Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA397330 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5903740.fastq.gz | Fastqsanger.gz | |||
| SRR5903741.fastq.gz | Fastqsanger.gz | |||
| SRR5903742.fastq.gz | Fastqsanger.gz | |||
| SRR5903743.fastq.gz | Fastqsanger.gz | |||
| SRR5903744.fastq.gz | Fastqsanger.gz |
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Project description:The microRNA-200 family is highly expressed in epithelial cells and frequently lost in metastatic cancer. Although the tumor-suppressing roles of this family are well documented and directly linked to the inhibition of mesenchymal genes, their targets and functions in normal epithelial tissues remain unclear. Furthermore, how the two sub-families of the five-microRNA family distinguished by a single nucleotide within the seed region regulate their targets is unclear. Here we show that the microRNA-200 family governs hair morphogenesis and fine-tunes stem cell specification by regulating cell adhesion, polarity and signaling pathways. By directly ligating microRNAs to their targeted mRNA regions, we identify numerous targets involved in the regulation of actin cytoskeleton, focal adhesion, cell cycle and Hippo/Yap signaling in a miRNA:mRNA pair-specific manner. The two sub-families bind to largely distinct target sites although many genes are regulated by both sub-families for a greater degree of regulation. Using inducible and knockout mouse models, we show that the microRNA-200 family enhances cell adhesion, inhibits migration and reduces cell division, contributing to precise stem cell specification. Our findings demonstrate that combinatorial targeting of many genes is critical for microRNA functions and provide new insights into microRNA-200s’ functions in normal epithelial tissues.
2018-03-16 | GSE102291 | GEO
Project description:Aging organs functionally and structurally decline with the loss of their regenerative capabilities, yet the existence of distinct cell division programs that determine organ fates is unknown. Hair follicles, mammalian mini-organs that grow hair, miniaturize by aging. Here we report that hair follicle regeneration and aging are driven by distinct cell division types of hair follicle stem cells (HFSCs). Cell fate tracing and cell division axis analysis in mice revealed that HFSCs undergo symmetric and asymmetric cell divisions to generate a new bulge, yet preferentially provoke “stress-responsive type” asymmetric cell divisions that generate aberrantly differentiating cells upon age/stress. That dynamic program with repetitive divisions efficiently eradicates those cells through defective association and stabilization of a hemidesmosomal protein COL17A1 and a cell-polarity-protein aPKCλ in HFSCs, thereby causing organ aging. The forced stabilization of COL17A1 rescued organ aging through aPKCλ stabilization. These results demonstrate that distinct cell division programs govern tissue/organ fates.
2020-12-25 | GSE124119 | GEO
Project description:The hair follicle is a biological oscillator that alternates growth, regression, and rest phases driven by the sequential activation of the proliferation/differentiation programs of resident stem cell populations. The activation of hair follicle stem cell niches and subsequent entry into the growing phase is mainly regulated by Wnt/β-catenin signalling, while regression and resting phases are mainly regulated by Tgf-β/Bmp/Smad activity. A major question still unresolved is the nature of the molecular switch that dictates the coordinated transition between both signalling pathways. Here we have focused on the role of Endoglin (Eng), a key co-receptor for members of the Tgf-β/Bmp family of growth factors.Using an Eng haploinsufficient mouse model, we report that Eng is required to maintain a correct follicle cycling pattern and for an adequate stimulation of hair follicle stem cell niches. We further report that β-catenin binds to the Eng promoter depending on Bmp signalling. Moreover, we show that β-catenin interacts with Smad4 in a Bmp/Eng-dependent context and both proteins act synergistically to activate Eng promoter transcription. These observations point to the existence of a growth/rest switching mechanism in the hair follicle that is based on an Eng-dependent feedback crosstalk between Wnt/β-catenin and Bmp/Smad signals. Implication of Endoglin, Wnt/β-catenin and Bmp/Smad signals in the growth/rest hair follicle
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| 2628246 | ecrin-mdr-crc
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.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
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:To fully interrogate location-specific variations of microRNAs of the hair follicle in AGA and normal persons, we sought to perform a thorough and comprehensive microRNA profiling of different locations of hair follicles (bulb portions, bugle portions)
2018-12-24 | GSE111788 | GEO
Project description:Through phenotypical study, we found that miR-205 can promote hair growth. The goals of this study is to identify direct targets of miR-205 in hair follicle stem cells and determine whether and how miR-205 promotes hair growth by activating hair follicle stem cell.
2023-06-07 | GSE185116 | GEO
Project description:Increasing evidence suggests that microRNAs may play important roles in regulating self-renewal and differentiation in mammalian stem cells (SCs). Here, we explore this issue in skin. We first characterize microRNA expression profiles of skin SCs versus their committed proliferative progenies and identify a microRNA subset associating with “stemness”. Of these, miR-125b is dramatically downregulated in early SC-progeny. We engineer an inducible mice system and show that when miR-125b is sustained in SC-progenies, tissue balance is reversibly skewed towards stemness at the expense of epidermal, oil-gland and HF differentiation. Using gain-and-loss of function in vitro, we further implicate miR-125b as a repressor of SC differentiation. In vivo, transcripts repressed upon miR-125b induction are enriched >700% for predicted miR-125b targets normally downregulated upon SC-lineage commitment. We verify some of these miR-125b targets, and show that Blimp1 and VDR in particular can account for many tissue imbalances we see when miR-125b is deregulated. We used microarrays to compare the global gene expression profile of P4 stage hair follicle ORS cells from DTG (K14-rtTA,TRE-miR-125b) and control littermates. Hair follicle cells were isolated from P4 Backskin of K14-RFP/Sox9-EGFP double transgenic mice as following: interfollicular epidermis sheet was pealed from hair follicle & dermis after dispase treatment. The hair follicle & dermis were first digested by collagenase (Sigma). Intact hair follicles were separated from dermal cells by low speed spinning (20g). The hair follicles were then digested by Trypsin and filtered by 40 µm cell strainers. The isolated hair follicle cells were FACS sorted. Dead cells and large differentiated cells were excluded based on DAPI and side scattering. Early bulge cells were gated as GFPHi,RFPHi. Non-bulge ORS cells were gated as GFP-, RFPHi.
2011-01-04 | E-GEOD-26394 | biostudies-arrayexpress
Project description:Wound Induced Hair Follicle neogenesis (WIHN) is a hair neogenesis phenomenon which occurred in the center of scar. Neonatal hair follicle are separated from the preexisting follicles by a hairless circular. We analysed the differentially expressed proteins between inner and outer area of scar at post-wound day 15 by iTRAQ technology.
2021-09-08 | PXD012868 | Pride
Project description:The homeostasis of both cornea and hair follicles depends on a constant supply of progeny cells produced by populations of keratin (K) 14-expressing stem cells localized in specific niches. To investigate the potential role of Co-factors of LIM domains (Clims) in such tissues, we generated transgenic mice expressing a dominant-negative Clim molecule (DN-Clim) under the control of the K14 promoter. As expected, the K14 promoter directed high level expression of the transgene to the basal cells of cornea and epidermis, as well as the outer root sheath of hair follicles. In corneal epithelium, the transgene expression causes decreased expression of adhesion molecule BP180 and defective hemidesmosomes, leading to detachment of corneal epithelium from the underlying stroma, which in turn causes blisters, wounds and an inflammatory response. After a period of epithelial thinning, the corneal epithelium undergoes differentiation to an epidermis-like structure. The K14-DN-Clim mice also develop progressive hair loss due to dysfunctional hair follicles that fail to generate hair shafts. The number of hair follicle stem cells is decreased by at least 50% in K14-DN-Clim mice, indicating that Clims are required for hair follicle stem cell maintenance. We hypothesize that Clim2 is an essential co-factor for the LIM homeodomain factor Lhx2, which was previously shown to play a role in hair follicle stem cell maintenance. Together, these data indicate that Clim proteins play important roles in the homeostasis of corneal epithelium and hair follicles. Experiment Overall Design: We profiled mRNA expression in mouse back skin from 3 time points, representing the initial hair follicle morphogenesis (P6 and P14) and the first telogen (P23); hair growth is synchronized during these time points. For each time point, RNA was isolated and analyzed from 3 to 5 transgenic mice and same number of wild-type littermates.
2008-06-16 | E-GEOD-8227 | biostudies-arrayexpress