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Gene expression profile of hair follicle stem cells (HFSCs) isolated from wild type and homozygous Dab2 cKO (Dab2 Fl/Fl) mice at postnatal day 35

ABSTRACT: Disabled 2 is an endocytic adaptor protein known to regulate various signaling pathways such Wnt , BMP, TGF and Ras/MAPK. In the present study, we observed that Dab2 is expressed in all the compartments of the hair follicle. K14 Cre specific homozygous Dab2 knockout resulted in delayed activation of HFSCs and delayed Ist hair follicle cycle initiation. At PD35, while WT progresses to anagen II, the Dab2 cKO mice still remains at telogen. In addition, loss of Dab2 alos led to reduced HFSCs pool extended quiescence, and reduced self renewal capacity of HFSCs at PD35. We performed expression profiling of HFSCs isolated from WT and Dab2 cKO mice at PD35 to check for the differentially regulated genes involved in HFSCs activation. The expression analysis helped us to elucidate the detailed molecular mechanisms involved in Dab2 mediated regulation of HFSCs activation and quiescence.

ORGANISM(S): Mus musculus

PROVIDER: GSE250300 | GEO | 2024/03/01

REPOSITORIES: GEO

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Gene expression profile of hair follicle stem cells (HFSCs) isolated from wild type and homozygous Dab2 cKO (Dab2 Fl/Fl) mice at postnatal day 68

Project description:Disabled 2 is an endocytic adaptor protein known to regulate various signaling pathways such Wnt , BMP, TGF and Ras/MAPK. In the present study, we observed that Dab2 is expressed in all the compartments of the hair follicle. K14 Cre specific homozygous Dab2 knockout resulted in delayed activation of HFSCs and delayed Ist hair follicle cycle initiation. At PD68, both WT and Dab2 cKO mice were at telogen. In addition, loss of Dab2 also led to reduced HFSCs pool extended quiescence, and reduced self renewal capacity of HFSCs at PD68. We performed expression profiling of HFSCs isolated from WT and Dab2 cKO mice at PD68 to check for the differentially regulated genes involved in HFSCs activation. The expression analysis helped us to elucidate the detailed molecular mechanisms involved in Dab2 mediated regulation of HFSCs activation and quiescence.

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Foxc1 reinforces quiescence in hair follicle stem cells

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2016-02-05 | E-GEOD-67404 | biostudies-arrayexpress

Stem cell quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors

Project description:In many organs, adult stem cells are uniquely poised to serve as cancer cells of origin. In the epidermis, hair follicle stem cells (HFSCs) cycle through stages of quiescence (telogen) and proliferation (anagen) to drive hair growth. Within the hair follicle, HFSCs are capable of initiating squamous cell carcinoma, yet it is unclear how the hair cycle contributes to tumorigenesis. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to gain of oncogenes (Ras) or loss of tumor suppressors (p53). Instead, prolonged oncogenic stimuli only exert their effects when HFSC quiescence mechanisms are removed by normal HFSC activation. Furthermore, Pten activity is necessary for quiescence based tumor suppression, since Pten deletion alleviates this stem cell specific ability without affecting proliferation per se. Small RNAs were cloned from Trizol-lysed cells sorted from mouse skin and sequenced with the Illumina HiSeq2000.

2013-10-28 | E-GEOD-51765 | biostudies-arrayexpress

Stem cell quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors

2013-10-28 | GSE51765 | GEO

Stem Cell Quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors

2013-10-30 | GSE51635 | GEO

Stem Cell Quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors

Project description:In some organs, adult stem cells are uniquely poised to serve as cancer cells of origin1-4. It is unclear, however, whether tumorigenesis is influenced by the activation state of the adult stem cell. Hair follicle stem cells (HFSCs) act as cancer cells of origin for cutaneous squamous cell carcinoma (SCC) and undergo defined cycles of quiescence and activation. The data presented here show that HFSCs are unable to initiate tumors during the quiescent phase of the hair cycle, indicating that the mechanisms that keep HFSCs dormant are dominant to the gain of oncogenes (Ras) or the loss of tumor suppressors (p53). Furthermore, Pten activity is necessary for quiescence based tumor suppression, as its deletion alleviates tumor suppression without affecting proliferation. These data demonstrate that stem cell quiescence is a form of tumor suppression in HFSCs, and that Pten plays a role in maintaining quiescence in the presence of tumorigenic stimuli. This experiment includes RNA profiling of hair follicle stem cells at various stages of tumorigenesis Briefly: HFSCs were lineage traced with YFP allele, FACS isolated from various genotypes, and then profiled by Affymetrix microarray Cell Isolation and FACS: Whole dorsal and ventral mouse K15-CrePR; LSLYFP, K15-CrePR; KrasG12D; LSLYFP and K15-CrePR; KrasG12D; Ptenff; LSLYFP was extracted, diced and digested with collagenase (20mg/ml) for 2 hours at 37C, then an equal volume of .25% trypsin was added and digestion continued for an additional hour at 37C. Digested tissue was mechanically dispersed via pipette and filtered with a 100uM cell strainer, collected at 300g and washed twice with PBS. The cells were then filtered through a 40uM cell strainer and FACS processed. YFP+ and YFP- cell populations were collected in RNA lysis buffer (Stratagene) and stored at -80C. Gene expression profiling Microarray analyses by GeneSpring software were performed

2013-10-30 | E-GEOD-51635 | biostudies-arrayexpress

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