ライフサイエンスコーパス: follicle

1 males), and 2 with alopecia (non-functioning follicles).

2 ath (IRS) as well as other parts of the hair follicle.

3 on of the cellular composition of the B cell follicle.

4 e-scale metabolic model of the mouse ovarian follicle.

5 rived from the outer root sheath of the hair follicle.

6 during their development within the ovarian follicle.

7 or the transition from primordial to primary follicle.

8 tion was predetermined in the primary B cell follicle.

9 rect mechanism of displacing MZ B cells into follicles.

10 nterpretation of these structures as ovarian follicles.

11 into granulosa cells of quiescent primordial follicles.

12 e expressed in the outer root sheath of hair follicles.

13 pigmentary status in canities-affected hair follicles.

14 cell trafficking into lymph node and splenic follicles.

15 es (PMFs), with smaller oocytes within these follicles.

16 integrated into clinically normal skin hair follicles.

17 nd their projections in mouse antral ovarian follicles.

18 d colocalized with B cells at the margins of follicles.

19 cells but dispensable for expression in hair follicles.

20 tent HAP stem cell colonies similar to fresh follicles.

21 t females AMH is produced by growing ovarian follicles.

22 ted in mouse oocytes beginning in primordial follicles.

23 l centres are tightly confined within B cell follicles.

24 re unable to efficiently disperse within the follicles.

25 cell-neurite complexes and abut primary hair follicles.

26 llicular dendritic cells (FDC) in the B cell follicles.

27 death pathways in the oocytes of primordial follicles.

28 dissemination of infected cells to lymphoid follicles.

29 e skin and eventually homing within the hair follicles.

30 sensory nerve endings that innervate whisker follicles.

31 olutionary conservation of mammalian ovarian follicles.

32 localization of germinal centers and B-cell follicles.

33 iors that drive elongation of the Drosophila follicle, a model system in which basement membrane stif

34 The formation of hair follicles, a landmark of mammals, requires complex mesen

35 ) T cells, and SIV-DNA and SIV-RNA in B cell follicles, a major site of viral persistence during ART.

36 selection of proper biomaterials improve the follicles adhesion and development.

37 rophages that is enriched within the resting follicle and deceases immediately prior to HFSC activati

38 hairy skin, we took bio-inspiration from the follicle and hypothesized that follicular fibroblasts wo

39 at the transition from primordial to primary follicle and is accompanied by dynamic changes in gene e

40 ccumulation of aberrant fibers in the dental follicle and periodontium.

41 n of the lower permanent portion of the hair follicle and play a vital role for repigmentation in vit

42 ctated GC output by retaining B cells in the follicle and steering their interaction with follicular

43 e melanocyte lineage progression in the hair follicle and underscore a key role for BMP signaling in

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

45 x2.3 impairs maturation of isolated lymphoid follicles and attenuates dextran sodium sulfate-induced

46 opins exhibit normal distribution of ovarian follicles and corpora lutea.

47 nchiolitis and alveolar ductitis with B-cell follicles and emphysema, in lung tissue samples from con

48 ed organ, equipped with appendages (that is, follicles and glands), that is critical for regulating b

49 ys post-vaccination) activation of tonsillar follicles and influenza-specific TFH-cell (CXCR5+CD57+CD

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

51 Cutaneous changes seem to start around hair follicles and involve activation of cells of the innate

52 fferentiated granulosa cells of preovulatory follicles and luteal cells of corpora lutea had no effec

53 e demonstrated a high sensitivity of ovarian follicles and spermatogenic cells to HZE particles.

54 dothelial venules within intragraft lymphoid follicles and the recruitment of B cells, but not Foxp3(

55 ring wound healing in adult mouse skin, hair follicles and then adipocytes regenerate.

56 formed lineage tracing to analyze primordial follicles and wave 1 medullar follicles during mouse fet

57 or Foxn1 Foxn1 is also expressed in the hair follicle, and disruption of Foxn1 function in mice resul

58 NIK) is highly active in intestinal lymphoid follicles, and is required for M-cell maintenance.

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

60 d distributions, resulting in defective hair follicle angling, a hallmark of disrupted PCP.

61 the reorientation of elongated cells at the follicle anterior.

62 we identify the dermal sheath that lines the follicle as the key driver of tissue regression and nich

63 natural tilt of the follicles, verifying the follicles as generators, with a time constant of about o

64 Finally, in organ-cultured human scalp hair follicles as well as in patients undergoing chemotherapy

65 and unearths new insights during primordial follicle assembly in mice.

66 Primordial follicle assembly in the mouse occurs during perinatal a

67 ls different intensities of fluorescence of "follicles" associated with a skeleton of the confuciusor

68 rofold (M) cells in ileum Peyer's patch (PP) follicle-associated epithelia (FAE) to limit entry point

69 tes directional electric fields (EFs) in the follicle-associated epithelium of mouse cecum.

70 ulge area of the hair follicle contains hair-follicle-associated pluripotent (HAP) stem cells.

71 Later, in autoreactive follicles, B-cells encounter T-follicular helper cells (

72 Hair follicle biopsy samples demonstrated evidence of Wee1 in

73 These models escape the preantral follicle block and in response to superovulatory gonadot

74 M) protein within melanocytes in anagen hair follicle bulbs.

75 MC and keratinocyte precursors from the hair follicle bulge of untreated vitiligo skin and vitiligo s

76 , the melanocyte (MC) precursors in the hair follicle bulge proliferate, migrate, and differentiate t

77 f the proteins MSY2 and NOBOX in the primary follicles but no difference in the level of protein sign

78 viously, we redirected CD8 T cells to B-cell follicles by ectopic expression of the CXCR5 homing prot

79 rowth can be induced from resting mouse hair follicles by topical application of JAK inhibitors, sugg

80 adaptations can be made to avoid toxicity to follicles caused by elevated levels of cryoprotectants.

81 se ovaries densely populated with primordial follicles, CCND2 protein co-localised and was detected i

82 average of 1100, 6200 and 2500 receptors per follicle cell (FC) at stages 8/9, 10 and >=11 of oogenes

83 er Fat2-dependent planar polarization of the follicle cell basal domain, oriented basement membrane (

84 z-f1's role in regulating Sim expression and follicle cell differentiation can be replaced by its mou

85 tic disruption of Ftz-f1 expression prevents follicle cell differentiation into the final maturation

86 ollicle maturation, particularly for somatic follicle cell differentiation, are poorly understood.

87 acts as a direct target of Ftz-f1 to promote follicle cell differentiation/maturation and that Ftz-f1

88 d-mediated cell proliferation in the ovarian follicle cell epithelium in response to mechanical stret

89 us, integrin function is dispensable for pre-follicle cell polarity but is required to maintain cellu

90 Finally, one follicle cell progenitor population has also been transc

91 This late follicle cell transition is characterized by upregulatio

92 Here, we identify a novel third follicle cell transition that occurs in the final stages

93 the transcriptional trajectory of the entire follicle-cell population over the course of their develo

94 FSCs produce transit-amplifying Follicle Cells (FCs) from their posterior face and quies

95 ansmitted from the oocyte to the surrounding follicle cells and in turn from the follicle cells back

96 , progenitor cell populations such as dental follicle cells are characterized by an open H3K4me3 chro

97 rounding follicle cells and in turn from the follicle cells back to the oocyte.

98 vertebrate tight junction, but proliferating follicle cells do not have mature septate junctions, and

99 During Drosophila oogenesis, the somatic follicle cells encasing oocytes undergo two distinct wel

100 We showed that hair follicle cells from HS patients had an increased number

101 FSC clones produce, on average, half of the follicle cells in each ovariole.

102 ors in Drosophila, is transiently induced in follicle cells in late stages of oogenesis via ecdystero

103 that inducing expression of Cut in stage 14 follicle cells is sufficient to inhibit follicle rupture

104 Here, we report that follicle cells lacking the RNA-binding protein IMP go th

105 in situ hybridization, we found that in the follicle cells of ovaries the 5'-ends of flam transcript

106 ly conserved and function within the somatic follicle cells of the ovary to regulate folliculogenesis

107 ine Delta signal that activates Notch in the follicle cells to induce them to cease proliferation and

108 Proliferating hair follicle cells were then shifted to DMEM/Ham's Nutrient

109 around the egg chamber on the basal side of follicle cells, emerges from polarized intercellular fil

110 We propose that normally in follicle cells, flam downstream transcript regions funct

111 controlled by cis-inhibition by Delta in the follicle cells, which is relieved when the miRNA pathway

112 racing of subpopulations of escort cells and follicle cells.

113 he anterior posterior axis of the Drosophila follicle cells.

114 intercellular filopodia and stress fibers in follicle cells.

115 essed in an overlapping domain to mid in the follicle cells.

116 tic staining in unruptured poorly luteinized follicles, consistent with dramatic reduction of progest

117 Primordial follicles, consisting of granulosa cell (GC)-enveloped o

118 e still unknown because almost all sebaceous follicles contain dense concentrations of bacteria yet o

119 The bulge area of the hair follicle contains hair-follicle-associated pluripotent (

120 fabricated and used as 3D system for porcine follicles culture.

121 in, essential for the regulation of the hair-follicle cycle, and required for the maintenance of both

122 regulate epidermal differentiation and hair follicle cycling and, in so doing, to promote barrier fu

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

124 ian transcriptomes and reductions in ovarian follicle density between juvenile alligators from Lake A

125 human skin wound closure, we found that hair follicle dermal papilla fibroblasts could accelerate clo

126 a metabolite of melatonin, could not prevent follicle destruction, implying that melatonin does not c

127 Lgr5-DTR-EGFP mice at E16.5 while first wave follicles developed normally and supported fertility.

128 cre/+);Runx2(flox/flox) mice were infertile; follicles developed to the preovulatory follicle stage b

129 s of disrupted oestrous cycling and in vitro follicle development being cause for concern.

130 ion of YAP1 activity disrupted mouse ovarian follicle development in vitro and in vivo.

131 ing cumulus and mural cells), during ovarian follicle development in vivo.

132 se Recon 2) and contains several key ovarian follicle development metabolic pathways.

133 Here, we investigate mouse hair follicle development to understand how morphogens operat

134 een limited due to dynamic nature of ovarian follicle development, thus warranting a systems approach

135 d plays a critical role in the regulation of follicle development.

136 in granulosa cells is essential for ovarian follicle development.

137 e Hippo signaling pathway influences ovarian follicle development; however, its exact roles remain un

138 indicated that the method failed to preserve follicles due to the high concentrations of DMSO used.

139 yze primordial follicles and wave 1 medullar follicles during mouse fetal and perinatal oogenesis.

140 ducted to characterize divergence in ovarian follicle dynamics and transcriptomes between sites, betw

141 in does not confer the protection of ovarian follicles, either directly or indirectly.

142 as conditional ablation of Igf1r in primary follicles elicits defective follicle-stimulating hormone

143 of MZ B cells between the MZ and the B-cell follicle enables them to efficiently capture and deliver

144 pha(V) deficiency impeding Tfh generation or follicle entry or the ability of alpha(V)-CD4 cKO Tfh to

145 tructural and biological changes in the hair follicle environment that may impact hair growth.

146 interfollicular epidermal, mammary and hair follicle epithelia that genotoxicity does not promote ap

147 -free MDV is produced in specialized feather follicle epithelial (FFE) cells of infected chickens, in

148 ally infects epithelial cells of the feather follicle epithelium from where it is shed into the envir

149 thal giant larvae (Lgl) using the Drosophila follicle epithelium.

150 y, the basal layer of the epidermis and hair follicles expressed p120-1 with reduced p120-3, whereas

151 tion had increased numbers of gastric B-cell follicles expressing CD19 (P < .0001); these follicles h

152 del where stem cells regenerate de novo hair follicles following deep wounding.

153 etic nerves, arrector pili muscles, and hair follicles form a tri-lineage unit to cause piloerection

154 ynthesis in a pattern that predicts new hair follicle formation after wounding in mice.

155 s and IL-27-mediated suppression of lymphoid follicle formation are all involved in governing the reg

156 gulate oocyte differentiation and primordial follicle formation during early, postnatal mouse oogenes

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

158 Dazl determines primordial follicle formation through the translational regulation

159 ollicular melanin unit in variably pigmented follicles from the aging human scalp of healthy individu

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

161 the medullary compartment, where the larger follicles grow and mature.

162 In older ovaries follicle growth was associated with nuclear exclusion of

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

164 ed delays in meiocyte differentiation and in follicle growth, even at the lowest in vitro dose exposu

165 fibrils and F-actin stress fibers constrain follicle growth, promoting its axial elongation.

166 follicles expressing CD19 (P < .0001); these follicles had features of mucosa-associated lymphoid tis

167 cultured pluripotent cells from human dental follicles (hDFC).

168 Hair follicle (HF) development is orchestrated by coordinated

169 wn that LGR4 plays an important role in hair follicle (HF) development, but the impact of LGR4 on the

170 ymphatics form intimate networks around hair follicle (HF) SCs.

171 noma, reside in the bulge region of the hair follicle (HF), an immune-privileged tissue niche with im

172 been successfully accomplished in human hair follicles (HuHF).

173 as cryptopatches (CPs) and isolated lymphoid follicles (ILFs) constitute steady-state activation hubs

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

175 The use of porcine follicles implied many advantages respect to the use of

176 tion of stem cells to regenerate anagen hair follicles in AA and intraepidermal melanocytes in vitili

177 anocytes in vitiligo and in regrowth of hair follicles in AA.

178 controls the tempo of maturation of primary follicles in An. albimanus in a similar manner to that p

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

180 We address the identity of putative ovarian follicles in Early Cretaceous bird fossils from the Jeho

181 level of protein signals or in the number of follicles in relation to treatment.

182 Tfh cells predominantly reside within B cell follicles in secondary lymphoid organs, they are challen

183 approaches and support growth of primordial follicles in vitro.

184 Proper development and maturation of a follicle is essential for successful ovulation and repro

185 The development of primordial follicles is controlled by a complex network of interact

186 In the Drosophila ovarian follicle, it has been proposed that after Fat2-dependent

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

188 w the outer root sheath (ORS) and inner hair follicle layers coordinate hair production.

189 l mesenchymal progenitor cells in the dental follicle lie at the heart of the coupling of these 2 pro

190 The local presence of B-cell follicle-like structures and oligoclonal bands in MS pat

191 n microenvironment, these cells express hair-follicle lineage markers and contribute to hair follicle

192 lls and prevented their commitment to a hair follicle lineage.

193 damage to the ovarian reserve, resulting in follicle loss, endocrine hormone deficiency, and inferti

194 sembles transit-amplifying cells of the hair follicle matrix, with AP-1 and TGFB cooperativity drivin

195 provides new insight into the regulation of follicle maturation in Drosophila and the conserved role

196 ction; however, the molecular mechanisms for follicle maturation, particularly for somatic follicle c

197 Despite normal oocyte numbers and follicle maturation, Plk1 cKO mice were infertile.

198 showed impaired spermatogenesis and ovarian follicle maturation.

199 role of ATM in the protection of human hair follicle melanocytes from oxidative stress/damage within

200 r in vitro model of primary human scalp hair follicle melanocytes, we showed that ATM expression incr

201 f competence during regeneration of new hair follicle mesenchyme.

202 Our systems approach to model follicle metabolism can guide future experimental studie

203 es that target Merkel cells in organoid hair follicles, mimicking the neural circuitry associated wit

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

205 lter or interfere with the typical spherical follicles morphology.

206 tion through the study of Wound Induced Hair follicle Neogenesis (WIHN), an adult organogenesis model

207 gen stage is actively maintained by the hair follicle niche.

208 nest breakdown with a 66% reduction in total follicle number and an increase in the proportion of pri

209 ogenic driver in the miniaturization of hair follicles of androgenetic alopecia by interfering with t

210 ication forks was altered in ORSCs from hair follicles of HS patients, leading to activation of the A

211 e botanical fossil record, showing that the "follicles" of some enantiornithine fossils resemble plan

212 skin competence explaining why aberrant hair follicles or sebaceous glands are sometimes observed in

213 an increase in the proportion of primordial follicles (PMFs), with smaller oocytes within these foll

214 Thus, the hair follicle possesses a unique, enhanced capacity to integr

215 gest that the cryopreserved whole human hair follicle preserves the ability to produce HAP stem cells

216 Teleost thyroid follicles produce the same thyroid hormones as in other

217 tulated embryonic HF development, and mature follicles produced hair co-occurring with epithelial tum

218 Interestingly, these cryopreserved hair follicles produced pluripotent HAP stem cell colonies si

219 a subset of Sox9-positive Lef1-negative hair follicle progenitors that give rise to the upper SG Over

220 tic nerve niche, which in turn controls hair follicle regeneration in adults.

221 d, sheath contraction is inhibited, impeding follicle regression and niche relocation.

222 e dermal sheath as smooth muscle that drives follicle regression for reuniting niche and stem cells i

223 In the hair cycle, during follicle regression, the niche traverses the skin throug

224 lves regulate the niche environment for hair follicle regrowth.

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

226 ging dermal environment on female scalp hair follicles remains unclear.

227 We therefore reaffirm that the "follicles" represent ingested food items, and even thoug

228 gh the cortical compartment, where quiescent follicles reside and the medullary compartment, where th

229 identified mechanoreceptors in the vibrissal follicle: ring-sinus Merkel; lanceolate; clublike; and r

230 e 14 follicle cells is sufficient to inhibit follicle rupture and ovulation through its negative regu

231 Ddr2 expression was detected in the dental follicle/sac and dental papilla mesenchyme of developing

232 g super-enhancer maintenance of the key hair follicle SC-specific TF genes.

233 licle lineage markers and contribute to hair follicles, sebaceous glands and/or epidermis renewal.

234 The hair follicle serves as a melanocyte reservoir for both hair

235 in submucosal and mucosal isolated lymphoid follicles (SM-ILFs and M-ILFs, respectively) as well as

236 disrupted touch-dome formation but not hair-follicle specification, demonstrating a temporally disti

237 oskeletal remodeling events that impact hair follicle specification, differentiation, downgrowth and

238 ile; follicles developed to the preovulatory follicle stage but failed to ovulate.

239 at are differentially active across multiple follicle stages.

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

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

242 novel cell type corresponding to the elusive follicle stem cell precursors and predicts subtypes of k

243 y defined for facilitating future studies on follicle stem cell regulation.

244 stigated how this is achieved for Drosophila Follicle Stem Cells (FSCs) by spatially-restricted niche

245 The follicle stem cells (FSCs) in the Drosophila ovary are a

246 vivo, conditional ablation of Ift20 in hair follicle stem cells (HF-SCs) similarly impairs their abi

247 es, leading researchers to propose that hair follicle stem cells (HFSCs) are either lost, differentia

248 T signaling is required for maintaining hair follicle stem cells (HFSCs) in a quiescent state.

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

250 In this work, we characterized hair follicle stem cells (HFSCs) isolated from HS patients an

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

252 ell carcinoma (SCC) can be initiated by hair follicle stem cells (HFSCs).

253 targeted an activating Hras mutation to hair follicle stem cells and discovered that Hras mutant cell

254 nd mono-ADP ribosylases, protects adult hair follicle stem cells from aging by ensuring their hair cy

255 lation of escort cells is able to convert to follicle stem cells in response to starvation or upon ge

256 nated stem cell units, germline, and somatic follicle stem cells maintain and renew an organ.

257 Hair follicle stem cells may themselves regulate the niche en

258 es form "synapse-like" connections with hair follicle stem cells to promote hair regeneration in resp

259 e germline stem cells and their niche cells, follicle stem cells, and previously undescribed subpopul

260 d a gradual decrease in the stemness of hair follicle stem cells, culminating in hair loss.

261 ased testosterone level, increased levels of follicle stimulating and luteinizing hormones, and 8.52-

262 treatment of male infertility is the use of follicle stimulating hormone (FSH) analogs which improve

263 fect on sperm count and concentration, serum follicle stimulating hormone (FSH), luteinizing hormone

264 is of serum and whole-blood from luteinizing/follicle-stimulating (LH/FSH)-secreting (n = 24), prolac

265 had a body-mass index of 19-35 kg/m(2) and a follicle-stimulating hormone (FSH) concentration of 3.0-

266 and c) test whether treatment with exogenous follicle-stimulating hormone (FSH) is capable of rescuin

267 >=60 years or aged <60 years if their serum follicle-stimulating hormone and oestradiol concentratio

268 nce last menses or since hysterectomy with a follicle-stimulating hormone concentration of >=40 U/L)

269 Igf1r in primary follicles elicits defective follicle-stimulating hormone responsiveness blocking dev

270 fl/fl)) Kras(G12D/+)(G12D mice) had abnormal follicle structures and developed low-grade serous ovari

271 (fl/fl)) Kras(G12V/+) (G12V mice) had normal follicle structures, and about 90% of them developed ute

272 gular location of the mechanoreceptor in the follicle, such alignment was observed only for Merkel af

273 ion of the functions of B cells within these follicles suggested diverse roles and the activation of

274 isplatin for 15 days can activate primordial follicles, suggesting that the response in the oocytes o

275 e their ovarian presence promotes oocyte and follicle survival vital for future ovarian health.

276 we reported their importance for oocyte and follicle survival within the developing ovary.

277 pidermis, fat-rich dermis and pigmented hair follicles that are equipped with sebaceous glands.

278 nocyte precursor cells in hair and vibrissal follicles that express the photopigment neuropsin (OPN5)

279 umps) requires concerted actions of the hair follicle, the arrector pili muscle (APM), and the sympat

280 present on and around the skin pilosebaceous follicles, the finding of multiple subtypes in deep tiss

281 sperse throughout the skin and populate hair follicles through long-range cell migration.

282 the maintenance and activation of primordial follicles, through SMAD-dependent and independent signal

283 ed BCL2 gene and protein expressions in hair follicle tissues.

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

285 rows always followed the natural tilt of the follicles, verifying the follicles as generators, with a

286 at the response in the oocytes of primordial follicles was dependent on cisplatin concentration and a

287 spatiotemporal gene ablation in murine hair follicles, we uncover a critical role for the transcript

288 arate somatic cellular lineages, second wave follicles were ablated by diptheria toxin treatment of L

289 s effects upon the progression of primordial follicles were assessed in cultures of mouse fetal ovari

290 or this, bovine granulosa cells from smaller follicles were cultured in vitro and after sub-confluenc

291 Hair follicles were shorter, not reaching the adipose layer.

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

293 ) macrophages localize in situ in the B cell follicles, where they can interact with Tfh cells.

294 expression were severely affected in feather follicles wherein MDV is shed, providing important infor

295 e expression of Runx1 and Runx2 in ovulatory follicles, while Cbfb is constitutively expressed.

296 skin repair, including regeneration of hair follicles with arrector pili muscles in healed wounds.

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

298 ity and the formation of protective lymphoid follicles within granulomas.

299 ts mediates B cell recruitment into lymphoid follicles within the allograft, resulting in a significa

300 isplatin: the death of oocytes in primordial follicles without indication of activation.