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What Is The Primary Function Of Melanin

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Hyperpigmentation: Causes, Types & Genetics Explained

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By Hugo Moreras Hugo Moreras Skillet Preprints.org Google Scholar † , Miguel C. Sibra Miguel C. Cyber ​​Skillet Preprints.org Google Scholar Duarte C. Baral Duarte C. Parallel Skillet Preprints.org Google Scholar *

Received: April 2, 2021 / Revised: April 20, 2021 / Accepted: April 21, 2021 / Published: April 24, 2021

British Journal Of Nursing

The mechanisms by which melanin pigment is transported from melanocytes and processed within keratinocytes to achieve skin pigmentation remain uncharacterized. However, numerous models have emerged in the past decades to explain the transfer process. Here, we review proposed models of melanin transport in the epidermis, the available evidence supporting each, and recent observations in favor of exo/phagocytosis and shedding vesicle models. In order to reconcile transmission models, we propose that different mechanisms may coexist to maintain skin pigmentation under different conditions. We also discuss the limited knowledge about melanin processing within keratinocytes. Finally, we identify new questions that need to be addressed to solve the long-standing quest to understand how basal skin pigmentation is controlled. This knowledge will allow the emergence of new strategies for treating pigmentary disorders that cause a significant social and economic burden on patients and healthcare systems worldwide, and could also have relevant cosmetic applications.

The skin is the largest organ in the human body and performs essential functions in protecting against external aggressions, including ultraviolet radiation (UVR) and infection, while maintaining water balance and body temperature [1]. The pigment system is an essential part of these functions and is responsible for variation in skin color traits within and between populations. In fact, skin pigmentation is one of the most distinctive and noticeable individual characteristics. We now understand that the association with UV protection underlies the development of skin pigmentation variation in humans. There are two main types of cells that make up the epidermis of the skin: keratinocytes, the most abundant cells, which are present in all layers of the epidermis and produce keratin to protect epithelial cells from mechanical and non-mechanical stress; Melanocytes are located in the basal layer of the epidermis and produce the protective pigment melanin [1, 2]. Melanocytes are neural crest-derived cells that arise from the dermal melanoblast lineage that migrate into the epidermis during embryonic development [3, 4, 5]. Keratinocytes continuously proliferate, migrate, and differentiate toward the upper layers of the epidermis, forming five layers or strata: stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, and stratum corneum [6, 7]. These five layers are only present in thick skin, while in the thin skin that covers most of the human body, the stratum pellucida is not observed. A single melanocyte can connect to up to 40 viable keratinocytes through its dendrites, forming the so-called epidermal melanin unit [8, 9].

Skin pigmentation results from three different processes: (1) melanin biogenesis and transport within melanocytes; (2) transfer of melanin from melanocytes to keratinocytes; and (iii) melanin internalization and processing by keratinocytes. Within keratinocytes, melanin accumulates in the supranuclear zone, protecting nuclear genetic material from damage caused by UV radiation [10].

Different classifications are used to classify humans according to their skin color. These include the Caucasian, Negro, and Mongoloid ethnic groups and the Fitzpatrick scale of six phototypes (I to VI), based on skin color and visual response to UV stimulation [10, 11]. Since these criteria do not represent the diversity of skin tones in humans, a new classification method is implemented using the Individual Classification Angle (ITA). This classification method is based on color parameters that best represent the variation of each person’s skin tone [10]. It is worth noting that racial diversity cannot be attributed to the higher number of melanocytes in dark skin [10]. Instead, differences in skin color are thought to be due to the type (eumelanin versus pheomelanin), the distribution and amount of melanin, as well as the size, number and type of melanin-containing compartments within the keratinocytes. Melanin is a group of biopolymers that are synthesized from tyrosine in melanocytes, within lysosome-associated organelles (LROs) called melanosomes. Dark melanin (ranging from brown to black pigment) is the product of successive hydroxylation, oxidation and carboxylation reactions, while pheomelanin formation (ranging from yellow to red pigment) requires at least one cysteine-based reduction step [12, 13]. The fate of melanin taken up by keratinocytes has been little studied, including the compartment in which it resides. We propose to call this compartment the melanocerasome, because it contains melanin and is formed within keratinocytes.

Unraveling The Structure And Function Of Melanin Through Synthesis

In dark skins, melanocerasomes have larger pigment nuclei and are individually distributed throughout the cytoplasm of keratinocytes, while in light skins they have smaller nuclei and are aggregated in clusters [14]. The ratio of clusters to single melanin granules decreases with increasing skin phototype [15, 16, 17]. It should be noted that light-pigmented skin does not contain melanin in the upper layers, while dark-pigmented skin maintains pigment in those layers [14]. These observations suggest that a critical factor, among others, in determining different skin phototypes is the mechanism of melanin transfer between pigment-producing melanocytes and pigment-receiving keratinocytes.

Melanosomes are considered LROs because they share proteins with lysosomes, are acidic in the early stages, and are secreted from melanocytes [18, 19, 20]. Melanin synthesis and melanosome transport within melanocytes are well characterized. Melanosomal biogenesis is divided into four organelle stages [18, 20]. During the first phase, non-pigmented premelanosomes containing endocytic membrane vesicles resembling early/sorting endosomes are formed [21]. This compartment is characterized by intraluminal protein fibers that begin to form at this stage and are completed by the second stage [22]. Melanin synthesis and melanosome maturation begin to acquire an oval shape at the end of the second stage. Stage III is characterized by the deposition of melanin on amyloid fibrils, causing them to thicken and darken, until they become fully melanized when stage IV is reached, when it is considered a fully mature melanosome [19, 20, 23].

In order to be transported to keratinocytes, melanosomes must be transported from the perinuclear area to the melanocyte dendrites. This is thought to occur in a cooperative two-step process, in which melanosomes first employ long-range, bidirectional microtubule-dependent transport. Indeed, melanosomes move in a kinesin II-dependent manner to the cell periphery, where they become attached to the actin cytoskeleton [24, 25]. In the periphery, melanosomes exhibit short-range movement on the cortical actin network that depends on the ternary complex consisting of Myosin Va, Melanophilin, and Rab27a [26, 27]. Melanosome distribution within melanocytes is hypothesized to result from competition between microtubule- and actin-dependent transport [28]. A recent report suggests that inter-melanosome repulsion based on actin filament dynamics can maintain the diffusion of melanosomes throughout the cytoplasm, without the need for microtubule-dependent transport [29]. Furthermore, another study showed that in retinal pigment epithelium (RPE) cells, microtubule transport is essential for the rapid, long-range transport of melanosomes and that cytoplasmic dynein is indispensable for the passage of these organelles to an actin filament-dependent transport [30]. Therefore, debate on this topic is still ongoing, as evidenced by the proposal for a role for dynein components in melanosome maturation, positioning, and transport to neighboring keratinocytes [31].

The molecular mechanisms controlling melanin transfer from melanocytes to keratinocytes remain controversial as there is still no consensus in this field. There are currently four models proposed to explain this process: (a) cellular phagocytosis of melanocyte dendrite tips by keratinocytes; (b) direct membrane fusion between melanocytes and keratinocytes, creating filopodia through which melanosomes are transported; (c) transport of pigment-laden vesicles from melanocytes, followed by internalization by keratinocytes; and (d) exocytosis of the melanin core by melanocytes and its subsequent internalization by keratinocytes (Figure 1). We will examine each model in more detail below.

The Layers Of The Skin: Interactive Anatomy Model

This model is based on the phagocytosis of part of the melanocyte by a keratinocyte and has been proposed for the first time yet

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