Homo sapiens
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PROVIDER: PRJNA400358 | ENA |
REPOSITORIES: ENA
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Project description:Human Hair follicles: Control Vs. 0.5 µM spermidine treatment
| PRJNA138843 | ENA
Project description:Inner Mongolia Cashmere Goat is a local excellent breed of cashmere and meat dual-purpose, which is a typical heterogeneous indumentum. The hair follicles cycle through periods of vigorous growth (anagen), a regression caused by apoptosis (catagen), and relative rest (telogen). At present, it is not clear which genes affect the cycle transformation of hair follicles and unclear how proteins impact the creation and expansion of hair follicles. In this work, we investigated the possible pathways of transformation and apoptosis in goat hair follicles using multi-omics joint analysis methodologies. The results showed that 917 , 1187 and 716 proteins were specifically expressed in anagen, catagen and telogen. The result of gene ontology (GO) annotation showed that differentially expressed proteins（DEPs) are in different growth cycle periods, and enriched GO items are mostly related to the transformation of cells and proteins. The Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment result indicated that the apoptosis process has a great impact on hair follicle's growth cycle. The results of the protein interaction network of differential proteins showed that the Ribosomal Protein family ( RPL4, RPL8, RPS16, RPS18, RPS2, RPS27A, RPS3 ) was the core protein in the network. The results of combined transcriptome and proteomics analysis showed that there were 16,34, and 26 overlapped DEGs and DEPs in the comparison of anagen VS catagen, catagen VS telogen and anagen VS telogen, of which API5 plays an important role in regulating protein and gene expression levels. We focused on API5 and Ribosomal protein and found that API5 affected the apoptosis process of hair follicles, and Ribosomal Protein was highly expressed in the resting stage of hair follicles. They are both useful as molecular marker candidate genes to study hair follicle growth and apoptosis, and they both have an essential function in the cycle transition process of hair follicles. The results of this study may provide a theoretical basis for further research on the growth and development of hair follicles in Inner Mongolian Cashmere goats.
2024-06-24 | PXD050798 | Pride
Project description:Since hair growth disorders can carry a major psychological burden, more effective human hair growth-modulatory agents need to be urgently developed. Here, we used the hypertrichosis-inducing immunosuppressant, cyclosporine A (CsA), as a lead compound to identify new hair growth-promoting targets. Through microarray analysis we identified the Wnt inhibitor, SFRP1, as being downregulated in the dermal papilla (DP) of CsA-treated human scalp hair follicles (HFs) ex vivo. Therefore, we further investigated the function of SFRP1 using a pharmacological approach and found that SFRP1 regulates intrafollicular canonical Wnt/β-catenin activity through inhibition of Wnt ligands in the human hair bulb. Conversely, inhibiting SFRP1 activity through the SFRP1 antagonist, WAY-316606, enhanced hair shaft production, hair shaft keratin expression and inhibited spontaneous HF regression (catagen) ex vivo. Collectively, these data (a) identify Wnt signaling as a novel, non-immune-inhibitory CsA target; (b) introduce SFRP1 as a physiologically important regulator of canonical β-catenin activity in a human (mini-)organ; and (c) demonstrate WAY-316606 to be a promising new promoter of human hair growth. Since inhibiting SFRP1 only facilitates Wnt signaling through ligands that are already present, this “ligand-limited” therapeutic strategy for promoting human hair growth may circumvent potential oncological risks associated with chronic Wnt over-activation. We used microarrays to identify novel hair growth promoting targets in human hair follicles through the use of cyclosporine A.
2018-05-09 | GSE109632 | GEO
Project description:Transcriptome analysis on Gata3 conditional knock out murine hair follicles. Background. The transcription factor Gata3 is critically involved in epidermis and hair follicle differentiation. Yet, little is known about how Gata3 co-ordinates stem cell lineage determination in skin, which processes are mostly implicated and how Gata3 differentially regulates distinct cell populations within the hair follicle. Here, we describe a conditional Gata3-/- mouse (K14-Gata3-/-) in which Gata3 is specifically deleted in epidermis and hair follicles. Principal findings. K14-Gata3-/- mice show aberrant postnatal growth and development, delayed hair growth and maintenance, abnormal hair follicle organization and irregular pigmentation. After the first hair cycle, the germinative layer surrounding the dermal papilla was not restored; instead, proliferation was pronounced in basal epidermal cells. Transcriptome analysis of laser-dissected K14-Gata3-/- hair follicles as compared to wild type littermate controls, revealed mitosis, epithelial differentiation and the Notch, WNT and BMP signalling pathways to comprise significantly overrepresented processes. Conclusions. Subsequent elucidation of these pathways at the RNA and protein levels and physiologic endpoints shows that Gata3 integrates diverse signalling networks to regulate the balance between hair follicle and epidermal cell fates.
2007-01-01 | E-MEXP-634 | biostudies-arrayexpress
Project description:This a model from the article:
The follicular automaton model: effect of stochasticity and of synchronization
of hair cycles.
Halloy J, Bernard BA, Loussouarn G, Goldbeter A. J Theor Biol
2002 Feb 7;214(3):469-79 11846603
,
Abstract:
Human scalp hair consists of a set of about 10(5)follicles which progress
independently through developmental cycles. Each hair follicle successively goes
through the anagen (A), catagen (C), telogen (T) and latency (L) phases that
correspond, respectively, to growth, arrest and hair shedding before a new
anagen phase is initiated. Long-term experimental observations in a group of ten
male, alopecic and non-alopecic volunteers allowed determination of the
characteristics of hair follicle cycles. On the basis of these observations, we
previously proposed a follicular automaton model to simulate the dynamics of
human hair cycles and the development of different patterns of alopecia [Halloy
et al. (2000) Proc. Natl Acad. Sci. U.S.A.97, 8328-8333]. The automaton model is
defined by a set of rules that govern the stochastic transitions of each
follicle between the successive states A, T, L and the subsequent return to A.
These transitions occur independently for each follicle, after time intervals
given stochastically by a distribution characterized by a mean and a standard
deviation. The follicular automaton model was shown to account both for the
dynamical transitions observed in a single follicle, and for the behaviour of an
ensemble of independently cycling follicles. Here, we extend these results and
investigate additional properties of the model. We present a deterministic
version of the follicular automaton. We show that numerical simulations of the
stochastic version of the automaton yield steady-state level of follicles in the
different phases which approach the levels predicted by the deterministic
equations as the number of follicles progressively increases. Only the
stochastic version can successfully reproduce the fluctuations of the fractions
of follicles in each of the three phases, observed in small follicle
populations. When the standard deviation is reduced or when the follicles become
otherwise synchronized, e.g. by a periodic external signal inducing the
transition of anagen follicles into telogen phase, large-amplitude oscillations
occur in the fractions of follicles in the three phases. These oscillations are
not observed in humans but are reminiscent of the phenomenon of moulting
observed in a number of mammalian species. Copyright 2002 Elsevier Science Ltd.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Halloy J, Bernard BA, Loussouarn G, Goldbeter A. (2002) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230014 | BioModels
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Human hair follicles undergo repetitive cycles of growth throughout their lifetime. During the hair follicle cycle, functional and structural changes occur within the surrounding skin environment. However, skin that experienced a deep injury lacks cycling hair follicles and turns into a mass of unremodelled scar tissue. We hypothesise that re-introducing cycling hair follicles into human scars will stimulate skin remodelling improving fibrotic tissue. To determine the transcriptional events underlying remodelling of scar dermis after hair follicle transplantation, we used Affymetrix microarrays to perform profiling of scar dermis before (0 mo), and at three time points after hair transplantation transplantation: 2, 4, and 6 months.
2022-12-31 | GSE145470 | GEO
Project description:Characterizing the expression of human olfactory receptor genes
| PRJNA97439 | ENA
Project description:Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (AGA); yet the mechanisms for decreased hair growth in this disorder are unclear. Here, we show that prostaglandin D2 synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D2 (PGD2), is similarly elevated in bald scalp. During normal follicle cycling in mice Ptgds and PGD2 levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD2 inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD2 receptor G protein-coupled receptor 44 (GPR44), but not the prostaglandin D2 receptor 1(PTGDR). Furthermore, we find that a transgenic mouse, K14-Ptgs2, which targets prostaglandin-endoperoxide synthase 2 expression to the skin, demonstrates elevated levels of PGD2 in the skin and develops alopecia, follicular miniaturization and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD2 as an inhibitor of hair growth in AGA and suggest the PGD2-GPR44 pathway as a potential target for treatment. 5 individuals with Androgenetic Alopecia were biopsied at both their haired and bald scalp for mRNA purification and microarray (total 10 arrays)
2012-03-26 | E-GEOD-36169 | biostudies-arrayexpress
Project description:Telogen (resting phase) hair follicles are more radioresistant than anagen (growth phase) ones. Irradiation of BALB/c mice in the anagen phase with γ-rays at 6 Gy induced hair follicle dystrophy, whereas irradiation in the telogen phase induced the arrest of hair follicle elongation without any dystrophy after post-irradiation depilation. In contrast, FGF18 was highly expressed in the telogen hair follicles to maintain the telogen phase and also the quiescence of hair follicle stem cells. Therefore, the inhibition of FGF receptor signaling at telogen induced the dystrophy after post-irradiation depilation. In addition, the administration of recombinant FGF18 suppressed cell proliferation in the hair follicles and enhanced the repair of radiation-induced DNA damage, so FGF18 protected the anagen hair follicles against radiation damage to enhance hair regeneration. Moreover, FGF18 reduced the expression of cyclin B1 and cdc2 in the skin and FGF18 signaling induced G2/M arrest in the keratinocyte cell line HaCaT, although no obvious change of the expression of DNA repair genes was detected by DNA microarray analysis. These findings suggest that FGF18 signaling for the hair cycle resting phase causes radioresistance in telogen hair follicles by arresting the proliferation of hair follicle cells.
2017-06-03 | GSE69501 | GEO