A practical guide for the study of human and murine sebaceous glands in situ

Abstract

The skin of most mammals is characterised by the presence of sebaceous glands (SGs), whose predominant constituent cell population is sebocytes, that is, lipid-producing epithelial cells, which develop from the hair follicle. Besides holocrine sebum production (which contributes 90% of skin surface lipids), multiple additional SG functions have emerged. These range from antimicrobial peptide production and immunomodulation, via lipid and hormone synthesis/metabolism, to the provision of an epithelial progenitor cell reservoir. Therefore, in addition to its involvement in common skin diseases (e.g. acne vulgaris), the unfolding diversity of SG functions, both in skin health and disease, has raised interest in this integral component of the pilosebaceous unit. This practical guide provides an introduction to SG biology and to relevant SG histochemical and immunohistochemical techniques, with emphasis placed on in situ evaluation methods that can be easily employed. We propose a range of simple, established markers, which are particularly instructive when addressing specific SG research questions in the two most commonly investigated species in SG research, humans and mice. To facilitate the development of reproducible analysis techniques for the in situ evaluation of SGs, this methods review concludes by suggesting quantitative (immuno-)histomorphometric methods for standardised SG evaluation.

Overexpression of Epigen during Embryonic Development Induces Reversible, Epidermal Growth Factor Receptor-Dependent Sebaceous Gland Hyperplasia

“…Quantitative morphometry (38) showed that SGs in K14-EPGN mice were nearly 7 times larger than control glands (Fig. 1F).…”

Primary sebocytes and sebaceous gland cell lines for studying sebaceous lipogenesis and sebaceous gland diseases

“…[8,10] Thus, increased and/or modified sebum production is a key feature of acne vulgaris, the most frequent skin disorder during adolescence, [11,12] while SG degeneration is a typical characteristic of psoriatic alopecia [13,14] and is also found in hidradenitis suppurativa, [15] lichen planopilaris, [16] pseudopelade of Brocq [17] and in some rare forms of cicatricial alopecia, such as primary cicatricial alopecia, [18] linear morphea [19] and Zouboulis syndrome. [20] Some animal models for studying SG biology and disease exist, [21,22] such as the asebia mouse, a well-studied animal model for primary cicatricial alopecia that develops SG atrophy due to a spontaneous mutation in the gene encoding the enzyme stearoylcoenzyme A desaturase 1. [23] Other examples include the use of rat preputial sebocytes [24] and hamster sebocytes.…”

“…For instance, keratin 7 and MUC1 are sebaceous markers in human but not in murine SGs. [21] These dissimilarities explain why SG-associated diseases also differ between species, the restriction of acne to human sebaceous follicles being an illustrative example. [27] Thus, although SG studies in rodents will greatly benefit from recent technical advances such as sebocyte-specific gene manipulation, [28] it is essential to study human sebocytes in order to understand SG biology, sebum functions and SG-associated diseases in humans.…”

Sebaceous lipids are essential for water repulsion, protection against UVB-induced apoptosis, and ocular integrity in mice

“…The prototype sebocyte is found in hair follicle-associated sebaceous glands (SGs), that produce sebum consisting essentially of triglycerides, wax esters, squalene (in humans only) and free fatty acids (Smith and Thiboutot, 2008). Sebum is reported to be important for skin and hair coat waterproofing, and its antioxidative and antimicrobial properties have led to the assumption that it is also important to maintain the epidermal barrier (Hinde et al, 2013;Schneider and Paus, 2010;Tóth et al, 2011). In addition to the hair follicle, sebocytes are found at several other locations of the mammalian body, forming so-called free or ectopic SGs, which are anatomically restricted and enlarged or otherwise modified.…”