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1 he onset of the first wave of HF regression (catagen).
2 F cycling by apoptosis-driven HF regression (catagen).
3 transition from active growth to regression (catagen).
4  interrupted by apoptosis-driven involution (catagen).
5  were more severe than in the other forms of catagen.
6 f melanogenic melanocytes during spontaneous catagen.
7 a/StEpiDelta) mice and hindered cycling into catagen.
8 nifest, whereas the HFPU disassembles during catagen.
9 e ex vivo growth of HFs and delayed onset of catagen.
10 ed high levels of glycogen that decreased in catagen.
11  phenotypes, and follicle loss occurs during catagen.
12 gulates apoptosis in HF keratinocytes during catagen.
13 rmal apoptosis reflects premature entry into catagen.
14 rious phases of the apoptotic process during catagen.
15 ct patterns of apoptosis and survival during catagen.
16  for the loss of gene expression observed at catagen.
17 lly declined, and reappeared again in middle catagen.
18 tosis induced by cytokines or hypoxia during catagen.
19 regressing hair follicle compartments during catagen.
20 nockout mice show significant retardation of catagen accompanied by significant decrease in the numbe
21 and to accelerated hair follicle regression (catagen), accompanied by an increase of CD8+ cells-expre
22       This study shows that both spontaneous catagen and dexamethasone-induced catagen display simila
23 and, and for understanding the regulation of catagen and hair follicle immunology.
24         Nrf2 preactivation reduced premature catagen and hair growth inhibition induced by oxidative
25 rating follicular matrix cells, facilitating catagen and maintaining follicular structures and their
26 epidermidis and other HF microbiota, delayed catagen and promoted autophagy, mitochondrial activity,
27  be detected in FP during anagen, but not in catagen and telogen phases of the hair cycle.
28  by normal mode ruby laser exposure, whereas catagen and telogen stage hair follicles were resistant
29     LEF1 and TOPGAL expression ceased during catagen and telogen, but reappeared at the start of the
30 increases during anagen and decreases during catagen and telogen.
31 ficiency shortens anagen phase, but prolongs catagen and telogen.
32 ng anagen and in the club hair sheath during catagen and telogen.
33  an inability to regrow hair after the first catagen and that the mutation displays semi-dominant inh
34 t is characterized by accelerated entry into catagen and through anagen, irregular hair follicle orie
35 ed by apoptosis were detected in spontaneous catagen and, more commonly, in dexamethasone-induced cat
36 gen) to a rapid apoptosis-driven involution (catagen) and finally a relative quiescent phase (telogen
37 ation (anagen), apoptosis-driven regression (catagen) and relative quiescence (telogen).
38 d is interrupted during follicle regression (catagen) and resting.
39 iogenic blood vessels during the involution (catagen) and the resting (telogen) phase.
40  two distinct pathways (dystrophic anagen or catagen) and why this makes RIA management so challengin
41 t growth, prematurely induced HF regression (catagen), and inhibited hair matrix keratinocyte prolife
42  as a regulator of hair follicle remodeling (catagen), and loss of Barx2 in mice causes a defect both
43 stages of rapid growth (anagen), regression (catagen), and relative "quiescence" (telogen).
44 of active regeneration (anagen), involution (catagen), and relative quiescence (telogen).
45  cycles between growth (anagen), regression (catagen), and relative quiescence (telogen).
46 prise phases of growth (anagen), regression (catagen), and rest (telogen).
47 ed during anagen, is reduced at the onset of catagen, and can be reamplified in the skin and surround
48  of catagen, resulting in a protracted first catagen, and later, causing short hair in adult gene-del
49 ir matrix keratinocytes, prematurely induced catagen, and up-regulated p53.
50 and, more commonly, in dexamethasone-induced catagen, and were identified using transmission electron
51 -induced apoptosis, it surprisingly promoted catagen- and chemotherapy-associated keratinocyte apopto
52 anisms underlying apoptosis in the HF during catagen, as well as differences in the regulation of apo
53 rast, forced hair follicles into "dystrophic catagen", associated with enhanced intrafollicular apopt
54 t genes and are implicated in the control of catagen (Bax, Bcl-2, insulin-like growth factor binding
55 rst spontaneous entry of hair follicles into catagen between TGF-beta1 null mice and age-matched wild
56 mal papilla cells of pelage follicles during catagen but not in anagen or telogen.
57 n to telogen involves an intermediate stage, catagen, consisting of a swift, apoptosis-driven involut
58 ed the potential involvement of TGF-beta1 in catagen control.
59 wth disorders based on premature or retarded catagen development (effluvium, alopecia, hirsutism).
60 thasone was demonstrated to induce premature catagen development accompanied by an abrupt termination
61                                              Catagen development accompanied by increased apoptosis i
62 into the back skin of mice induced premature catagen development.
63 ng spontaneous and pharmacologically induced catagen development.
64 activates premature but predominantly normal catagen development.
65 pontaneous catagen and dexamethasone-induced catagen display similar changes in the pigmentary unit.
66                                       During catagen, Eda A1 mRNA and Edar protein were expressed in
67 a neonatal short-hair phenotype due to early catagen entry compared with matched wild-type siblings.
68  the vascular changes as well as the delayed catagen exhibited by these mice.
69             During hair follicle regression (catagen), expression levels decrease until expression is
70 lso detected in the permanent portion of the catagen follicle.
71 ions, and that substance P treatment induces catagen follicles along with activated CD8+ T cells.
72 ls and fewer apoptotic cells than comparable catagen follicles from +/+ mice.
73                               In comparison, catagen follicles had low levels of telomerase activity
74                          Importantly, mutant catagen follicles undergo delayed regression and display
75 calization of apoptotic nuclei and TGFRII in catagen follicles.
76 gulated during anagen, then downregulated in catagen follicles.
77                                              Catagen hair follicles exhibited pigment incontinence in
78 -22 is not an effector of apoptosis in mouse catagen hair follicles.
79  papilla and lower epithelial strand of late-catagen hair follicles.
80 ression of the hair follicles from anagen to catagen (hair follicle maturation and regression), group
81 en suggests that secondary hair germ of late catagen HF is most likely repopulated by melanocytes ari
82 ot sheath or follicular papilla of early/mid-catagen HF.
83 d premature, apoptosis-driven HF regression (catagen), HF cytotoxicity/dystrophy, and most important
84                                       During catagen, hr gene expression gradually declined in the re
85 rally abnormal hairs are easily dislodged in catagen implying a precocious exogen.
86                Ha1 expression is lost during catagen in all mice but recovers more slowly in the knoc
87 n regulating basic cellular processes during catagen, including club hair formation, maintenance of D
88 odel for general hair pigmentation research, catagen induced by cyclophosphamide offers an interestin
89 -express Lgr5, do not express Shh and escape catagen-induced apoptosis.
90 s among the elusive endogenous regulators of catagen induction in vivo, possibly via the inhibition o
91 lopecia, whereas a shift towards "dystrophic catagen" initially enhanced the hair loss, yet subsequen
92 en but was highly upregulated throughout the catagen involution phase.
93                                          How catagen is coordinated, and spares the progenitor cells
94                                 The onset of catagen is repressed by R-spondin2 injection, and the an
95        The functional role of osteopontin in catagen is unclear but it may promote the formation of a
96      The regression phase of the hair cycle (catagen) is an apoptosis-driven process accompanied by t
97    The hair follicles fail to regress during catagen leading to abnormally long follicles.
98 F development was disturbed during the first catagen leading to formation of epithelial-lined HF cyst
99 itro cultured HFs has been shown to induce a catagen-like process.
100               Although dexamethasone-induced catagen may provide a useful model for general hair pigm
101 llicular damage-response towards "dystrophic catagen" mitigates cyclophosphamide-induced alopecia, wh
102 regressive phase of the hair follicle cycle (catagen), occurred earlier than usual.
103 eceptors during late anagen and the onset of catagen of the hair cycle.
104 oblasts migrate out of the late anagen/early catagen papilla and re-enter the proximal connective tis
105 riven by the dystrophic anagen or dystrophic catagen pathway, play important parts in the degree of h
106 ed to result from a premature entry into the catagen phase of the hair cycle.
107 papilla cells, during the anagen but not the catagen phase.
108 ed a significant acceleration of spontaneous catagen progression.
109 transforming growth factor beta 2 (TGFbeta2; catagen promoter) was enhanced.
110         Neutralizing TGFbeta antagonized the catagen-promoting effects of P-cadherin silencing.
111 ced perifollicular angiogenesis, whereas the catagen regression phase is characterized by apoptosis-d
112  failure of hair follicles to enter a normal catagen regression phase, eventual follicular degradatio
113 F during cyclical rounds of anagen (growth), catagen (regression), and telogen (quiescence).
114 ses: telogen (resting), anagen (growth), and catagen (regression).
115 s been proposed to play an important role in catagen regulation.
116 iven physiological hair follicle regression (catagen) remains to be elucidated.
117 rain and skin, which is believed to regulate catagen remodeling in the hair cycle.
118  undergo cyclic behavior through regression (catagen), rest (telogen), and regeneration (anagen) duri
119 ct both in the initiation and progression of catagen, resulting in a protracted first catagen, and la
120 n-specific genes (e.g., nexin 1), but also a catagen-specific gene.
121 differentiation, short hair shafts, aberrant catagen stage of the hair cycle, and eventual loss of th
122 le morphogenesis and late onset of the first catagen stage.
123 ng early and middle anagen and during middle catagen stages.
124 orders characterized by premature entry into catagen, such as androgenetic alopecia, alopecia areata,
125 eration in the follicular melanocytes during catagen suggests that secondary hair germ of late catage
126  follicular pigmentary unit during HF anagen-catagen-telogen transition and may be used for the estab
127 suggest that Gsdma3 has an important role in catagen-telogen transition by balancing the Wnt signalin
128 wever, whether there is a switch controlling catagen-telogen transition remains largely unknown.
129                       Furthermore, anagen to catagen/telogen ratios were lower in individuals with al
130 age of the hair cycle, being switched-off in catagen to remain absent through telogen.
131  Here we show that hair follicles cycle from catagen to the next anagen without transitioning through
132 2B GFP mice led to significant hair follicle catagen transformation compared with controls.
133                             As the anagen-to-catagen transformation of microdissected human scalp HFs
134  melanocytes were examined during the anagen-catagen transformation, comparing spontaneous and pharma
135 d in hair cycle control, i.e., the anagen-to-catagen transformation, was tested.
136 ir follicle cycling via entry into the first catagen transformation.
137 blast growth factor-5 regulate the anagen to catagen transition by independent pathways.
138 hat TNFalpha is required for a timely anagen-catagen transition in mouse pelage follicles, and that i
139 tor combination might regulate the anagen to catagen transition of the hair cycle.
140 es in anagen VI, decreased during the anagen-catagen transition phase.
141 follicular adipocytes declined during anagen-catagen transition, whereas fluorescence-lifetime imagin
142 ect promotion of apoptosis during the anagen-catagen transition.
143 ng was observed in this region at the anagen-catagen transition.
144 naling molecules that regulate the anagen to catagen transition.
145                                  During late catagen, TUNEL and Ki-67 negative melanocytes expressing
146        By contrast, cyclophosphamide-induced catagen was characterized by the initial retention of me
147       This cell loss, which continued during catagen, was not associated with intra-follicular papill
148  may be one of the triggers for the onset of catagen when the follicles are in anagen and the onset o
149 le, and in the bulge during anagen and early catagen, whereas Aldh1a3 expression was primarily in the
150 es in TGF-beta1 -/- mice were still in early catagen, whereas hair follicles of +/+ littermates had a
151 hed off during the transition from anagen to catagen, which implies a regulatory role for IGF-I durin
152 nce that specific genes are turned on during catagen, which is therefore not simply a passive "degene

 
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