Non-senescent, conventional marker-negative geriatric muscle stem cells identified by new CD63/CD200 markers [scRNA-seq]
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PROVIDER: PRJNA1070639 | ENA |
REPOSITORIES: ENA
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Project description:During aging, the accumulation of senescent cells has a pivotal role in age-related dysfunctions. At geriatric age, the emergence of muscle stem cells (MuSCs) exhibiting senescence markers identified in vitro studies have been reported. However, whether they are in cellular senescence and thus have lost their function is unclear, due to the lack of specific marker for senescent cells. Here, by tracing genetically labeled MuSCs throughout life, we found an unknown MuSC population termed GERI-MuSCs that lost conventional MuSC markers at geriatric age. Although they have several known senescence features, they retain considerable functionalities of in vitro proliferation and in vivo myogenesis, suggesting they are not in cellular senescence. These results highlight the potential discrepancies between aging process in vivo and cellular senescence characterized in vitro. Importantly, we found new markers, CD63 and CD200, inclusive of GERI-MuSCs, which provide a crucial tool for a deeper investigation on in vivo senescence.
2024-12-31 | GSE254476 | GEO
Project description:During aging, the accumulation of senescent cells has a pivotal role in age-related dysfunctions. At geriatric age, the emergence of muscle stem cells (MuSCs) exhibiting senescence markers identified in vitro studies have been reported. However, whether they are in cellular senescence and thus have lost their function is unclear, due to the lack of specific marker for senescent cells. Here, by tracing genetically labeled MuSCs throughout life, we found an unknown MuSC population termed GERI-MuSCs that lost conventional MuSC markers at geriatric age. Although they have several known senescence features, they retain considerable functionalities of in vitro proliferation and in vivo myogenesis, suggesting they are not in cellular senescence. These results highlight the potential discrepancies between aging process in vivo and cellular senescence characterized in vitro. Importantly, we found new markers, CD63 and CD200, inclusive of GERI-MuSCs, which provide a crucial tool for a deeper investigation on in vivo senescence.
2024-12-31 | GSE254475 | GEO
Project description:Non-senescent, conventional marker-negative geriatric muscle stem cells identified by new CD63/CD200 markers
| PRJNA1070635 | ENA
Project description:Non-senescent, conventional marker-negative geriatric muscle stem cells identified by new CD63/CD200 markers [RNA-seq]
| PRJNA1070632 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-12-31 | GSE254477 | GEO
Project description:Mouse back skin was disassociated to single cells, sorted by cell surface markers and tested by microarrray To compare the gene expression of mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+) xx Bald scalp retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells Androgenetic alopecia (AGA) or common baldness results from a marked decrease in hair follicle size. This miniaturization may be related to loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from the same individuals for the presence of hair follicle stem and progenitor cells using flow cytometry to quantitate cells expressing CYTOKERATIN 15 (KRT15), CD200, CD34 and ALPHA-6-INTEGRIN (ITGA6). High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. Cells with the highest level of KRT15 expression were maintained in bald scalp; however, distinct populations of CD200high ITGA6high cells and CD34-positive cells were markedly diminished. Consistent with a progenitor cell phenotype, the diminished populations localized closely to the stem-cell rich bulge area but were larger and more proliferative than the bulge stem cells. In functional assays, analogous CD200 high /Itga6 high cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings suggest that a defect in stem cell activation plays a role in the pathogenesis of AGA. 4 independent biologic replicates (each pooled from 3 distinct mice) were sorted for Mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+)
2011-01-12 | E-GEOD-21568 | biostudies-arrayexpress
Project description:The tetraspanin CD63 is implicated in pro-metastatic signaling pathways, but so far, it is unclear how CD63 levels affect the tumor cell phenotype. Here, we investigated the effect of CD63 modulation in different metastatic tumor cell lines. In vitro, knock down of CD63 induced a more epithelial-like phenotype concomitant with increased E-cadherin expression, downregulation of its repressors Slug and Zeb1, and decreased N-cadherin. In addition, β-catenin protein was markedly reduced, negatively affecting expression of the target genes MMP-2 and PAI-1. β-catenin inhibitors mimicked the epithelial phenotype induced by CD63 knock down. Inhibition of β-catenin upstream regulators PI3K/AKT or GSK3β could rescue the mesenchymal phenotype underlining the importance of the β-catenin pathway in CD63-regulated cell plasticity. CD63 knock down-induced phenotypical changes correlated with a decrease of experimental metastasis, while CD63 overexpression enhanced the tumor cell-intrinsic metastatic potential. Taken together, our data show that CD63 is a crucial player in the regulation of the tumor cell-intrinsic metastatic potential by affecting cell plasticity. Stable knock down of CD63 was performed in SKOV3ipL ovarian carcinoma cell line using 2 shRNAs lentiviral constructs (sh49 and sh51), and as a negative control, a shNT construct. Parental cells, control shNT and the 2 shCD63 cell lines were seeded 24 hours prior to RNA isolation on a 10 cm dish, labelling and hybridization on microarrays. One color experiment with 2 biological replicates of the 4 experimental conditions: SKOV3ipL, SKOV3ipL_shNT, SKOV3ipL_sh49 and SKOV3ipL_sh51.
2015-01-23 | E-GEOD-61957 | biostudies-arrayexpress
Project description:Human hair follicles from normal areas of the scalp were disassociated to single cells, sorted and tested by microarrray To compare the expression of human CD200+ CD49+ hair follicle keratinocytes versus CD200-CD49+ keratinocytes
2011-01-12 | GSE21567 | GEO
Project description:Mouse back skin was disassociated to single cells, sorted by cell surface markers and tested by microarrray To compare the gene expression of mouse bulge (CD34+CD200+CD49+) versus secondary hair germ (CD34-CD200+CD49+) versus interfollicular epidermis (CD34-CD200-CD49+) xx Bald scalp retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells Androgenetic alopecia (AGA) or common baldness results from a marked decrease in hair follicle size. This miniaturization may be related to loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from the same individuals for the presence of hair follicle stem and progenitor cells using flow cytometry to quantitate cells expressing CYTOKERATIN 15 (KRT15), CD200, CD34 and ALPHA-6-INTEGRIN (ITGA6). High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. Cells with the highest level of KRT15 expression were maintained in bald scalp; however, distinct populations of CD200high ITGA6high cells and CD34-positive cells were markedly diminished. Consistent with a progenitor cell phenotype, the diminished populations localized closely to the stem-cell rich bulge area but were larger and more proliferative than the bulge stem cells. In functional assays, analogous CD200 high /Itga6 high cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings suggest that a defect in stem cell activation plays a role in the pathogenesis of AGA.
2011-01-12 | GSE21568 | GEO
Project description:Purpose: Understanding immunosuppression in AML is critical . The goals of this study are to compare the transcriptomics of human CD3+ T cells from humanized mice exposed to CD200+/- AML. Methods: NSG mice were humanized with 10x10^6 healthy PBMCs prior to the introduction of CD200+ or CD200- OCI-AML3 cells. After 10 days, CD3+ T cells were isolated and RNA was sequenced. Results: T cells from mice with CD200+ AML were characterized by an enrichment of T cell activation pathways and a downregulation of numerous metabolic pathways, including OXPHOS and glycolysis. Conclusions: Our results demonstrate, for the first time, that CD200+ AML can directly impair T cell metbolism.
2021-04-24 | GSE173194 | GEO