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Received Dec 28, 2017; Accepted Mar 6, 2018
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1. Introduction
Sebocytes can produce lipid-rich sebum to function in epidermal barrier, hair follicle integrity, and antibacterial and antioxidant properties [1, 2]. Abnormal sebum secretion is involved in some common dermatosis including acne vulgaris, atopic dermatitis, psoriasis, rosacea, and seborrheic dermatitis [3, 4]. Sebocyte differentiation in mice is divided into undifferentiated (stem and proliferating cells) and differentiated (maturating and fully differentiated cells) stages that are, respectively, characterized by keratin 5 (K5) and peroxisome proliferator-activated receptor γ (PPARγ) expression [5]. The terminal differentiation of human sebocytes presents with increased cell size, cytoplasmic accumulation of lipid droplets, and nuclear degeneration, followed by holocrine secretion and cell death [6, 7]. A recent study of mouse model unraveled that holocrine secretion of sebum is a DNase2-mediated form of programmed cell death distinct from apoptosis, necroptosis, and cornification [8]. Zouboulis et al. firstly compared the markers of human sebocyte versus keratinocyte differentiation in vitro in 1991 [9]. Cell confluence levels generally serve as differentiation stages of in vitro cultured sebocytes [10, 11]. However, to date a well-established differentiation model of human primary sebocytes has been unavailable, and the feasible markers of sebocyte differentiation have not been fully elucidated, which may hinder to understand the physiological function of sebaceous glands and pathophysiological mechanisms of sebaceous gland-related diseases.
PPARγ, liver X receptors (LXR), sterol regulatory element binging protein (SREBP1), and Forkhead box O1 (FoxO1) may be main lipogenic factors for sebocytes [12–15]. PPARγ could be a potential marker of sebocyte differentiation because its expression correlates with the differentiation stage of sebocytes [12]. LXR agonists inhibited proliferation but promoted lipogenesis in SZ95 sebocytes [13]. SREBP1 may be a key regulator of lipid synthesis in sebaceous glands through inducing expression of lipogenic genes [14, 16]. FoxO1 might be implicated in acne pathogenesis by mediating androgen receptor, PPARγ, LXR, and SREBP1 expression [15, 17, 18]. Additionally, our previous study showed that sex determining region Y-related high mobility group box 9 (Sox9) can promote sebocyte proliferation, differentiation, and lipogenesis [10]. However,...