Abstract
Caffeic acid phenethyl ester (CAPE), a naturally occurring bioactive compound, displays anti-inflammatory, anti-carcinogenic, and anti-microbial effects. However, the effect of CAPE on skin photoaging is unknown. Herein, we investigated the inhibitory effect of CAPE against ultraviolet (UV) irradiation-mediated matrix metalloproteinase (MMP)-1 expression and its underlying molecular mechanism. CAPE treatment suppressed UV-induced MMP-1 levels in both human dermal fibroblasts (HDF) and human skin tissues. While CAPE did not display any significant effects against the upstream regulatory pathways of MMP-1, CAPE was capable of reversing UV-mediated epigenetic modifications. CAPE suppressed UV-induced acetyl-histone H3 (Lys9) as well as total lysine acetylation in HDF cells. Similarly, CAPE also attenuated UV-induced lysine acetylations in human skin tissues, suggesting that the CAPE-mediated epigenetic alterations can be recapitulated in ex vivo conditions. CAPE was found to attenuate UV-induced histone acetyltransferase (HAT) activity in HDF. Notably, CAPE was able to directly inhibit the activity of several HATs including p300, CREP-binding protein (CBP), and p300/CBP-associated factor (PCAF), further confirming that CAPE can function as an epigenetic modulator. Thus, our study suggests that CAPE maybe a promising agent for the prevention of skin photoaging via targeting HATs.
Highlights
Photoaging is mainly caused by ultraviolet (UV) exposure, free radicals, and physical stimuli [1]
After 10 days, matrix metalloproteinase (MMP)-1 levels were examined in the UV-irradiated skin tissue (Figure 3A)
It was found that the 2.5 μM of Caffeic acid phenethyl ester (CAPE) treatment reduced MMP-1 expression in UV-irradiated skin tissues (Figure 3B)
Summary
Photoaging is mainly caused by ultraviolet (UV) exposure, free radicals, and physical stimuli [1]. The UV light reaching our skin is composed of 90–95% UVA (315–400 nm) and 5–10% UVB (280–315 nm). Overexposure to UVA/UVB is known to be associated with skin aging characterized by wrinkle formation, skin pigmentation, and laxity [2,3]. UV irradiation causes the expression of various matrix metalloproteinases (MMPs) in dermal fibroblasts, which contribute to the degradation of extracellular matrixes including collagen, leading to skin wrinkle formation [4]. Among the UV-inducible enzymes, MMP-1 has been known to play a key role in collagen degradation, and has been a major interest in skin aging [4,5]. MMP-1 inhibitors can be an attractive strategy in preventing skin aging due to UV exposure
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