ライフサイエンスコーパス: anagen

1 on of an exaggerated, aberrant growth phase (anagen).

2 and progression into the hair growth phase (anagen).

3 hinner hair follicles and shafts during late anagen.

4 pression patterns in the Cl during postnatal anagen.

5 trix cells were positive for PS2 during late anagen.

6 , pre-cortex, and hair shaft during mid-late anagen.

7 activation of beta-catenin produced a normal anagen.

8 tion or proliferation of matrix cells during anagen.

9 growth cycle, the largest peak is coupled to anagen.

10 n and reentry of telogen hair follicles into anagen.

11 , however, appeared to remain blocked in pro-anagen.

12 to terminate precursor cell division during anagen.

13 n differentiating hair cortical cells during anagen.

14 ls, suggesting that 5-FU killed the cells in anagen.

15 an increased proportion in the growth phase, anagen.

16 s highly expressed in late telogen and early anagen.

17 tors Bmp2, Dkk1, and Sfrp4 increase in early anagen.

18 in human anagen HFs significantly prolonged anagen.

19 ferent stages of the hair cycle, telogen and anagen.

20 uiescent phase (telogen) before returning to anagen.

21 Treatment of mice at 59 days of age (when in anagen 1) with topical 5-FU delayed hair regrowth by 10

22 Hairs irradiated in anagen and analyzed during the second cycle exhibited a

23 pression of miR-31 markedly increases during anagen and decreases during catagen and telogen.

24 ression was detected during early and middle anagen and during middle catagen stages.

25 s of the hair cycle, and in the bulge during anagen and early catagen, whereas Aldh1a3 expression was

26 panion layer of the outer root sheath during anagen and in the club hair sheath during catagen and te

27 hannel blockers act through Cav1.2 to induce anagen and overcome the TS phenotype.

28 P cells there was an increase in the size of anagen and telogen DP, but the proportion of tdTomato-la

29 in the epidermis and the epithelium of both anagen and telogen hair follicles.

30 e onset of catagen when the follicles are in anagen and the onset of anagen when the follicles are in

31 n of TGF-beta1 and its receptors during late anagen and the onset of catagen of the hair cycle.

32 licles cycle between stages of rapid growth (anagen) and metabolic quiescence (telogen) throughout li

33 ir follicles cycle between stages of growth (anagen) and metabolic quiescence (telogen) throughout li

34 periods of relative resting, active growth (anagen), and regression.

35 ases of active hair growth and pigmentation (anagen), apoptosis-driven regression (catagen) and relat

36 of fibrosis markers, increased induction of anagen around wounds, and HF regeneration in the wound c

37 es induced in the dermal papilla (DP) during anagen as a result of the interaction with epithelial ma

38 that epithelial Wnt ligands are required for anagen, as loss of Wls in the follicular epithelium resu

39 hifted it towards a mild form of "dystrophic anagen", associated with a significant reduction in apop

40 ly proliferating hair-producing cells of the anagen bulb (matrix cells), while these cells were stron

41 In anagen bulbs, kazrin was expressed by a band of cells wi

42 of label-retaining cells to define the human anagen bulge.

43 es Shh target genes and epithelial tumors at anagen but not other stages, pointing to a restricted co

44 e., the follicular papilla cells, during the anagen but not the catagen phase.

45 and dermal papilla cells during early to mid-anagen but was highly upregulated throughout the catagen

46 Existing hair follicles entered anagen, but no ectopic follicles formed.

47 t manner, as it can be detected in FP during anagen, but not in catagen and telogen phases of the hai

48 r resulted in a delay in the first postnatal anagen, but subsequent hair cycles were normal.

49 al stem cell maintenance, and stimulation of anagen by hair plucking caused follicular proliferation

50 ained in the follicle following induction of anagen by plucking of the hairs.

51 ir germs through 48 h following induction of anagen by plucking, but instead remained in their subseb

52 eintegration and activation, and only during anagen can the phenotype of hair graying and repigmentat

53 ollicle melanocytes were examined during the anagen-catagen transformation, comparing spontaneous and

54 find that TNFalpha is required for a timely anagen-catagen transition in mouse pelage follicles, and

55 st values in anagen VI, decreased during the anagen-catagen transition phase.

56 of perifollicular adipocytes declined during anagen-catagen transition, whereas fluorescence-lifetime

57 r indirect promotion of apoptosis during the anagen-catagen transition.

58 staining was observed in this region at the anagen-catagen transition.

59 of the follicular pigmentary unit during HF anagen-catagen-telogen transition and may be used for th

60 or Dicer during an established growth phase (anagen) caused failure of hair follicles to enter a norm

61 During anagen, cell proliferation in the germinative matrix of

62 This production was associated with anagen-dependent expression of the tyrosinase gene and e

63 embled neonatal dermis than adult telogen or anagen dermis.

64 postnatal hair cycle results in accelerated anagen development and altered stem cell activity in the

65 Furthermore, acceleration of wound-induced anagen development in Lhx2(+/-) mice is inhibited by adm

66 n contrast, BMP4 induces selective arrest of anagen development in the non-tylotrich (secondary) HF.

67 Anagen development is accompanied by down-regulation of

68 ses of the hair cycle results in accelerated anagen development, and altered differentiation of hair

69 populations gradually lost expression of the anagen DP signature gene, versican.

70 a shorter telogen and a premature entry into anagen during the second phase of hair cycling without a

71 (catagen), rest (telogen), and regeneration (anagen) during postnatal life.

72 ing that fibroblasts migrate out of the late anagen/early catagen papilla and re-enter the proximal c

73 onstrate that forced MSI2 expression retards anagen entry and consequently delays hair growth, wherea

74 specific deletion of Lgr4 results in delayed anagen entry during the physiological hair cycle and com

75 of EF epidermis was most similar to that of anagen epidermis, consistent with activation of beta-cat

76 r root sheath, hair fiber perforation of the anagen follicle base, and progressive follicular replace

77 g a prominent marker of sebaceous glands and anagen follicle bulbs.

78 receptor mice displayed the same pattern of anagen follicle formation as the wild-type mice.

79 that diffusible factors associated with the anagen follicle influence cell proliferation in the epid

80 a critical role of TSP-1 in the induction of anagen follicle involution, with potential implications

81 hin the dermal papilla regulates the telogen-anagen follicle transition and suggest that diffusible f

82 kely to contribute to the formation of a new anagen follicle.

83 Anagen follicles in mutants exhibit decreased proliferat

84 In anagen follicles, high levels of telomerase activity wer

85 sebaceous gland hypoplasia, abnormally long anagen follicles, retained inner root sheath, hair fiber

86 he existence of quiescent noncycling KSCs in anagen follicles.

87 above telogen follicles to 7.0% above early anagen follicles.

88 of all developing HFs and also by postnatal anagen follicles.

89 of the infundibulum; the companion layer in anagen follicles; and the single layer of outer root she

90 a single defined source; and possess a long anagen growth phase, we initiated a study of them in cul

91 rved in the outer root sheath throughout the anagen growth phase.

92 ed in telogen rather than transitioning into anagen growth, confirmed by retention of bromodeoxyuridi

93 growth cycle in 3 phases: telogen (resting), anagen (growth), and catagen (regression).

94 regenerate the HF during cyclical rounds of anagen (growth), catagen (regression), and telogen (quie

95 e RASopathy, Noonan-like syndrome with loose anagen hair (NS/LAH).

96 e responsible for Noonan Syndrome with Loose anagen Hair (NSLH).

97 the subsequent hair cycle, i.e., after a new anagen hair bulb has been constructed, which points to t

98 rmatitis, and the proliferative cells of the anagen hair bulb.

99 melanogenically-active melanocytes from the anagen hair bulbs of affected human scalp remains unclea

100 idermis and, for the cyclic formation of new anagen hair bulbs.

101 layer of the inner root sheath of the lower anagen hair follicle and weak staining of the telogen fo

102 Mutated (ATM) protein within melanocytes in anagen hair follicle bulbs.

103 Shh target genes normally occurs only in the anagen hair follicle in response to expression of Shh.

104 /SPRR1 is localized to specific areas of the anagen hair follicle with weak staining in the telogen f

105 haracterized by a marked increase in size of anagen hair follicles (HFs) and by the replacement of zi

106 er, these models are based on the culture of anagen hair follicles and have only partially been used

107 the mobilization of stem cells to regenerate anagen hair follicles in AA and intraepidermal melanocyt

108 the effects of TGF-beta1 injection on murine anagen hair follicles in vivo.

109 ntary unit during the cyclical involution of anagen hair follicles is unknown.

110 CD31 staining revealed that the late anagen hair follicles of the KrP mice were surrounded by

111 Dsg1 compensates for the loss of Dsg3 in the anagen hair follicles of these Dsg3-/- mice.

112 ession profiles revealed that in contrast to anagen hair follicles of wild-type mice, tumors of trans

113 marked proliferation of the root sheaths of anagen hair follicles, limited to the region within the

114 dian clock activity specific to regenerating anagen hair follicles, namely epithelial matrix and mese

115 Such observations indicate that, in anagen hair follicles, the fragments containing cells ac

116 s and Xenopus, being confined to the bulb of anagen hair follicles, the infundibulum, and parakeratot

117 In developing and mature anagen hair follicles, whn is expressed at high levels i

118 pilla, and connective tissue sheath of human anagen hair follicles.

119 nst melanogenesis-associated proteins in the anagen hair follicles.

120 a (AA) is an autoimmune disease that attacks anagen hair follicles.

121 t deprives both MeSCs and melanocytes of the anagen hair matrix of proinflammatory signals required f

122 s basal pigmentation in the epidermis and in anagen hair shafts.

123 sg1 and Dsg3 in this layer, in anchoring the anagen hair to the follicle.

124 +/+ or Dsg3+/- mice, showed striking loss of anagen hair, which was confirmed and quantitated by gent

125 d remained in the follicle after loss of the anagen hair.

126 known as the Noonan-like syndrome with loose anagen hair.

127 mmune disease that targets actively growing (anagen) hair follicles in humans and other mammals.

128 mmune disease that targets actively growing (anagen) hair follicles in humans, mice, rats, dogs, hors

129 ry cell infiltrates around actively growing (anagen) hair follicles.

130 mechanism for the inflammation that targets anagen hairs in alopecia areata.

131 ut) mice lose hair during telogen, but their anagen hairs remain anchored to the follicle.

132 by a reduced number of anagen HFs, decreased anagen HF proliferation, hair pigmentary changes, and de

133 cells, rather than quiescent bulge SCs, for anagen HF repair can be a potential approach to prevent

134 Wnt target Lef1, known to be required for HF anagen/HF-activation and regeneration.

135 knockout mice also show an increased size of anagen HFs associated with increased cell proliferation

136 cell proliferation and controls the size of anagen HFs by modulating the expression of cell-cycle-as

137 Anagen HFs have high demands for energy and biosynthesis

138 Markedly enlarged anagen HFs of TG mice show increased proliferation in th

139 nockdown of either BMAL1 or Period1 in human anagen HFs significantly prolonged anagen.

140 strophy as determined by a reduced number of anagen HFs, decreased anagen HF proliferation, hair pigm

141 econdary hair germ of late telogen and early anagen HFs, suggesting a potential role for NF-kappaB in

142 r matrix and outer and inner root sheaths of anagen HFs.

143 lated CD133 + and CD133- DP cells from mouse anagen HFs.

144 StEpiDelta/StEpiDelta) mice presented solely anagen HFs.

145 eath (IRS) markers, with expression onset at anagen IIIa above the new hair bulb and subsequent sprea

146 curring in the Cl, mK6a expression begins at anagen IIIb in differentiating cells located proximal to

147 of Shh target gene transcription only during anagen in follicular and interfollicular keratinocytes.

148 tivation improved hair regrowth by promoting anagen in hair follicles and accelerated regrowth of car

149 More hair follicles were in anagen in mice fed high vitamin A.

150 were in anagen VI, whereas none (0%) were in anagen in the control group.

151 ostnatal skin would accelerate initiation of anagen in the hair follicle cycle, with concomitant acce

152 onic development of hair follicles, and that anagen in the postnatal cycling follicle has morphologic

153 human HF cycling and manipulate long-lasting anagen in vivo.

154 Genes induced in the DP during anagen included modulators of genes expressed additional

155 decreased Wnt/beta-catenin signaling during anagen induction compared with control hair follicles.

156 uired for Wnt/beta-catenin activation during anagen induction is unknown.

157 kinase 2 ablation causes alterations during anagen induction, giving rise to abnormal cyst-like stru

158 in HF stem/progenitor cell activation during anagen induction.

159 Loss of Fgf18 signaling markedly accelerates anagen initiation, whereas loss of Tgf-beta2 signaling s

160 nocytes demonstrated a defective response to anagen initiation.

161 lopecia--the last a consequence of defective anagen initiation.

162 In animals exposed during anagen, intermediate fluences induced nonscarring alopec

163 ely regulated cycles of active regeneration (anagen), involution (catagen), and relative quiescence (

164 follicles, transition from telogen back into anagen involves the activation, proliferation, and diffe

165 y accelerated entry into catagen and through anagen, irregular hair follicle orientation, and increas

166 ronments are created as the HF cycles: early anagen is the most conducive phase for melanocytic reint

167 e show that Wnt signaling is elevated during anagen, is reduced at the onset of catagen, and can be r

168 ting the apoptotic death of ORS cells during anagen leads to a more rapid termination of progenitor c

169 tro, and shows that P-cadherin is needed for anagen maintenance by regulating canonical Wnt signaling

170 om the middle back region of the spontaneous anagen mice that received PTH (7-34) revealed that 19 +/

171 Similarly, in induced anagen mice treated with PTH (7-34), 22.3 +/- 1.4 (mean

172 At mid-anagen, NF-kappaB activity was observed in the inner roo

173 The onset of anagen of the first postnatal hair follicle cycle was al

174 llicle development and for the growth phase (anagen) of postnatal follicles.

175 d each other's effects on the growing phase (anagen) of scalp follicles cultured in media with and wi

176 w premature termination of the growth phase (anagen) of the hair cycle, an event that is regulated in

177 lar vascularization during the growth phase (anagen) of the hair cycle, followed by regression of ang

178 ninER expressing hair follicles also entered anagen on 4OHT treatment.

179 we demonstrate its direct role in promoting anagen onset and HFSC proliferation.

180 Wnt and Endothelin niche signals during hair anagen onset are hijacked to promote McSC malignant tran

181 terozygous Lhx2 knockout (+/-) mice, whereas anagen onset in the HFs located closely to the wound is

182 naling in the dermal papilla is required for anagen onset in the murine hair cycle.

183 tenuated HFs and epithelial proliferation at anagen onset; in their absence, Demodex colonization led

184 py through two distinct pathways (dystrophic anagen or catagen) and why this makes RIA management so

185 ycle abnormalities, driven by the dystrophic anagen or dystrophic catagen pathway, play important par

186 During early anagen or growth phase of the hair follicle, nestin-expr

187 f pelage follicles during catagen but not in anagen or telogen.

188 -expressing lower outer root sheath cells in anagen, our studies indicate an alternative origin, and

189 he suprabasal cells of the telogen bulge and anagen outer root sheath (ORS).

190 n in the field is whether the bulb region of anagen pelage follicles contains multipotential progenit

191 at triggers their growth, proliferation, and anagen phase expansion.

192 issected human hair follicle segments during anagen phase in ex vivo culture.

193 gnificant acceleration of healing during the anagen phase of HF cycling in vivo, associated with alte

194 rement for the vitamin D receptor during the anagen phase of the first (developmental) hair cycle, bu

195 und healing and those upregulated during the anagen phase of the hair cycle in unwounded skin.

196 heath and medulla of the follicle during the anagen phase of the hair growth cycle.

197 s repressed by R-spondin2 injection, and the anagen phase persists.

198 y expressed in the hair shaft cuticle during anagen phase, and its expression is decreased in Alopeci

199 ing the hair cycle, Msx2 deficiency shortens anagen phase, but prolongs catagen and telogen.

200 ches were characterized by hair follicles in anagen phase, implicating keratinocytes in the aberrant

201 ehog monoclonal antibody during the growing (anagen) phase of the hair cycle.

202 hair follicle, and for inciting the growth (anagen) phase of the hair cycle.

203 During its growth (anagen) phase, the proximal-distal axis of the mouse coa

204 ation that resides in the lower hair bulb of anagen-phase follicles and expresses Hopx.

205 Wnts, but not Sonic hedgehog (Shh), maintain anagen-phase gene expression in vitro and hair inductive

206 d/or thickness of hairs and/or the number of anagen-phase hair follicles after minoxidil or acyclovir

207 tivation/regeneration results in accelerated anagen progress, whereas treatment of wounds with sitagl

208 erin silencing reduced the expression of the anagen-promoting growth factor, IGF-1, whereas that of t

209 hair follicle stem cells and contributes to anagen re-entry but does so in a calcium flux-independen

210 sed hair density, altered hair types, faster anagen re-entry, and formation of compound vibrissa foll

211 , and spares the progenitor cells needed for anagen re-entry, is poorly understood.

212 hair follicles may affect each other during anagen re-entry, thus forming propagating regenerative h

213 t were either spontaneously in or induced to anagen received either PTH (7-34) or placebo.

214 s further, and the probability of successful anagen reentry decreases, leading to progressive alopeci

215 ollicle generation and regeneration, telogen-anagen reentry, and extra-follicular macro-environmental

216 progressing through stages of rapid growth (anagen), regression (catagen), and relative "quiescence"

217 deled mini organ that cycles between growth (anagen), regression (catagen), and relative quiescence (

218 lly recognized to comprise phases of growth (anagen), regression (catagen), and rest (telogen).

219 evels in VDR(-/-) keratinocytes and restored anagen responsiveness in vivo in VDR(-/-) mice, resultin

220 ar adipocytes affect the physiology of human anagen scalp HFs.

221 rization (terminal-to-vellus conversion) and anagen shortening.

222 cles with a Gsdma3 mutation enter the second anagen simultaneously as WT mice.

223 blasts from neonatal skin, adult telogen and anagen skin and adult skin in which ectopic hair follicl

224 The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former domina

225 Mouse anagen skin fragments, maintained in histoculture, were

226 his issue, Ansell et al. show that wounds on anagen skin heal faster than those on telogen skin, sugg

227 s can lead to the identification of not only anagen-specific genes (e.g., nexin 1), but also a catage

228 roxylase activities during the telogen/early anagen stage (days 0-1).

229 Actively growing and pigmented anagen stage hair follicles were sensitive to hair remov

230 tive mesenchymal expression during postnatal anagen stage hair-follicle cycling.

231 logen hair follicles into the hair-producing anagen stage in mature skin remain incompletely understo

232 FM is stringently coupled to the anagen stage of the hair cycle, being switched-off in ca

233 by histology that these follicles are in the anagen stage of their first hair growth cycle.

234 on from the resting (telogen) to the growth (anagen) stage of the hair cycle in adult mouse skin.

235 essed in the upper matrix and medulla of the anagen-stage hair.

236 telogen hair follicles into a proliferative (anagen) state, whereas 100% of the hair follicles in the

237 generalized follicular hamartoma, and loose anagen syndrome, may be associated with developmental de

238 resting phase of the hair follicle cycle) to anagen (the active phase), thereby facilitating robust h

239 od) and remained continuously in an abnormal anagen (the growth phase of the hair cycle).

240 However, in mid- and late anagen, the GFP-expressing cells are located in the uppe

241 During telogen or resting phase and in early anagen, the GFP-positive cells are mainly in the bulge a

242 orrelated with a decrease in the duration of anagen, the growth phase of the hair cycle.

243 tein-alpha and -beta were upregulated during anagen, then downregulated in catagen follicles.

244 telogen, significantly upregulated in early anagen, then gradually declined, and reappeared again in

245 the hair follicles to exit telogen and enter anagen, thereby initiating hair growth.

246 d the progression of the hair follicles from anagen to catagen (hair follicle maturation and regressi

247 and fibroblast growth factor-5 regulate the anagen to catagen transition by independent pathways.

248 gand receptor combination might regulate the anagen to catagen transition of the hair cycle.

249 other signaling molecules that regulate the anagen to catagen transition.

250 o be switched off during the transition from anagen to catagen, which implies a regulatory role for I

251 Furthermore, anagen to catagen/telogen ratios were lower in individua

252 in grafts of null skin did not progress from anagen to telogen and scanning electron micrografts reve

253 Transition from anagen to telogen involves an intermediate stage, catage

254 The transition from anagen to telogen is marked by downregulation of hair co

255 repetitively progresses from a growth phase (anagen) to a rapid apoptosis-driven involution (catagen)

256 As the anagen-to-catagen transformation of microdissected human

257 is involved in hair cycle control, i.e., the anagen-to-catagen transformation, was tested.

258 NF-kappaB participates in telogen-anagen transition in awl and zigzag HFs, and is required

259 JAK-inhibition is able to induce telogen-to-anagen transition in wild-type mice.

260 ecome increasingly clear that the telogen-to-anagen transition is controlled jointly by at least the

261 as a crucial proximal signal for the telogen-anagen transition.

262 te of HFSCs in the process of the telogen-to-anagen transition.

263 During mid-anagen, two types of deleted in colon carcinoma staining

264 cells were created by Atoh1 induction during anagen versus telogen and following disruption of Notch

265 ultured, human scalp hair follicles (HFs) in anagen VI can be exploited for dissecting and manipulati

266 1.4 (mean +/- SEM) of the follicles were in anagen VI compared to only 1.3 +/- 0.7% in the control m

267 topical application of dexamethasone during anagen VI decreased the concentration of POMC, MC1-R, an

268 lable-transcriptomic atlas of distinct human anagen VI HF compartments, which can be utilized to deve

269 lorimetric quantitative assay showing ORS of anagen VI HFs contained high levels of glycogen that dec

270 and single-cell RNA-sequencing data on human anagen VI HFs or selected cell populations showed that w

271 profiles of 8 selected compartments of human anagen VI HFs.

272 atin 15+ (K15), CD200+ or CD34+ cells within anagen VI hHFs by immunohistomorphometry, using Ki-67 an

273 umber and total papilla size were maximal by anagen VI, but intriguingly, decreased by 25% during thi

274 h, and, after reaching the highest values in anagen VI, decreased during the anagen-catagen transitio

275 - 4% (mean +/- SEM) of the follicles were in anagen VI, whereas none (0%) were in anagen in the contr

276 dShh, but not in controls, acceleration into anagen was evident, since hair follicle size and melanog

277 When anagen was induced by hair depilation at day 20 after bi

278 p of follicles put into culture when in late anagen were attempting to cycle in vitro.

279 the follicles are in anagen and the onset of anagen when the follicles are in telogen.

280 The second peak was observed at mid-anagen, when melanogenesis takes place.

281 a dominant-negative manner to markedly delay anagen, while L-type channel blockers act through Cav1.2

282 that induces resting hair follicles to enter anagen with consequent hair growth.

283 Hair follicles cannot enter the second anagen with ectopic WT Gsdma3 overexpression.

284 air follicles cycle from catagen to the next anagen without transitioning through a morphologically t