytes and keratinocytes. The skin employs a number of antioxidant agents to protect the oxidative balance, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), ascorbic acid, and tocopherols. The results presented here indicate that antioxidant treatments may be effective when applied in the therapy of cutaneous diseases where oxidative stress plays a prominent pathogenic role.

show abstract

“…p < .05 was considered to be statistically significant. (Kostyuk, et al, 2010;Vafaee, Rokos, Salem, & Schallreuter, 2010;Ozturk, Batcioglu, Karatas, Hazneci, & Genc, 2008). Dysregulated Nrf2/ARE pathway leads to impaired antioxidant capability of melanocytes, contributing to the pathogenesis of vitiligo [7].…”

Section: Discussionmentioning

confidence: 99%

Paeonol protects melanocytes against hydrogen peroxide‐induced oxidative stress through activation of Nrf2 signaling pathway

Guo

Zhang

2021

Drug Development Research

View full text Add to dashboard Cite

Oxidative stress plays a pivotal role in the pathogenesis of vitiligo. Paeonol, a phenolic compound found in the root bark of Cortex Moutan, has been suggested to have therapeutic effects on various diseases through nuclear factor Nrf2 mediated antioxidant pathways. However, the therapeutic effects of paeonol on vitiligo have not been investigated. In this study, we investigated whether paeonol could protect melanocytes against oxidative stress through Nrf2 activation. Hydrogen peroxide (H 2 O 2 ) was used to mimic the oxidative stress. PIG1 cells were pretreated with paeonol for 24 h, and then were treated with H 2 O 2 for 24 h. To detect the role of Nrf2, siRNA method was used to knockdown the Nrf2 expression. After that, cell viability, melanin content, tyrosinase activity, intracellular reactive oxygen species, antioxidant enzymes activities, nuclear translocation of Nrf2, and mRNA expression of Nrf2 downstream antioxidant genes were detected. Paeonol improved cell viability and melanogenesis in PIG1 cells treated with H 2 O 2 . Paeonol also alleviated oxidative stress by restoring the activities of superoxide dismutase, catalase, and glutathione peroxidase. Paeonol promoted Nrf2 nuclear translocation and the expression of its downstream-regulated antioxidative genes under oxidative stress. Furthermore, Nrf2 knockdown by siRNA abolished the protective effects of paeonol on PIG1 cells against oxidative damage. Paeonol protected melanocytes against H 2 O 2 -induced oxidative stress by Nrf2 mediated antioxidant pathways. Paeonol is a potential therapeutic drug for vitiligo.

show abstract

In vivo and in vitro evidence for epidermal H₂O₂‐mediated oxidative stress in piebaldism

Cited by 8 publications

References 31 publications

Hypothalamic–Pituitary–Thyroid Axis Hormones Stimulate Mitochondrial Function and Biogenesis in Human Hair Follicles

Hypothalamic–Pituitary–Thyroid Axis Hormones Stimulate Mitochondrial Function and Biogenesis in Human Hair Follicles

Reactive Oxygen Species in Skin Repair, Regeneration, Aging, and Inflammation

Paeonol protects melanocytes against hydrogen peroxide‐induced oxidative stress through activation of Nrf2 signaling pathway

Contact Info

Product

Resources

About