Abstract
Recent studies have revealed that adiponectin can suppress cellular inflammatory signaling pathways. This study aimed to elucidate the effect of adiponectin on the unregulated production of hBD2 in UVB-induced premature senescent keratinocytes. We constructed an in vitro model of premature senescent keratinocytes through repeated exposure to low energy UVB. After repeated low energy UVB exposure, there was significant generation of reactive oxygen species (ROS) and induction of senescence-associated markers, including senescence associated beta-galactosidase activity and expression of p16INK4a and histone H2AX. In addition, the present clinical study showed higher expression of hBD2 in sun-exposed skin of elderly group, and the overexpression of hBD2 was observed by c-Fos activation in vitro. Adiponectin has the ability to scavenge ROS and consequently inhibit MAPKs and SA-markers in UVB-exposed keratinocytes. An inhibitor study demonstrated that adiponectin downregulated hBD2 mRNA expression through suppression of the AP-1 transcription factor components c-Fos via inactivation of p38 MAPK. Collectively, the dysregulated production of hBD2 by the induction of oxidative stress was attenuated by adiponectin through the suppression of p38 and JNK/SAPK MAPK signaling in UVB-mediated premature senescent inducible conditions. These results suggest the feasibility of adiponectin as an anti-photoaging and anti-inflammatory agent in the skin.
Highlights
As the skin is the most exposed tissue to environmental stress, repeated exposure to environmental stimuli include ultraviolet (UV) light leads to an enhanced inflammatory state and even aging of skin and a reduction of barrier function [1, 2]
Reports showed that the overexpression of human beta defensin 2 (hBD2) stimulated epidermal keratinocyte migration and proliferation, and even played an oncogenic role in esophageal carcinogenesis and basal cell carcinoma [3, 10, 11], and could result in excessive inflammation similar to that seen in psoriasis and rosacea [12, 13]
We suggest that there is the correlation between photoaging and hBD2 expression and the adiponectin plays a role in protective effect against hBD2 dysregulation in UVB-induced premature senescent keratinocytes
Summary
As the skin is the most exposed tissue to environmental stress, repeated exposure to environmental stimuli include ultraviolet (UV) light leads to an enhanced inflammatory state and even aging of skin and a reduction of barrier function [1, 2]. An essential component of the cutaneous defensive barrier, human beta defensin 2 (hBD2) is a cysteine-rich cationic 41 amino acid antimicrobial peptide, which is induced in cutaneous infection and inflammatory dermatitis [3]. It plays a role in cellular immune reactions and antimicrobial cytotoxic activities against bacteria, fungi, and viruses and as a sacrificial sunscreens in UV exposed tissue [4, 5]. Clinical studies reported that high hBD2 levels were found in elderly individuals and UV exposed condition, possibly due to age-dependent skin changes, including barrier disruption, that were caused by an accumulated inflammatory response [2, 14]. Loss of hBD2 homeostasis may mediate the excessive inflammatory responses and the correlation between photoaging and hBD2 expression is hypothesized in this study
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