ライフサイエンスコーパス: catagen

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 phenotypes, and follicle loss occurs during catagen.

9 gulates apoptosis in HF keratinocytes during catagen.

10 rmal apoptosis reflects premature entry into catagen.

11 rious phases of the apoptotic process during catagen.

12 ct patterns of apoptosis and survival during catagen.

13 for the loss of gene expression observed at catagen.

14 lly declined, and reappeared again in middle catagen.

15 tosis induced by cytokines or hypoxia during catagen.

16 regressing hair follicle compartments during catagen.

17 nockout mice show significant retardation of catagen accompanied by significant decrease in the numbe

18 and to accelerated hair follicle regression (catagen), accompanied by an increase of CD8+ cells-expre

19 This study shows that both spontaneous catagen and dexamethasone-induced catagen display simila

20 and, and for understanding the regulation of catagen and hair follicle immunology.

21 Nrf2 preactivation reduced premature catagen and hair growth inhibition induced by oxidative

22 rating follicular matrix cells, facilitating catagen and maintaining follicular structures and their

23 be detected in FP during anagen, but not in catagen and telogen phases of the hair cycle.

24 by normal mode ruby laser exposure, whereas catagen and telogen stage hair follicles were resistant

25 LEF1 and TOPGAL expression ceased during catagen and telogen, but reappeared at the start of the

26 increases during anagen and decreases during catagen and telogen.

27 ficiency shortens anagen phase, but prolongs catagen and telogen.

28 ng anagen and in the club hair sheath during catagen and telogen.

29 an inability to regrow hair after the first catagen and that the mutation displays semi-dominant inh

30 t is characterized by accelerated entry into catagen and through anagen, irregular hair follicle orie

31 ed by apoptosis were detected in spontaneous catagen and, more commonly, in dexamethasone-induced cat

32 gen) to a rapid apoptosis-driven involution (catagen) and finally a relative quiescent phase (telogen

33 d is interrupted during follicle regression (catagen) and resting.

34 iogenic blood vessels during the involution (catagen) and the resting (telogen) phase.

35 t growth, prematurely induced HF regression (catagen), and inhibited hair matrix keratinocyte prolife

36 as a regulator of hair follicle remodeling (catagen), and loss of Barx2 in mice causes a defect both

37 stages of rapid growth (anagen), regression (catagen), and relative "quiescence" (telogen).

38 of active regeneration (anagen), involution (catagen), and relative quiescence (telogen).

39 cycles between growth (anagen), regression (catagen), and relative quiescence (telogen).

40 prise phases of growth (anagen), regression (catagen), and rest (telogen).

41 ed during anagen, is reduced at the onset of catagen, and can be reamplified in the skin and surround

42 of catagen, resulting in a protracted first catagen, and later, causing short hair in adult gene-del

43 ir matrix keratinocytes, prematurely induced catagen, and up-regulated p53.

44 and, more commonly, in dexamethasone-induced catagen, and were identified using transmission electron

45 -induced apoptosis, it surprisingly promoted catagen- and chemotherapy-associated keratinocyte apopto

46 anisms underlying apoptosis in the HF during catagen, as well as differences in the regulation of apo

47 rast, forced hair follicles into "dystrophic catagen", associated with enhanced intrafollicular apopt

48 t genes and are implicated in the control of catagen (Bax, Bcl-2, insulin-like growth factor binding

49 rst spontaneous entry of hair follicles into catagen between TGF-beta1 null mice and age-matched wild

50 mal papilla cells of pelage follicles during catagen but not in anagen or telogen.

51 n to telogen involves an intermediate stage, catagen, consisting of a swift, apoptosis-driven involut

52 ed the potential involvement of TGF-beta1 in catagen control.

53 wth disorders based on premature or retarded catagen development (effluvium, alopecia, hirsutism).

54 thasone was demonstrated to induce premature catagen development accompanied by an abrupt termination

55 Catagen development accompanied by increased apoptosis i

56 into the back skin of mice induced premature catagen development.

57 ng spontaneous and pharmacologically induced catagen development.

58 activates premature but predominantly normal catagen development.

59 pontaneous catagen and dexamethasone-induced catagen display similar changes in the pigmentary unit.

60 During catagen, Eda A1 mRNA and Edar protein were expressed in

61 a neonatal short-hair phenotype due to early catagen entry compared with matched wild-type siblings.

62 the vascular changes as well as the delayed catagen exhibited by these mice.

63 During hair follicle regression (catagen), expression levels decrease until expression is

64 lso detected in the permanent portion of the catagen follicle.

65 ions, and that substance P treatment induces catagen follicles along with activated CD8+ T cells.

66 ls and fewer apoptotic cells than comparable catagen follicles from +/+ mice.

67 In comparison, catagen follicles had low levels of telomerase activity

68 Importantly, mutant catagen follicles undergo delayed regression and display

69 calization of apoptotic nuclei and TGFRII in catagen follicles.

70 gulated during anagen, then downregulated in catagen follicles.

71 Catagen hair follicles exhibited pigment incontinence in

72 -22 is not an effector of apoptosis in mouse catagen hair follicles.

73 papilla and lower epithelial strand of late-catagen hair follicles.

74 ression of the hair follicles from anagen to catagen (hair follicle maturation and regression), group

75 en suggests that secondary hair germ of late catagen HF is most likely repopulated by melanocytes ari

76 ot sheath or follicular papilla of early/mid-catagen HF.

77 During catagen, hr gene expression gradually declined in the re

78 rally abnormal hairs are easily dislodged in catagen implying a precocious exogen.

79 Ha1 expression is lost during catagen in all mice but recovers more slowly in the knoc

80 n regulating basic cellular processes during catagen, including club hair formation, maintenance of D

81 odel for general hair pigmentation research, catagen induced by cyclophosphamide offers an interestin

82 -express Lgr5, do not express Shh and escape catagen-induced apoptosis.

83 s among the elusive endogenous regulators of catagen induction in vivo, possibly via the inhibition o

84 lopecia, whereas a shift towards "dystrophic catagen" initially enhanced the hair loss, yet subsequen

85 en but was highly upregulated throughout the catagen involution phase.

86 How catagen is coordinated, and spares the progenitor cells

87 The onset of catagen is repressed by R-spondin2 injection, and the an

88 The functional role of osteopontin in catagen is unclear but it may promote the formation of a

89 The regression phase of the hair cycle (catagen) is an apoptosis-driven process accompanied by t

90 The hair follicles fail to regress during catagen leading to abnormally long follicles.

91 itro cultured HFs has been shown to induce a catagen-like process.

92 Although dexamethasone-induced catagen may provide a useful model for general hair pigm

93 llicular damage-response towards "dystrophic catagen" mitigates cyclophosphamide-induced alopecia, wh

94 regressive phase of the hair follicle cycle (catagen), occurred earlier than usual.

95 eceptors during late anagen and the onset of catagen of the hair cycle.

96 oblasts migrate out of the late anagen/early catagen papilla and re-enter the proximal connective tis

97 riven by the dystrophic anagen or dystrophic catagen pathway, play important parts in the degree of h

98 ed to result from a premature entry into the catagen phase of the hair cycle.

99 papilla cells, during the anagen but not the catagen phase.

100 ed a significant acceleration of spontaneous catagen progression.

101 transforming growth factor beta 2 (TGFbeta2; catagen promoter) was enhanced.

102 Neutralizing TGFbeta antagonized the catagen-promoting effects of P-cadherin silencing.

103 ced perifollicular angiogenesis, whereas the catagen regression phase is characterized by apoptosis-d

104 failure of hair follicles to enter a normal catagen regression phase, eventual follicular degradatio

105 ses: telogen (resting), anagen (growth), and catagen (regression).

106 s been proposed to play an important role in catagen regulation.

107 iven physiological hair follicle regression (catagen) remains to be elucidated.

108 rain and skin, which is believed to regulate catagen remodeling in the hair cycle.

109 undergo cyclic behavior through regression (catagen), rest (telogen), and regeneration (anagen) duri

110 ct both in the initiation and progression of catagen, resulting in a protracted first catagen, and la

111 n-specific genes (e.g., nexin 1), but also a catagen-specific gene.

112 differentiation, short hair shafts, aberrant catagen stage of the hair cycle, and eventual loss of th

113 le morphogenesis and late onset of the first catagen stage.

114 ng early and middle anagen and during middle catagen stages.

115 orders characterized by premature entry into catagen, such as androgenetic alopecia, alopecia areata,

116 eration in the follicular melanocytes during catagen suggests that secondary hair germ of late catage

117 follicular pigmentary unit during HF anagen-catagen-telogen transition and may be used for the estab

118 suggest that Gsdma3 has an important role in catagen-telogen transition by balancing the Wnt signalin

119 wever, whether there is a switch controlling catagen-telogen transition remains largely unknown.

120 age of the hair cycle, being switched-off in catagen to remain absent through telogen.

121 Here we show that hair follicles cycle from catagen to the next anagen without transitioning through

122 2B GFP mice led to significant hair follicle catagen transformation compared with controls.

123 As the anagen-to-catagen transformation of microdissected human scalp HFs

124 melanocytes were examined during the anagen-catagen transformation, comparing spontaneous and pharma

125 d in hair cycle control, i.e., the anagen-to-catagen transformation, was tested.

126 ir follicle cycling via entry into the first catagen transformation.

127 blast growth factor-5 regulate the anagen to catagen transition by independent pathways.

128 hat TNFalpha is required for a timely anagen-catagen transition in mouse pelage follicles, and that i

129 tor combination might regulate the anagen to catagen transition of the hair cycle.

130 es in anagen VI, decreased during the anagen-catagen transition phase.

131 ect promotion of apoptosis during the anagen-catagen transition.

132 ng was observed in this region at the anagen-catagen transition.

133 naling molecules that regulate the anagen to catagen transition.

134 During late catagen, TUNEL and Ki-67 negative melanocytes expressing

135 By contrast, cyclophosphamide-induced catagen was characterized by the initial retention of me

136 This cell loss, which continued during catagen, was not associated with intra-follicular papill

137 may be one of the triggers for the onset of catagen when the follicles are in anagen and the onset o

138 le, and in the bulge during anagen and early catagen, whereas Aldh1a3 expression was primarily in the

139 es in TGF-beta1 -/- mice were still in early catagen, whereas hair follicles of +/+ littermates had a

140 hed off during the transition from anagen to catagen, which implies a regulatory role for IGF-I durin

141 nce that specific genes are turned on during catagen, which is therefore not simply a passive "degene