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Adipocytes in Skin Health and Disease

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Adipocytes in Skin Health and Disease Downloaded from http://perspectivesinmedicine.cshlp.org/ on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press Adipocytes in Skin Health and Disease Guillermo Rivera-Gonzalez1, Brett Shook1, and Valerie Horsley Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06520 Correspondence: [email protected] Adipocytes are intimately associated with the dermal compartment of the skin, existing in a specialized dermal depot and displaying dynamic changes in size during tissue homeostasis. However, the roles of adipocytes in cutaneous biology and disease are not well understood. Traditionally, adipocytes within tissues were thought to act as reservoirs of energy, as thermal, or as structural support. In this review, we discuss recent studies revealing the cellular basis of the dynamic development and regenerative capacity of dermal adipocytes associated with the hair cycle and following injury. We discuss and speculate on potential roles of dermal adipocytes in cutaneous biology with an emphasis on communication during hair follicle growth and wound healing. Finally, we explore how alterations in the dermal adipose tissue may support clinical manifestations of cutaneous diseases such as lipodystrophy,obesity, and alopecia. ADIPOCYTE DEVELOPMENT AND control adipocyte differentiation, exist within HOMEOSTASIS IN THE SKIN the dermis of mouse skin a few days before birth (Wojciechowicz et al. 2008), suggesting that ad- n mammals, white adipose tissue (WAT) forms ipocyte precursor cells exist in the skin during Iat specific bodily sites or depots. Major sites of the formation of the dermis. adipocyte development include the visceral de- The developmental origin of adipocytes has pot in the abdomen, subcutaneous adipocytes not fully been defined. Genetic lineage tracing below the skin, and dermal adipocytes within using mice expressing Cre recombinase under www.perspectivesinmedicine.org the dermis of the skin (Gesta et al. 2007). The the control of the Sox10 promoter, expressed in timing of adipocyte formation and gene expres- neural crest cells, revealed that many mesenchy- sion patterns is different between distinct adi- mal cell types including cephalic adipocytes in pose depots (Gesta 2006). Mature dermal adi- the salivary gland and ear are of neural crest pocytes form postnatally after the formation of origin, but not adipocytes in trunk depots, the hair follicle (Hausman et al. 1981). However, such as subcutaneous adipocytes (Le Douarin adipocyte precursor cells are present in murine 2004). Recent studies have shown that Pdgfr-a embryonic skin by E14 (Wojciechowicz et al. expressing cells form adipocytes during devel- 2013) and cells expressing C/EBPa, which can opment in several depots (Fig. 1) (Berry and 1These authors contributed equally to this work. Editors: Anthony E. Oro and Fiona M. Watt Additional Perspectives on The Skin and Its Diseases available at www.perspectivesinmedicine.org Copyright # 2014 Cold Spring Harbor Laboratory Press; all rights reserved; doi: 10.1101/cshperspect.a015271 Cite this article as Cold Spring Harb Perspect Med 2014;4:a015271 1 Downloaded from http://perspectivesinmedicine.cshlp.org/ on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press G. Rivera-Gonzalez et al. Differentiation gradient Adipogenesis Hypertrophy Mature Adipocyte Preadipocyte adipocyte progenitor Pdgfr-α CD29 CD29 Lipid CD34 PDGFR-α Pparγ C/ebp Sca1 CD24 Pparγ Sca1 CD34 Perillipin Secreted adipokines Leptin IGF-1 IL-6 NGF BMP TGF-β Adiponectin Figure 1. Mechanisms of adipose tissue growth. Adipose tissue growth can occur through two different mech- anisms: adipogenesis and hypertrophy. Adipogenesis generates new mature adipocytes through proliferation and differentiation of proliferative adipocyte precursor cells (identified by the cell surface markers Lin-, CD34, CD29, Sca1, CD24, and PDGFR-a). These cells give rise to preadipocytes that lose CD24 expression and begin to express higher levels of adipogenic transcription factors such as PPARg. Preadipocytes differentiate into post- mitotic mature adipocytes and can grow in size as they fill with lipid during hypertrophy. Mature adipocytes express perilipin and secrete adipokines that have the potential to impact skin biology. Rodeheffer 2013). However, because Pdgfr-a follicular regression, the adipocyte layer dimin- is expressed by multiple mesenchymal lineages ishes to a thin layer of mature adipocytes under- (Karlsson et al. 1999; Collins et al. 2011), the neath the dermal papillae. Following initiation precise developmental origin of dermal adipo- of hair follicle growth, the size of the dermal cytes is unknown. adipocyte layer expands. Classic studies in the 1950s studying the The dynamic nature of dermal adipocytes www.perspectivesinmedicine.org death and regrowth of the postnatal hair follicle during the hair cycle is controlled in part by noted that the dermal adipocyte layer dramat- the formation of new mature adipocytes by im- ically changes its thickness in synchrony with mature adipocyte precursorcells(Fig. 1). Imma- the spontaneous regeneration of the hair follicle ture adipocyte lineage cells can be identified (Fig. 2) (Chase et al. 1953). The hair follicle is based on their expression of CD34, CD29, and maintained by cyclic growth (anagen), death Sca1 (Rodeheffer et al. 2008; Festa et al. 2011; (catagen), and quiescent (telogen) stages dur- Berry and Rodeheffer 2013). Labeling of prolif- ing its maintenance. The initiation of hair re- erative cells during the initiation of hair growth growth involves the activation of epithelial stem revealed that immature adipocyte precursorcells cells in the bulge region of the hair follicle (Cot- are activated to proliferate in parallel with the sarelis et al. 1990; Blanpain et al. 2004; Zhang hair cycle and new mature adipocytes are et al. 2009) and their interaction with mesen- formed by proliferative cells (Festa et al. 2011). chymal cells in the dermal papillae (Jahoda et al. Furthermore, treatment of mice during the ini- 1984; Rompolas et al. 2012). During hair follicle tiation of hair growth with a pharmacological morphogenesis, lipid-filled dermal adipocytes inhibitor of a key adipogenic transcription fac- surround the growing hair follicle (Fig. 2). On tor, PPARg, blocks the growth of dermal adipo- 2 Cite this article as Cold Spring Harb Perspect Med 2014;4:a015271 Downloaded from http://perspectivesinmedicine.cshlp.org/ on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press Adipocytes in Cutaneous Biology Telogen Epidermis Sebaceous gland Catagen Early anagen Key Dermal papilla Preadipocyte Fibroblasts Adipocyte progenitor Bulge stem cells Mature adipocyte Extracellular Lipid-filled Hair germ matrix mature adipocyte Adipocyte Anagen signaling Hair matrix Figure 2. Changes in dermal adipose tissue during the hair follicle cycle. During the transition of the hair follicle from rest (telogen) to growth (anagen), dermal adipose tissue increases in size via activation of immature adipocyte precursor cells. These cells generate an increased number of adipocytes that, via hypertrophy, grow in size to surround the hair follicle during anagen. As the hair follicle regresses (catagen), dermal adipose tissue significantly decreases in size via unknown mechanisms. www.perspectivesinmedicine.org cytes during the hair cycle. Thus, adipogenesis atinocytes and fibroblasts proliferate and mi- within the dermal adipocyte depot occurs in grate to restore the epidermal barrierand initiate parallel with the hair follicle cycle. dermal repair, respectively. Adiponectin- and Adipogenesis of dermal adipocytes also oc- perilipin-expressing adipocytes repopulate skin curs following injury (Schmidt and Horsley wounds during the proliferative stage of healing 2013) as the ensuing wound-healing process re- concomitant with fibroblast activation and mi- pairs epidermal and dermal integrity and com- gration (Schmidt and Horsley 2013). This re- position to its original structure (Fig. 3) (Alexaki population of adipocytes following wounding etal.2012;Forcheronetal.2012;Riccobonoetal. is associated with proliferation of adipocyte pre- 2012; Schmidt and Horsley 2013). Immediately cursor cells and can be inhibited by pharmaco- following a skin injury, the inflammatory re- logical inhibition of PPARg, indicating that adi- sponse protects the damaged skin from external pogenesis occurs during wound healing. pathogens and clears cellular debris created by In general, the cellular and molecular path- the injury (Delavary et al. 2011). Immune cells ways that promote adipogenesis in vivo are not initiate the proliferative response by which ker- well understood. The dynamic nature of dermal Cite this article as Cold Spring Harb Perspect Med 2014;4:a015271 3 Downloaded from http://perspectivesinmedicine.cshlp.org/ on September 25, 2021 - Published by Cold Spring Harbor Laboratory Press G. Rivera-Gonzalez et al. Fibrin scab Wound Injury/ Clotting/ hemostasis platelets Inflammation Epidermal Dermal repair repair Proliferation Key Fibroblast Predipocyte Macrophage Adipocyte progenitor Extracellular Mature adipocyte matrix (LCM) Remodeling Lipid-filled Nascent ECM mature adipocyte Recurring wound/scab Remodeling www.perspectivesinmedicine.org Proliferation Adipogenesis inhibition Figure 3. The role of adipocytes in wound healing. Wound healing occurs in four main stages: injury, inflam- mation, proliferation, and remodeling. Immediately after wounding, platelets generate
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