ライフサイエンスコーパス: hair follicle

1 aling in the various stem cell niches of the hair follicle.

2 tem/early progenitor cell compartment of the hair follicle.

3 ow that FGF5 induces regression of the human hair follicle.

4 trated on the caudal (downward) side of each hair follicle.

5 e nucleus and cytoplasm in the epidermis and hair follicle.

6 ity and that Shh is its direct target in the hair follicle.

7 re the main site of androgen activity in the hair follicle.

8 oupled receptor 5-positive stem cells in the hair follicle.

9 ermis to reach the epidermis of the skin and hair follicles.

10 n in peripheral nerve endings of cutaneous D-hair follicles.

11 ells, and defective postnatal development of hair follicles.

12 iquely accessible human (mini-) organ: scalp hair follicles.

13 lusters with antigen presenting cells around hair follicles.

14 s the relative numbers of eccrine glands and hair follicles.

15 cells [hEPI-NCSC(s)] present in the bulge of hair follicles.

16 eta-catenin/Wnt signaling pathways in murine hair follicles.

17 expected heterogeneity among SCs and TACs of hair follicles.

18 nhancer that drives expression in developing hair follicles.

19 y reduced scar formation and regeneration of hair follicles.

20 nds in mice lead to de novo morphogenesis of hair follicles.

21 nature as EpSCs directly isolated from human hair follicles.

22 d by factors both intrinsic and extrinsic to hair follicles.

23 cells near F4/80(+) mouse macrophages around hair follicles.

24 tial endings wrapping the base of individual hair follicles.

25 he effects of chemotherapeutic agents on the hair follicle, a number of experimental models have been

26 ing cells, we found that SHH does not act on hair follicles, adipocytes, endothelial cells, and hemat

27 Microarray and qRT-PCR analysis of human hair follicles after Nrf2 activation using sulforaphane

28 Regeneration of skin and hair follicles after wounding--a process known as wound-

29 protecting human organ function (i.e., scalp hair follicles) against redox insult.

30 G2D(+)CD8(+) T cells actively infiltrate the hair follicle and are responsible for its destruction in

31 wly identified and reciprocal determinant of hair follicle and eccrine gland density and identify a p

32 econstitute the epithelial components of the hair follicle and interfollicular epidermis.

33 ent to which frizzled 3 (Fz3) can rescue the hair follicle and Merkel cell polarity defects in frizzl

34 n precursors and mature melanocytes from the hair follicle and the epidermis of untreated and narrow

35 in modulation of melanocyte functions in the hair follicle and the epidermis with attendant effects o

36 body skin ectopic K8+ cells were confined to hair follicles and absent from interfollicular regions.

37 ows predominantly in lipid-rich areas around hair follicles and associated skin folds.

38 aging causes the stepwise miniaturization of hair follicles and eventual hair loss in wild-type mice

39 mation of cutaneous accessory organs such as hair follicles and mammary glands has proved elusive, a

40 nd light sheet microscopy in cultured bovine hair follicles and plucked human hairs.

41 racteristic has been used to identify SCs in hair follicles and sweat glands; however, whether a quie

42 d by reduced or absent eccrine sweat glands, hair follicles and teeth, and defective formation of sal

43 ing the early development of mouse teeth and hair follicles and the evaluation of the likely effects

44 man skin, mTregs preferentially localized to hair follicles and were more abundant in skin with high

45 ts the complexity of interactions within the hair follicle, and encourages further discussion on the

46 aling is required for the development of the hair follicle, and for inciting the growth (anagen) phas

47 normal rapidly proliferating organs, such as hair follicles, and causes massive apoptosis in hair mat

48 and pharmacodynamics were measured in blood, hair follicles, and circulating tumor cells.

49 dermally derived structures including teeth, hair follicles, and cutaneous glands.

50 Ectodermal organs such as teeth, hair follicles, and mammary glands begin their developme

51 progenitors that give rise to the epidermis, hair follicles, and Merkel cells.

52 ngs and are localized in fingertips, whisker hair follicles, and other touch-sensitive spots.

53 er in the stomach and intestinal epithelium, hair follicles, and ovarian surface epithelium.

54 yo to specific locations within the skin and hair follicles, and to other sites in the body.

55 Hair follicle apoptosis induced by DXR was significantly

56 Hence, hair follicles are a widely studied model for stem cell

57 Hair follicles are mammalian skin organs that periodical

58 g that Adelta-LTMR lanceolate endings around hair follicles are polarized; they are concentrated on t

59 Stem cells located at the bulges of the hair follicles are responsible for hair cycling and cont

60 Conversely, hair follicles are specified when mesenchymal BMP signal

61 We found that TSC processes at hair follicles are tiled and that individual TSCs host a

62 Hair follicles are unique structures in the skin that co

63 We used the hair follicle as a model to link changes in the keratin

64 Using the hair follicle as a model, Hsu at al. demonstrate that th

65 Using hair follicle as a model, we map the global chromatin do

66 s high level of micro-injuries and a lack of hair follicles as a back-up source of SCs.

67 at leads to cell disruption, can be found in hair follicle-associated sebaceous glands (SGs) or in fr

68 cells remained in deep regions of body skin hair follicles at 3 months post-induction.

69 to regulate the developmental progression of hair follicles beyond the germ stage.

70 ntal role for T-box genes and new aspects of hair follicle biology and pigmentation.

71 hair follicle, improved characterization of hair follicle biology, and methods development in precis

72 Epithelial stem cells (EpSCs) in the hair follicle bulge are required for hair follicle growt

73 we verify that Tcf3-expressing cells in the hair follicle bulge are self-renewing stem cells with mu

74 equent whole transcriptome RNA sequencing of hair follicle bulge melanocyte precursors and compared t

75 up-regulation of TNC, GJB6, and THBS1 in the hair follicle bulge melanocytes and of TYR in the epider

76 transcription factor expressed primarily in hair follicle bulge stem cells in mice.

77 ed an initial expansion and later decline of hair follicle bulge stem cells, accompanied by an enrich

78 is repopulated by melanocyte precursors from hair follicle bulge that proliferate, migrate, and diffe

79 erm was present in the untreated and treated hair follicle bulge, whereas a possible secondary melano

80 The hair follicle bulge, which contains melanocyte stem cell

81 oimmune disease resulting from damage of the hair follicle by T cells.

82 e stem cells (McSCs) located in the bulge of hair follicles can regenerate mature melanocytes for hai

83 Hair follicles cannot enter the second anagen with ectop

84 kin from K14-H2B GFP mice led to significant hair follicle catagen transformation compared with contr

85 wn (small interfering RNA) in cultured human hair follicles confirmed the regulation of key Nrf2 targ

86 llicle response to chemotherapy, human scalp hair follicles cultured ex vivo were treated with doxoru

87 Here we show that hair follicles cycle from catagen to the next anagen wit

88 role during epidermal ontogenesis and normal hair follicle cycling and that its absence may aggravate

89 r 1,25-dihydroxyvitamin D3 and/or calcium in hair follicle cycling is not clear despite their impact

90 btype, which leads to fibrosis and disrupted hair follicle cycling.

91 KS-TG mice had reduced cutaneous hair-follicle density, microvascular density, and pannic

92 dependent function of activated prostasin in hair follicles, dependent on zymogen conversion by matri

93 These findings implicate hair follicle-derived cytokines as regulators of maligna

94 ell localization depended on the presence of hair follicle-derived IL-7.

95 ombination of L1 and a feeder layer of human hair follicle-derived mesenchymal stem cells (hHF-MSCs).

96 We performed in vivo fate mapping of adult hair follicle dermal sheath (DS) cells to determine thei

97 Ablating these hair follicle dermal stem cells and their progeny retard

98 h factor production that in turn facilitates hair follicle development and cycling.

99 ch lead to hyperthickened epidermis, ectopic hair follicle development and increased skin tumor susce

100 udies suggest that the major events of human hair follicle development are similar to those in mice,

101 Early hair follicle development is characterised by the rapid

102 s of Lgr5+follicular epithelium and impaired hair follicle development were only observed in Lgr4/5dK

103 Scharschmidt et al. (2017) show that during hair follicle development, commensals induce regulatory

104 inoma and Ptch1;Ptch2 loss disrupts skin and hair follicle development.

105 Hedgehog signaling gradient that may specify hair follicle development.

106 ctopic Merkel cells, and defective postnatal hair follicle development.

107 but appears to be dispensable for embryonic hair follicle development.

108 the interfollicular epidermis and for normal hair follicle development.

109 tion of follicular keratinocytes, leading to hair follicle developmental defects.

110 istal-less 3 (Dlx3), a critical regulator of hair follicle differentiation and cycling, was decreased

111 comorbid acne inversa (AI), an inflammatory hair follicle disorder, and had a history of nicotine ab

112 ing in peripheral blood lymphocyte (PBL) and hair follicle DNA from two Caucasian adults.

113 mal adipose layer expands concomitantly with hair follicle downgrowth, providing a paradigm for study

114 thelial stem cell (eSC) niche of human scalp hair follicles, during the inflammatory permanent alopec

115 ickened interfollicular epidermis, alopecia, hair follicle dystrophy, claw dystrophy, and abnormal pi

116 sor protein p53 upon the cell cycle entry of hair follicle early progenitor cells and in cultured ker

117 he stem cell compartment and induces ectopic hair follicles (EFs).

118 cell-neurite complexes, and circumferential hair follicle endings.

119 FGF22, a hair follicle-enriched gene, exhibited pseudogenization,

120 Moreover, ablation of BDNF in hair follicle epithelial cells disrupts polarization of

121 The dystrophic hair follicle epithelium is stratified and is positive f

122 in immunity, reside predominantly within the hair follicle epithelium of the unperturbed epidermis.

123 ressing and partially reversing EMT in human hair follicles eSCs ex vivo, including in lichen planopi

124 that this enzyme is highly expressed in the hair follicle, especially the inner root sheath, and tha

125 gnature even in lesional lichen planopilaris hair follicles ex vivo.

126 Hair follicle expression of IL-15 was required for CD8(+

127 le, in contrast, TSCs remain associated with hair follicles following skin denervation in adult mice

128 epigmented by melanocyte precursors from the hair follicles, following stimulation with UV light.

129 ure increase in adipocytes in the absence of hair follicle formation, demonstrating that Wnt activati

130 ypes in embryonic mouse skin at the onset of hair follicle formation.

131 tegrin-linked kinase (ILK), are critical for hair follicle formation.

132 homeostasis, stem cells of the epidermis and hair follicle fuel their respective tissues.

133 nchiolar epithelial cells, the epidermis and hair follicles, gall bladder epithelium, choroid plexus,

134 . demonstrate that (i) the response of human hair follicles grafted onto immunodeficient mice to cycl

135 in the hair follicle bulge are required for hair follicle growth and cycling.

136 It has long been recognized that the hair follicle growth cycle and oscillation in the thickn

137 epair and stress response in general and for hair follicle growth in particular.

138 ological inhibition of Wnt production delays hair follicle growth.

139 es during a high-fat diet and in skin during hair follicle growth.

140 -TACs abrogates both dermal adipogenesis and hair follicle growth.

141 ate complexes associated with three types of hair follicles, guard, awl/auchene and zigzag, serve as

142 The hair follicle has become the main model to understand th

143 ve oxygen species (ROS) in the regulation of hair follicle (HF) cycle and skin homeostasis is poorly

144 hat miR-214 regulates skin morphogenesis and hair follicle (HF) cycling by targeting beta-catenin, a

145 Tfam(EKO) mice showed significantly reduced hair follicle (HF) density and morphogenesis, fewer intr

146 Here we show that hair follicle (HF) development facilitates the accumulat

147 on factor NF-kappaB controls key features of hair follicle (HF) development, but the role of NF-kappa

148 The hair follicle (HF) is a continuously remodeled mini orga

149 tous latent skin infection within long-lived hair follicle (HF) keratinocyte stem cells.

150 eous glands (SGs) to differentiate along the hair follicle (HF) lineages.

151 Hair follicle (HF) morphogenesis and cycling are a resul

152 lly regulated in dermal papilla cells during hair follicle (HF) morphogenesis and the postnatal hair

153 Right after birth, hair follicle (HF) morphogenesis was transiently delayed

154 Here, we co-isolate embryonic hair follicle (HF) placode and dermal condensate cells,

155 factor-kappa B (NF-kappaB) activity, primary hair follicle (HF) pre-placode formation is initiated wi

156 Here, we define genetic changes altered in hair follicle (HF) SCs in mice treated with a potent SC

157 FE) are generally well differentiated, while hair follicle (HF) stem cell-derived SCCs frequently exh

158 clic on-off switching of pigmentation in the hair follicle (HF).

159 ibroblasts in the dermal papilla (DP) of the hair follicle (HF).

160 In growing hair follicles (HF), quiescent stem cells (SC) are maint

161 nd thyrotropin (TSH), are expressed in human hair follicles (HFs) and regulate mitochondrial function

162 Here, using hair follicles (HFs) as a paradigm, we show that emergin

163 New hair follicles (HFs) do not form in adult mammalian skin

164 The immune privilege (IP) of hair follicles (HFs) has been well established in previo

165 in 2), also known as BCL11B, is expressed in hair follicles (HFs) of embryonic and adult skin.

166 l adipose tissue plays an essential role for hair follicles (HFs) regeneration by regulating hair cyc

167 Hair follicles (HFs) undergo cyclical periods of growth,

168 Hair follicles (HFs) undergo lifelong cyclical transform

169 Hair follicles (HFs) undergo precisely regulated cycles

170 ations in hairless gene manifest rudimentary hair follicles (HFs), epidermal cysts, hairless phenotyp

171 s (Tregs) in skin preferentially localize to hair follicles (HFs), which house a major subset of skin

172 Human scalp hair follicles (hHF) harbour several epithelial stem (eH

173 pressed in skin MCs are involved in skin and hair follicle homeostasis.

174 cing in patients with diseases affecting the hair follicle, improved characterization of hair follicl

175 lleles in DNA extracted from lymphocytes and hair follicles in infants postnatally.

176 is suppressed in the dermal endothelium and hair follicles in KS-TG mice.

177 By studying regeneration of hair follicles in response to patterned hair plucking, w

178 Human iMels generate pigmented epidermis and hair follicles in skin reconstitution assays in vivo.

179 n treated with BMP or when placed with human hair follicles in vitro.

180 ells on the caudal, but not rostral, side of hair follicles, in close proximity to Adelta-LTMR lanceo

181 In contrast, we found that hair follicle induction and polarization and the develop

182 ce and migration but also secretion of known hair follicle inhibitory factors.

183 Mice deficient for Sun2 exhibited irregular hair follicle intercellular adhesions, defective follicl

184 e find that mesenchymal cell condensation at hair follicles is locally directed by an epidermal prepa

185 lular domain activity operating in the first hair follicles is responsible for a delay in follicular

186 ting that Wnt activation, rather than mature hair follicles, is required for adipocyte generation.

187 of the terminal differentiation programs in hair follicle keratinocytes.

188 ss the origin of repeating patterns, such as hair follicles, limb digits, and intestinal villi, durin

189 ITGA6(+) cells are capable of generating all hair follicle lineages including the hair shaft, and the

190 tological studies showed markedly dystrophic hair follicles, loss of hair shafts with increased apopt

191 Wound healing, angiogenesis, and hair follicle maintenance are often impaired in the skin

192 Ectodermal organs, which include teeth, hair follicles, mammary ducts, and glands such as sweat,

193 rm diverse ectodermal organs, such as teeth, hair follicles, mammary glands, and salivary glands.

194 ce were characterized by the presence of the hair follicle marker Sox 9, keratins 10 and 14, and norm

195 We show that in the absence of ILK, the hair follicle matrix lineage fails to develop, likely du

196 alps in fostering vascularization around the hair follicle may contribute to the development of AGA.

197 tion is narrow-band UVB (NBUVB), but how the hair follicle melanocyte precursors are activated by UV

198 which in turn determines the distribution of hair follicle melanocytes.

199 tifies a bipotent stem cell within the adult hair follicle mesenchyme and has important implications

200 l epidermal differentiation, thereby causing hair follicle miniaturization.

201 suggests that CtBP1 has a pathogenic role in hair follicle morphogenesis and differentiation.

202 ractions are also required in adult mice for hair follicle morphogenesis and spindle orientation with

203 Disrupting ciliogenesis results in hair follicle morphogenesis defects due to attenuated Hh

204 ression of the Gorab gene in mice results in hair follicle morphogenesis defects that were characteri

205 PGRIP1L, a ciliopathy gene, is essential for hair follicle morphogenesis likely through regulating pr

206 Hair follicle morphogenesis of Ift27-null mice was sever

207 Hair follicle morphogenesis requires coordination of mul

208 Hair follicle morphogenesis requires precisely controlle

209 lly and functionally dependent manner during hair follicle morphogenesis.

210 We found that RPGRIP1L is essential for hair follicle morphogenesis.

211 f CD133 stem cells in enhanced capillary and hair follicle neogenesis, contributing to more rapid and

212 showed reduced basal cell proliferation and hair follicle numbers in the developing skin, as well as

213 s, which also showed lower expression in the hair follicle of AA patients.

214 nd to be expressed in both the epidermis and hair follicle of normal skin, but its expression was dra

215 CRABP2 and FABP5 were expressed in hair follicles of lid skin in both groups, whereas the C

216 c mites of the genus Demodex live within the hair follicles of mammals and are ubiquitous symbionts o

217 dant in fingertips, touch domes, and whisker hair follicles of mammals.

218 . report that transplantation of human scalp hair follicles onto chemotherapy-treated immunodeficient

219 ipulate specific cellular populations of the hair follicle or microenvironment to test their regenera

220 erexpression of the BMP antagonist Noggin in hair follicles or deletion of the BMP receptor in myofib

221 Using hair follicle organ cultures, we show that FGF5 induces

222 cesses - including axon growth and guidance, hair follicle orientation, and stereociliary bundle orie

223 tle is known about the energetics of growing hair follicles, particularly in the mitochondrially abun

224 d mesenchymal self-organisation processes in hair follicle patterning, identifying a network of fibro

225 This hair follicle phenotype was associated with markedly sup

226 lia makes it impossible to determine whether hair follicle phenotypes in these cilia mutants are caus

227 mutant cells, and Ift25-null mice displayed hair follicle phenotypes similar to those of Ift27 mutan

228 In mice, hair follicle placode "budding" is initiated by invagina

229 nctions in Wnt signaling, a prerequisite for hair follicle placode induction.

230 hereby CD133 promotes morphogenesis in early hair follicle placodes through the localized removal of

231 ng central nervous system development and in hair follicle polarity during skin development.

232 e-cell level and at the macroscopic level of hair follicle populations.

233 The regenerated hair follicles possess a KRT15(+) stem cell population a

234 ectodermal organ morphogenesis and disrupted hair follicle regeneration and homeostasis, as well as i

235 he transcription factor Gata6 in adult mouse hair follicle regeneration where it controls the renewal

236 hat developmental programs utilized for skin hair follicle regeneration, such as Wnt, are hijacked to

237 wnstream effectors IL-6 and STAT3 to promote hair follicle regeneration.

238 activate epithelial progenitors and initiate hair follicle regeneration.

239 led as one such negative regulator of WNT in hair follicle regeneration.

240 l keratinocytes with increased expression of hair follicle-related molecules (keratin 25, trichohyali

241 To define the molecular signature of hair follicle response to chemotherapy, human scalp hair

242 data demonstrate that the early phase of the hair follicle response to DXR includes upregulation of a

243 y mutations impairing TBX3 expression in the hair follicle, resulting in a more circumferential distr

244 from peripheral clock cells in participants' hair follicle samples.

245 factor Forkhead box C1 (FOXC1) expressed in hair follicle SCs (HFSCs).

246 In this study, we show that murine hair follicle SCs induce the Foxc1 transcription factor

247 a dynamic, cell-intrinsic mechanism used by hair follicle SCs to reinforce quiescence upon self-rene

248 holemounts to allow systematic annotation of hair follicle, sebaceous gland and interfollicular epide

249 ing stem cells in affected tissues including hair follicles, sebaceous glands, taste buds, nails and

250 companion layer and inner root sheath of the hair follicle, SG, and epidermis.

251 Instead, in Par3-deficient hair follicles, spindles were shifted toward planar orie

252 We show that hair follicle stem cell (HFSC) aging causes the stepwise

253 +) Treg cells preferentially localize to the hair follicle stem cell (HFSC) niche to control HFSC-med

254 of apoptosis before the onset of epithelial hair follicle stem cell activation during the murine hai

255 TLR3 activation promotes expression of hair follicle stem cell markers and induces elements of

256 artments in mice, we show here that multiple hair follicle stem cell populations readily develop BCC-

257 We conclude that signalling couples hair follicle stem cell quiescence with reduced H3 K4/K9

258 orneal epithelium were compared to epidermal hair follicle stem cell RNA-Seq to identify genes repres

259 tify SOX9 as a crucial chromatin rheostat of hair follicle stem cell super-enhancers, and provide fun

260 Hair follicle stem cells (HFSCs) and their transit ampli

261 els actively reduced in adult mouse skin and hair follicle stem cells (HFSCs) during G0 quiescence.

262 Hair follicle stem cells (HFSCs) play important roles in

263 odel, we map the global chromatin domains of hair follicle stem cells and their committed progenitors

264 conclude that R-spondin2 treatment activates hair follicle stem cells and therefore may have therapeu

265 In mammalian hair, it is unclear how hair follicle stem cells can enter an extended period of

266 r niche, either in vitro or in wound-repair, hair follicle stem cells dynamically remodel super-enhan

267 on of beta-catenin specifically within mouse hair follicle stem cells generates new hair growth throu

268 Hair follicle stem cells have emerged as a prime model t

269 ate the proliferation and differentiation of hair follicle stem cells through Notch signaling.

270 b and others that demonstrate the ability of hair follicle stem cells to serve as cancer cells of ori

271 e types of stem cells--embryonic stem cells, hair follicle stem cells, and intestinal epithelial stem

272 Nfatc1 locus allowed labeling and tracing of hair follicle stem cells.

273 ing enabling time-resolved imaging of single hair follicle stem cells.

274 y regulator of the undifferentiated state of hair follicle stem cells.

275 T-cells is the preferential proliferation of hair follicle stem cells.

276 s well as beta-catenin-induced activation of hair follicle stem/early progenitor cells and trichofoll

277 ve activity promoting the hyperactivation of hair follicle stem/progenitor cells and tumorigenesis.

278 of longitudinal lanceolate complexes at each hair follicle subtype.

279 pocytes in large skin wounds that regenerate hair follicles, suggesting a new source of adipogenic pr

280 alopecia and excoriation) mouse skin rescues hair follicle telogen entry and significantly decreases

281 areata (AA) is an autoimmune disease of the hair follicle that results in hair loss of varying sever

282 In mouse hair follicles, those chemotherapeutic agents that disru

283 Here, we discover that hair follicle transit-amplifying cells (HF-TACs) play an

284 Hair follicles undergo cyclic behavior through regressio

285 orneum (p<0.001) and the imaging of the skin hair follicles using multiphoton microscopy showed that

286 es in expression of 504 genes in DXR-treated hair follicles versus controls.

287 n be reamplified in the skin and surrounding hair follicles via intradermal injection of recombinant

288 , in non-transplanted animals, the number of hair follicles was reduced.

289 he relative patterning of eccrine glands and hair follicles, we exploited natural variation in the de

290 Using mouse whisker hair follicles, we show herein that tactile stimuli are

291 Using rat whisker hair follicles, we show that Merkel cells rather than Ab

292 Only nodules containing at least 1 visible hair follicle were biopsied.

293 scence microscopy to be localized around the hair follicles, when applied to the skin using hypobaric

294 ological tissue regression, we use the mouse hair follicle, which cycles stereotypically between phas

295 f the T-box 3 (TBX3) transcription factor in hair follicles, which in turn determines the distributio

296 yofibroblast reprogramming required neogenic hair follicles, which triggered bone morphogenetic prote

297 ablation leads to loss of LTMR terminals at hair follicles while, in contrast, TSCs remain associate

298 Subsequently, hair follicles with a Gsdma3 mutation enter the second a

299 nsistently, K5.CtBP1 mice displayed abnormal hair follicles with decreased expression of Dlx3 downstr

300 e, hairs are lost and replaced by dystrophic hair follicles with dilated infundibulae.