Suppression of melanogenesis by a newly synthesized compound, MHY966 via the nitric oxide/protein kinase G signaling pathway in murine skin

Choi, Yeon Ja; Uehara, Yohei; Park, Ji Young; Chung, Ki Wung; Ha, Young Mi; Kim, Ji Min; Song, Yu; Chun, Pusoon; Park, June Whan; Moon, Hyung Ryong; Chung, Hae Young

doi:10.1016/j.jdermsci.2012.09.014

Cited by 23 publications

(15 citation statements)

References 26 publications

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“…In the present study, we found that MHY 966 activates PPAR α and γ, but the potency was less than that of fenofibrate, a PPAR α agonist, and rosiglitazone, a PPAR γ agonist, in in vitro transcriptional activity (Figure 1). However, this result conflict with the conclusion in our previous study [13]. In our previous study, we performed the Lantha Screen TR-FRET PPAR γ competitive binding assay.…”

Section: Discussioncontrasting

confidence: 73%

“…In fact, lipid peroxidation induced by oxidative stress is a cause of the mass of keratinocytes, the cellular membranes of which contain considerable amounts of unsaturated lipid and cholesterol. In a previous study, we found that MHY 966 treatment reduces NO level increases caused by UVB exposure [13]. On the other hand, we found MHY 966 suppressed UVB-induced inflammatory response, including COX-2 and iNOS, by inhibited not ROS generation (data not shown) but NF-κB activation (Figure 3), thus we supposed that MHY 966 attenuated the UVB-induced overexpression of ONOO - , and inhibited lipid peroxidation processes (Figure 4).…”

Section: Discussionmentioning

confidence: 99%

“…In the previous study, we reported that MHY 966 suppresses melanogenesis by inhibiting the generation of NO [13]. This study was undertaken to identify a novel PPAR α/γ dual agonist and to explore the hypothesis that MHY 966 prevents UVB-induced collagen degrdation by inhibiting inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

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The Novel PPAR α/γ Dual Agonist MHY 966 Modulates UVB–Induced Skin Inflammation by Inhibiting NF-κB Activity

Park

Lee

et al. 2013

PLoS ONE

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Ultraviolet B (UVB; 290~320nm) irradiation-induced lipid peroxidation induces inflammatory responses that lead to skin wrinkle formation and epidermal thickening. Peroxisome proliferator-activated receptor (PPAR) α/γ dual agonists have the potential to be used as anti-wrinkle agents because they inhibit inflammatory response and lipid peroxidation. In this study, we evaluated the function of 2-bromo-4-(5-chloro-benzo[d]thiazol-2-yl) phenol (MHY 966), a novel synthetic PPAR α/γ dual agonist, and investigated its anti-inflammatory and anti-lipid peroxidation effects. The action of MHY 966 as a PPAR α/γ dual agonist was also determined in vitro by reporter gene assay. Additionally, 8-week-old melanin-possessing hairless mice 2 (HRM2) were exposed to 150 mJ/cm2 UVB every other day for 17 days and MHY 966 was simultaneously pre-treated every day for 17 days to investigate the molecular mechanisms involved. MHY 966 was found to stimulate the transcriptional activities of both PPAR α and γ. In HRM2 mice, we found that the skins of mice exposed to UVB showed significantly increased pro-inflammatory mediator levels (NF-κB, iNOS, and COX-2) and increased lipid peroxidation, whereas MHY 966 co-treatment down-regulated these effects of UVB by activating PPAR α and γ. Thus, the present study shows that MHY 966 exhibits beneficial effects on inflammatory responses and lipid peroxidation by simultaneously activating PPAR α and γ. The major finding of this study is that MHY 966 demonstrates potential as an agent against wrinkle formation associated with chronic UVB exposure.

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Section: Discussioncontrasting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

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The Novel PPAR α/γ Dual Agonist MHY 966 Modulates UVB–Induced Skin Inflammation by Inhibiting NF-κB Activity

Park

Lee

et al. 2013

PLoS ONE

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“…As far as we know, only a small portion of the pathways involved in pigmentation have been validated to date, including the protein kinase C pathway [ 49 , 50 ], cAMP pathway [ 51 ], SCF-KIT pathway [ 52 ], cGMP pathway [ 53 ], phosphatidylinositol 3-kinase-Akt pathway [ 54 ], protein kinase A pathway [ 55 ], BMP signaling [ 56 ], Notch pathway [ 57 ], ERK pathway [ 58 ], Wnt signal [ 59 ], KITLG and the KITLG/c-Kit pathway [ 60 ], CXCR3-mediated pathway [ 61 ], JAK2-STAT6 signaling pathway [ 62 ], nitric oxide/protein kinase G signaling pathway [ 63 ], FGF/MAPK/Ets signaling [ 64 ], p38MAPK [ 65 ], MITF-GPNMB pathway [ 66 ], Galphas-SASH1-IQGAP1-E-cadherin pathway [ 67 ], CREB/MITF/tyrosinase pathway [ 68 ], and necrosis factor receptor-associated factor 2 (TRAF2)-caspases pathway [ 69 ]. However, reports on the role of lncRNA in pigmentation are limited.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide analysis of long non-coding RNAs at early stage of skin pigmentation in goats (Capra hircus)

et al. 2016

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BackgroundLong noncoding RNAs (lncRNAs) play roles in almost all biological processes; however, their function and profile in skin development and pigmentation is less understood. In addition, because lncRNAs are species-specific, their function in goats has not been established.ResultWe systematically identified lncRNAs in 100-day-old fetal skin by deep RNA-sequencing using the Youzhou dark goat (dark skin) and Yudong white goat (white skin) as a model of skin pigmentation. A total of 841,895,634 clean reads were obtained from six libraries (samples). We identified 1336 specific lncRNAs in fetal skin that belonged to three subtypes, including 999 intergenic lncRNAs (lincRNAs), 218 anti-sense lncRNAs, and 119 intronic lncRNAs. Our results demonstrated significant differences in gene architecture and expression among the three lncRNA subtypes, particularly in terms of density and position bias of transpose elements near the transcription start site. We also investigated the impact of lncRNAs on its target genes in cis and trans, indicating that these lncRNAs have a strict tissue specificity and functional conservation during skin development and pigmentation.ConclusionThe present study provides a resource for lncRNA studies in diseases involved in pigmentation and skin development. It expands our knowledge about lncRNA biology as well as contributes to the annotation of the goat genome.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2365-3) contains supplementary material, which is available to authorized users.

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“…UV, particularly longer-wavelength UVA, is a well-known inducer of ROS, and UV-induced oxidative stress may be an important contributive factor for melanoma [80–82]. ROS can inappropriately activate signaling pathways, interfere with genome maintenance and affect apoptosis.…”

Section: Oxidative Stress and Agingmentioning

confidence: 99%

Ultraviolet Radiation, Aging and the Skin: Prevention of Damage by Topical cAMP Manipulation

2014

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Being the largest and most visible organ of the body and heavily influenced by environmental factors, skin is ideal to study long-term effects of aging. Throughout our lifetime, we accumulate damage generated by UV radiation. UV causes inflammation, immune changes, physical changes, impaired wound healing and DNA damage that promotes cellular senescence and carcinogenesis. Melanoma is the deadliest form of skin cancer and among the malignancies of highest increasing incidence over the last several decades. Melanoma incidence is directly related to age, with highest rates in individuals over the age of 55 years, making it a clear age-related disease. In this review, we will focus on UV-induced carcinogenesis and photo aging along with natural protective mechanisms that reduce amount of “realized” solar radiation dose and UV-induced injury. We will focus on the theoretical use of forskolin, a plant-derived pharmacologically active compound to protect the skin against UV injury and prevent aging symptoms by up-regulating melanin production. We will discuss its use as a topically-applied root-derived formulation of the Plectranthus barbatus (Coleus forskolii) plant that grows naturally in Asia and that has long been used in various Aryuvedic teas and therapeutic preparations.

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Suppression of melanogenesis by a newly synthesized compound, MHY966 via the nitric oxide/protein kinase G signaling pathway in murine skin

Cited by 23 publications

References 26 publications

The Novel PPAR α/γ Dual Agonist MHY 966 Modulates UVB–Induced Skin Inflammation by Inhibiting NF-κB Activity

The Novel PPAR α/γ Dual Agonist MHY 966 Modulates UVB–Induced Skin Inflammation by Inhibiting NF-κB Activity

Genome-wide analysis of long non-coding RNAs at early stage of skin pigmentation in goats (Capra hircus)

Ultraviolet Radiation, Aging and the Skin: Prevention of Damage by Topical cAMP Manipulation

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