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COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE
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Retinoid Receptors
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Retinoid-binding proteins were first discovered in the 1970s9 In 1987, the discovery of retinoic acid receptors led to the realization that tretinoin is a hormone10,11 Since that time, much research has been performed to determine the exact roles of these binding proteins and receptors The biologic effects of retinoic acid are now known to be mediated by several biologic systems: binding proteins such as cellular retinoic acid binding proteins I and II (CRABP I and II); cellular retinol binding protein (CRBP)2; and nuclear receptors that are divided into two categories, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs)12 All of these nuclear receptors are members of a large superfamily called nuclear hormone superfamily receptors, which includes the
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In 1931, the Nobel Prize was awarded to Karrer et al for determining the structure
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FIGURE 30-1 Chemical structures of the three generations of retinoids Addition of aromatic rings has made third-generation retinoids more stable and more speci c for certain receptors
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Retinoid binding prevents AP-1 binding to AP-1 site RETINOID RETINOID
AP-1
AP-1 SITE PROLIFERATION GENES
DIFFERENTIATION GENES RETINOID RESPONSE ELEMENT
RAR AP-1
CHAPTER 30 RETINOIDS
INACTIVE COMPLEX
Differentiation of keratinocytes Intercellular adhesion Normalize keratinization
FIGURE 30-2 Retinoid mechanism of action in acne
Block pro-proliferative and pro-inflammatory effects of AP-1
receptors for vitamin D, estradiol, glucocorticoids, and thyroid hormone13 The retinoic acid receptor family is composed of two types of receptors, the RARs and the RXRs The RARs and the RXRs are divided into , , and subtypes The RAR , RAR , and RAR genes have been localized to chromosomes 17q21, 3p24, and 12q13, respectively, and the RXR , RXR , and RXR genes have been mapped to chromosomes 9q343, 6p213, and 1q22-23, respectively14 These receptors are able to regulate gene expression in two ways: (1) they induce gene expression by binding to specific DNA sequences known as retinoic acid responsive elements (RAREs), or (2) they inhibit gene expression by downregulating the actions of other transcription factors (such as AP-1 and NF-IL6) All the , , and subtypes exhibit distinct affinities for retinoic acid and show a characteristic tissue distribution For example, epidermis is a privileged tissue for the expression of RAR and RXR , the major isoforms of their respective families in this tissue, whereas RAR is ubiquitous In the skin, RAR is primarily found in the dermis, and it is also found in other body tissues7 Ninety percent of the RARs in the epidermis and cultured keratinocytes are
RAR , which is the receptor associated with terminal differentiation; therefore, this receptor is the target of the retinoids used in dermatology15 The interactions of the retinoid receptors among themselves and other receptors of the nuclear hormone superfamily are complex RARs are known to heterodimerize with RXR in order to interact with their RAREs and mediate classic retinoid activity and toxicity RXRs, however, are more promiscuous, heterodimerizing with several other members of the steroid receptor superfamily including peroxisome proliferator-activated receptors (PPAR), vitamin D receptors, thyroid hormone receptors, and a number of orphan receptors, such as LXR, PXR, and FXR16 The interactions of these receptors are being studied intensively; however, more research is necessary to fully delineate the mechanisms of action of retinoid agents
RETINOIDS AS ANTIAGING AGENTS
Photodamage and Matrix Metalloproteinases
Although tretinoin has been approved for many years for the treatment of photoaging, evidence suggests that it also plays a
role in the prevention of aging This can be linked to inhibitory effects of retinoids on damaging metalloproteinases UVB exposure dramatically upregulates the production of several collagen-degrading enzymes known as matrix metalloproteinases (MMPs) (see 6) Activation of MMP genes results in production of collagenase, gelatinase, and stromelysin, which have been shown to fully degrade skin collagen17 (Box 30-1) Fisher et al demonstrated that application of tretinoin inhibits the induction of all three of these harmful MMPs1 In addition to increasing levels of destructive enzymes such as collagenase, UV exposure has also been shown to decrease collagen production Fisher et al demonstrated that expression of collagen types I and III is substantially reduced within 24 hours after a single UV exposure18 Pretreatment of the skin with alltrans-retinoic acid (tretinoin) was shown to inhibit this loss of procollagen synthesis Therefore, pretreatment of the skin with topical retinoids, when used consistently, is likely to be beneficial in preventing as well as treating photodamage19
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