The matrix cells are referred to as transit-amplifying cellsbecause they undergo a limited number of cell divisions beforedifferentiating. As the supply of matrix cells declines, HSand IRS differentiation slow and the follicle enters a destructivephase called catagen. The timing of the first catagen onsetvaries slightly between strains of mice and varies significantlyfrom one skin region to another. In pigmented mice, the progressionof catagen is evident from the color of the skin, which changesfrom the dark gray to black of anagen to pale pink by telogen.As with morphogenesis, the first catagen begins in a wave, spreadingfrom the top of the head caudally towards the tail and laterallydown the sides of the animal. In back skin taken from the midline,the onset of the first catagen ranges from P14 at the upperback near the head to P18 in the lower back near the tail. Catagenlasts 3-4 days in mice.
Some molecular regulators of the anagen-catagen transition havebeen identified, although how they work together to promotecatagen or terminate anagen is not yet understood. Moleculesthat promote the transition to catagen include the growth factorsFGF5 and EGF, neurotrophins such as BDNF and possibly the p75-neurotrophinreceptor, p53 and TGFß-family pathway members suchas TGFß1 and the BMPRIa (Andl et al., 2004
; Foitziket al., 2000; Hansen et al., 1997; Hebert et al., 1994; Schmidt-Ullrichand Paus, 2005). Factors known to maintain anagen include SGK3and Msx2 (Alonso et al., 2005; Ma et al., 2003).
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