Melanocyte

It takes 3-7 weeks for cells to pass from the basal layer to the corneal layer. The corneal cells then slowly desquamate. 

Thickness of the epidermis varies considerably according to the location, from about 50 pm at the thinnest places (eyelids), to 100 pm on the rest of the body, and eventually to nearly a millimeter on the palms of the hands and the soles of the feet. 

This mechanism has a precise function and can easily interfere with internal attacks or external attacks (physical or chemical). The keratin layer can thus increase in a normal fashion to make up for a very significant wearing down or pathologic conditions, for example, in psoriasis (Fig. 2.4) (of which the causes remain obscure). 

These cells exit from the neural crest and migrate toward the epidermis where their dendritic extensions are in contact with the surrounding cells. On 

Merkel cells are not distributed homogenously throughout the body (they are abundant on the lips, digits, and mouth), and they remain the most mysterious cells of the skin. Their origin has even been debated origin from the neural crest or from epidermal precursors. Merkel cells possess secretory granules contaiifing various biochemical 

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Endorphin (143) is produced from pto-opiomelanocottin, a precursor for a-, P-, and y-melanocyte stimulating hormones (MSH), adtenocorticotropin (ACTH), which includes the a-MSH sequence, and P-Hpotropin (P-LPH), which includes P-MSH and P-endotphin sequences. 

CART (cocaine- and amphetamine-regulated transcript) is a hypothalamic peptide that inhibits both normal and starvation-induced feeding when injected into cerebral ventricles of rats. CART is co-localized with the anorexigenic peptide a-melanocyte-stimulating hormone in neurons of the arcuate nucleus. Secretion of CART is stimulated by leptin and CART may be an endogenous inhibitor of food intake. 

MC3R is expressed both within the periphery and central nervous system (CNS) with detection in immune cells, gut, placenta but no detection in the adrenal gland or melanocytes. Unlike other MCR, most melanocortins (ACTHi 39, a-, (3- and y-MSH) display equipotent binding and full biological activity with truncated peptides, ACTH o and ACTH o MC3R... 

Proopiomelanocortin (POMC) is the precursor peptide of hormones and neuropeptides expressed in the pituitary and the hypothalamus (adrenocorticotropic hormone (ACTH), lipotropin, a-melanocyte-stimulating hormone (aMSH), yMSH, 3-endorphin, and others). The main clinical consequences of POMC deficiency are adrenal insufficiency (due to absence of ACTH), red hair pigmentation (due to absence of MSH) and severe early-onset obesity (due to the lack of aMSH). 

Inhibition of the passage of melanosomes from melanocytes to keratinocytes... 

Johansson O, Ljungberg A, Han SW, Vaalasti A (1991) Evidence for gamma-melanocyte stimulating hormone containing nerves and neutrophilic gran-... 

Morelli JG, Yohn JJ, Lyons MB, Murphy RC, Norris DA (1989) Leukotrienes C4 and D4 as potent mitogens for cultures human neonatal melanocytes. Invest Dermatol 93(6) 719-722... 

Tomita Y, Iwamoto M, Masuda T, Tagami H (1987) Stimulatory effect of prostaglandin E2 on the configuration of normal human melanocytes in vitro. J Invest Dermatol 89(3) 299-301... 

Tomita Y, Maeda K, Tagami H (1992) Melanocyte-stimulation properties of arachidonic acid metabolites, possible role of post-inflammatory. Cell Res 5 357-361... 

Costa JJ, Demetri GD, Harris TJ. Dvorak AM. Hayes DF, Merica EA, Menchaca DM. Gringeri AJ. Schwartz LB, Galli SJ Recombinant human stem cell factor (kit ligand) promotes human mast cell and melanocyte hyperplasia and functional activation in vivo. J Exp Med 1996 183 2681-2686. 

Otfier fiormones accelerate tfie release of free fatty acids from adipose tissue and raise tfie plasma free fatty acid concentration by increasing the rate of lipolysis of the triacylglycerol stores (Figure 25—8). These include epinephrine, norepinephrine, glucagon, adrenocorticotropic hormone (ACTH), a- and P-melanocyte-stimulat-ing hormones (MSH), thyroid-stimulating hormone (TSH), growth hormone (GH), and vasopressin. Many of these activate the hormone-sensitive hpase. For an optimal effect, most of these lipolytic processes require the presence of glucocorticoids and thyroid hormones. These hormones act in a facilitatory or permissive capacity with respect to other lipolytic endocrine factors. 

Neural cells convert tyrosine to epinephrine and norepinephrine (Figure 31—5). While dopa is also an intermediate in the formation of melanin, different enzymes hydroxylate tyrosine in melanocytes. Dopa decarboxylase, a pyridoxai phosphate-dependent enzyme, forms dopamine. Subsequent hydroxylation by dopamine P-oxidase then forms norepinephrine. In the adrenal medulla, phenylethanolamine-A -methyltransferase uti-hzes S-adenosyhnethionine to methylate the primary amine of norepinephrine, forming epinephrine (Figure 31-5). Tyrosine is also a precursor of triiodothyronine and thyroxine (Chapter 42). 

Luteinizing hormone Melanocyte-stimulating hormone Parathyroid hormone Somatostatin... 

Figure 42-15. Products of pro-opiomelanocortin (POMQ cleavage. (MSH, melanocyte-stimulating hormone CLIP, corticotropin-like intermediate lobe peptide LPH, lipotropin.)...

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