ライフサイエンスコーパス: hair follicle

1 issues such as mammary gland, cornea and the hair follicle.

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

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

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

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

6 t sheath (IRS) as well as other parts of the hair follicle.

7 re derived from the outer root sheath of the hair follicle.

8 ng the skin and eventually homing within the hair follicles.

9 anches that redundantly innervate individual hair follicles.

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

11 expected heterogeneity among SCs and TACs of hair follicles.

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

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

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

15 tial endings wrapping the base of individual hair follicles.

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

17 ells, and defective postnatal development of hair follicles.

18 lusters with antigen presenting cells around hair follicles.

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

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

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

22 to be expressed in the outer root sheath of hair follicles.

23 with pigmentary status in canities-affected hair follicles.

24 t are integrated into clinically normal skin hair follicles.

25 lial cells but dispensable for expression in hair follicles.

26 rkel cell-neurite complexes and abut primary hair follicles.

27 in the brain but also in the bone marrow and hair follicles(2-6).

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

29 The formation of hair follicles, a landmark of mammals, requires complex

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

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

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

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

34 region of the lower permanent portion of the hair follicle and play a vital role for repigmentation i

35 strate melanocyte lineage progression in the hair follicle and underscore a key role for BMP signalin

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

37 s in adult mice can heal by regenerating new hair follicles and adipocytes in their center.

38 s of the skin are intimately associated with hair follicles and control HF development, cycling, and

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

40 HOPX is a stem cell marker in hair follicles and intestines.

41 Cutaneous changes seem to start around hair follicles and involve activation of cells of the in

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

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

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

45 During wound healing in adult mouse skin, hair follicles and then adipocytes regenerate.

46 factor Foxn1 Foxn1 is also expressed in the hair follicle, and disruption of Foxn1 function in mice

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

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

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

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 uctures in skin such as nerves, vasculature, hair follicles, and sebaceous glands.

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

54 arized distributions, resulting in defective hair follicle angling, a hallmark of disrupted PCP.

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

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

57 Conversely, hair follicles are specified when mesenchymal BMP signal

58 Hair follicles are unique structures in the skin that co

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

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

61 Finally, in organ-cultured human scalp hair follicles as well as in patients undergoing chemoth

62 Forming the hair follicle-associated sebaceous gland, sebocytes are

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

64 The bulge area of the hair follicle contains hair-follicle-associated pluripotent (HAP) stem cells.

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

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

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

68 Hair follicle biopsy samples demonstrated evidence of We

69 d (ATM) protein within melanocytes in anagen hair follicle bulbs.

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

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

72 ion, MC and keratinocyte precursors from the hair follicle bulge of untreated vitiligo skin and vitil

73 iligo, the melanocyte (MC) precursors in the hair follicle bulge proliferate, migrate, and differenti

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

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

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

77 The hair follicle bulge, which contains melanocyte stem cell

78 air growth can be induced from resting mouse hair follicles by topical application of JAK inhibitors,

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

80 Hair follicles cannot enter the second anagen with ectop

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

82 We showed that hair follicle cells from HS patients had an increased nu

83 Proliferating hair follicle cells were then shifted to DMEM/Ham's Nutr

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

85 The bulge area of the hair follicle contains hair-follicle-associated pluripot

86 in skin, essential for the regulation of the hair-follicle cycle, and required for the maintenance of

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

88 D to regulate epidermal differentiation and hair follicle cycling and, in so doing, to promote barri

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 HH gene correlates with chemotherapy-induced hair follicle damage or the degree of CIA, respectively.

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

95 s of human skin wound closure, we found that hair follicle dermal papilla fibroblasts could accelerat

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

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

98 Early hair follicle development is characterised by the rapid

99 Here, we investigate mouse hair follicle development to understand how morphogens o

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

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

102 Hedgehog signaling gradient that may specify hair follicle development.

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

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

105 the interfollicular epidermis and for normal hair follicle development.

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

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

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

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

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

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

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

113 ing structural and biological changes in the hair follicle environment that may impact hair growth.

114 mouse interfollicular epidermal, mammary and hair follicle epithelia that genotoxicity does not promo

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

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

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

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

119 ersely, the basal layer of the epidermis and hair follicles expressed p120-1 with reduced p120-3, whe

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

121 is model where stem cells regenerate de novo hair follicles following deep wounding.

122 mpathetic nerves, arrector pili muscles, and hair follicles form a tri-lineage unit to cause piloerec

123 RA) synthesis in a pattern that predicts new hair follicle formation after wounding in mice.

124 ordia without a wave, akin to the process of hair follicle formation in mammalian embryos.

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

126 hair bulb region of normal and miniaturized hair follicles from vertex and occipital region in males

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

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

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

130 Unexpectedly, SOX9, a hair follicle growth regulator, was aberrantly expressed

131 role of redox sensing in the status of human hair follicle growth, differentiation and pigmentation.

132 interfollicular epidermis (IFE) and delayed hair follicle growth.

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

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

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

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

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

138 The hair follicle (HF) dermal condensate (DC) is a cluster o

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

140 Hair follicle (HF) development is orchestrated by coordi

141 s known that LGR4 plays an important role in hair follicle (HF) development, but the impact of LGR4 o

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

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

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

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

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

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

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

149 in, lymphatics form intimate networks around hair follicle (HF) SCs.

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

151 melanoma, reside in the bulge region of the hair follicle (HF), an immune-privileged tissue niche wi

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

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

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

155 Hair follicles (HFs) undergo lifelong cyclical transform

156 Hair follicles (HFs) undergo precisely regulated cycles

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

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

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

160 yet been successfully accomplished in human hair follicles (HuHF).

161 cular mast cells, in maintaining physiologic hair follicle immune privilege (IP); the extent to which

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

163 ilization of stem cells to regenerate anagen hair follicles in AA and intraepidermal melanocytes in v

164 h melanocytes in vitiligo and in regrowth of hair follicles in AA.

165 subset of RORgammat(+) ILCs residing within hair follicles in close proximity to sebaceous glands.

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

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

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

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

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

171 Whole hair follicles isolated from human scalp were cryopreser

172 that the OSM source is not intrinsic to the hair follicle itself and is instead a subset of TREM2(+)

173 al how the outer root sheath (ORS) and inner hair follicle layers coordinate hair production.

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

175 em cells and prevented their commitment to a hair follicle lineage.

176 n skin microenvironment, these cells express hair-follicle lineage markers and contribute to hair fol

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

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

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

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

181 te resembles transit-amplifying cells of the hair follicle matrix, with AP-1 and TGFB cooperativity d

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

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

184 e key role of ATM in the protection of human hair follicle melanocytes from oxidative stress/damage w

185 ng our in vitro model of primary human scalp hair follicle melanocytes, we showed that ATM expression

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

187 ate of competence during regeneration of new hair follicle mesenchyme.

188 bundles that target Merkel cells in organoid hair follicles, mimicking the neural circuitry associate

189 l epidermal differentiation, thereby causing hair follicle miniaturization.

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

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

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

193 lly and functionally dependent manner during hair follicle morphogenesis.

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

195 cells are the only cells that can respond to hair follicle morphogenetic signals in vivo.

196 question through the study of Wound Induced Hair follicle Neogenesis (WIHN), an adult organogenesis

197 key modulators of these reactions, including hair follicles, neurons, and commensal microbes.

198 telogen stage is actively maintained by the hair follicle niche.

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

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

201 pathogenic driver in the miniaturization of hair follicles of androgenetic alopecia by interfering w

202 replication forks was altered in ORSCs from hair follicles of HS patients, leading to activation of

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

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

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

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

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

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

209 tent skin competence explaining why aberrant hair follicles or sebaceous glands are sometimes observe

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

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

212 This hair follicle phenotype was associated with markedly sup

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

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

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

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

217 Thus, the hair follicle possesses a unique, enhanced capacity to i

218 s suggest that the cryopreserved whole human hair follicle preserves the ability to produce HAP stem

219 Interestingly, these cryopreserved hair follicles produced pluripotent HAP stem cell coloni

220 d in a subset of Sox9-positive Lef1-negative hair follicle progenitors that give rise to the upper SG

221 implying a therapeutic potential of SKPs in hair follicle regeneration and bioengineering.

222 pathetic nerve niche, which in turn controls hair follicle regeneration in adults.

223 , have been shown to induce hair genesis and hair follicle regeneration in mice, implying a therapeut

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

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

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

227 hemselves regulate the niche environment for hair follicle regrowth.

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

229 The genesis of the hair follicle relies on signals derived from mesenchymal

230 the aging dermal environment on female scalp hair follicles remains unclear.

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

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

233 erning super-enhancer maintenance of the key hair follicle SC-specific TF genes.

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

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

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

237 r-follicle lineage markers and contribute to hair follicles, sebaceous glands and/or epidermis renewa

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

239 The hair follicle serves as a melanocyte reservoir for both

240 d cytoskeletal remodeling events that impact hair follicle specification, differentiation, downgrowth

241 E14.5 disrupted touch-dome formation but not hair-follicle specification, demonstrating a temporally

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

243 rves form a dual-component niche to modulate hair follicle stem cell (HFSC) activity.

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

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

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

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

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

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

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

251 In vivo, conditional ablation of Ift20 in hair follicle stem cells (HF-SCs) similarly impairs thei

252 patches, leading researchers to propose that hair follicle stem cells (HFSCs) are either lost, differ

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

254 K-STAT signaling is required for maintaining hair follicle stem cells (HFSCs) in a quiescent state.

255 Skin vasculature cross-talking with hair follicle stem cells (HFSCs) is poorly understood.

256 In this work, we characterized hair follicle stem cells (HFSCs) isolated from HS patien

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

258 ous cell carcinoma (SCC) can be initiated by hair follicle stem cells (HFSCs).

259 , we targeted an activating Hras mutation to hair follicle stem cells and discovered that Hras mutant

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

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

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

263 ses and mono-ADP ribosylases, protects adult hair follicle stem cells from aging by ensuring their ha

264 Hair follicle stem cells may themselves regulate the nic

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

266 nerves form "synapse-like" connections with hair follicle stem cells to promote hair regeneration in

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

268 s, and a gradual decrease in the stemness of hair follicle stem cells, culminating in hair loss.

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

270 The up-regulation of hair-follicle stem cell genes is consistent with reduced

271 In response to skin injury, hair-follicle stem cells (HFSCs), normally poised for ha

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

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

274 ive cryopreservation procedures of the human hair follicle that preserve the differentiation potentia

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

276 ied epidermis, fat-rich dermis and pigmented hair follicles that are equipped with sebaceous glands.

277 oosebumps) requires concerted actions of the hair follicle, the arrector pili muscle (APM), and the s

278 ts disperse throughout the skin and populate hair follicles through long-range cell migration.

279 creased BCL2 gene and protein expressions in hair follicle tissues.

280 We then discuss the epidermis and hair follicle, to provide a non-skeletal example of a ti

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

282 Hair follicles undergo cyclic behavior through regressio

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

284 in symptoms: benign lesions originating from hair follicles, variously shaped cysts in the lungs, and

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

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

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

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

289 using spatiotemporal gene ablation in murine hair follicles, we uncover a critical role for the trans

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

291 tingly, Foxn1 expression and function in the hair follicle were unaffected.

292 Hair follicles were shorter, not reaching the adipose la

293 ield over the human head produced by healthy hair follicles when the scalp is lightly pressed.

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

295 used to collect the upper parts of the human hair follicles which were cultured for four weeks in a D

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

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

298 hance skin repair, including regeneration of hair follicles with arrector pili muscles in healed woun

299 respect to their cutaneous end organs (e.g., hair follicles), with Abeta rapidly adapting-LTMRs being

300 overlapping with respect to their associated hair follicles, with the notable exception of C-LTMRs, w