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  • 1
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    Spatial organization within a niche as a determinant of stem-cell fate (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-10-08
    Description: Stem-cell niches in mammalian tissues are often heterogeneous and compartmentalized; however, whether distinct niche locations determine different stem-cell fates remains unclear. To test this hypothesis, here we use the mouse hair follicle niche and combine intravital microscopy with genetic lineage tracing to re-visit the same stem-cell lineages, from their exact place of origin, throughout regeneration in live mice. Using this method, we show directly that the position of a stem cell within the hair follicle niche can predict whether it is likely to remain uncommitted, generate precursors or commit to a differentiated fate. Furthermore, using laser ablation we demonstrate that hair follicle stem cells are dispensable for regeneration, and that epithelial cells, which do not normally participate in hair growth, re-populate the lost stem-cell compartment and sustain hair regeneration. This study provides a general model for niche-induced fate determination in adult tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895444/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895444/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rompolas, Panteleimon -- Mesa, Kailin R -- Greco, Valentina -- 1R01AR063663-01/AR/NIAMS NIH HHS/ -- R01 AR063663/AR/NIAMS NIH HHS/ -- T32 GM007223/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Oct 24;502(7472):513-8. doi: 10.1038/nature12602. Epub 2013 Oct 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Department of Dermatology, Yale Stem Cell Center, Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24097351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Division ; *Cell Lineage ; Epithelial Cells/cytology ; Hair Follicle/cytology ; Male ; Mice ; Regeneration ; *Stem Cell Niche ; Stem Cells/*cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Niche-induced cell death and epithelial phagocytosis regulate hair follicle stem cell pool (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-04-08
    Description: Tissue homeostasis is achieved through a balance of cell production (growth) and elimination (regression). In contrast to tissue growth, the cells and molecular signals required for tissue regression remain unknown. To investigate physiological tissue regression, we use the mouse hair follicle, which cycles stereotypically between phases of growth and regression while maintaining a pool of stem cells to perpetuate tissue regeneration. Here we show by intravital microscopy in live mice that the regression phase eliminates the majority of the epithelial cells by two distinct mechanisms: terminal differentiation of suprabasal cells and a spatial gradient of apoptosis of basal cells. Furthermore, we demonstrate that basal epithelial cells collectively act as phagocytes to clear dying epithelial neighbours. Through cellular and genetic ablation we show that epithelial cell death is extrinsically induced through transforming growth factor (TGF)-beta activation and mesenchymal crosstalk. Strikingly, our data show that regression acts to reduce the stem cell pool, as inhibition of regression results in excess basal epithelial cells with regenerative abilities. This study identifies the cellular behaviours and molecular mechanisms of regression that counterbalance growth to maintain tissue homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457634/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457634/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mesa, Kailin R -- Rompolas, Panteleimon -- Zito, Giovanni -- Myung, Peggy -- Sun, Thomas Y -- Brown, Samara -- Gonzalez, David G -- Blagoev, Krastan B -- Haberman, Ann M -- Greco, Valentina -- 1R01AR063663-01/AR/NIAMS NIH HHS/ -- 2P50CA121974/CA/NCI NIH HHS/ -- 5 P30 AR053495-07/AR/NIAMS NIH HHS/ -- 5T32 GM007223/GM/NIGMS NIH HHS/ -- K08 AR066790/AR/NIAMS NIH HHS/ -- P30 AR053495/AR/NIAMS NIH HHS/ -- R01 AR063663/AR/NIAMS NIH HHS/ -- T32 GM007223/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Jun 4;522(7554):94-7. doi: 10.1038/nature14306. Epub 2015 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA. ; Department of Biopathology and Medical Biotechnology, University of Palermo, via Divisi 83, 90100 Palermo, Italy. ; 1] Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA [2] Department of Dermatology, Yale School of Medicine, New Haven, Connecticut 06510, USA. ; Department of Laboratory Medicine, Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut 06510, USA. ; 1] National Science Foundation, Arlington, Virginia 22230, USA [2] AA Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. ; 1] Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA [2] Department of Dermatology, Yale School of Medicine, New Haven, Connecticut 06510, USA [3] Yale Stem Cell Center, Yale School of Medicine, New Haven, Connecticut 06510, USA [4] Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25849774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *Cell Death ; Dermis/cytology/metabolism ; Epithelial Cells/*cytology/metabolism ; Hair Follicle/*cytology/metabolism ; Homeostasis ; Mice ; Phagocytes/cytology ; *Phagocytosis ; Regeneration ; Signal Transduction ; Stem Cell Niche/*physiology ; Stem Cells/*cytology/metabolism ; Transforming Growth Factor beta/metabolism ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Live imaging of stem cell and progeny behaviour in physiological hair-follicle regeneration (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-07-06
    Description: Tissue development and regeneration depend on cell-cell interactions and signals that target stem cells and their immediate progeny. However, the cellular behaviours that lead to a properly regenerated tissue are not well understood. Using a new, non-invasive, intravital two-photon imaging approach we study physiological hair-follicle regeneration over time in live mice. By these means we have monitored the behaviour of epithelial stem cells and their progeny during physiological hair regeneration and addressed how the mesenchyme influences their behaviour. Consistent with earlier studies, stem cells are quiescent during the initial stages of hair regeneration, whereas the progeny are more actively dividing. Moreover, stem cell progeny divisions are spatially organized within follicles. In addition to cell divisions, coordinated cell movements of the progeny allow the rapid expansion of the hair follicle. Finally, we show the requirement of the mesenchyme for hair regeneration through targeted cell ablation and long-term tracking of live hair follicles. Thus, we have established an in vivo approach that has led to the direct observation of cellular mechanisms of growth regulation within the hair follicle and that has enabled us to precisely investigate functional requirements of hair-follicle components during the process of physiological regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772651/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772651/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rompolas, Panteleimon -- Deschene, Elizabeth R -- Zito, Giovanni -- Gonzalez, David G -- Saotome, Ichiko -- Haberman, Ann M -- Greco, Valentina -- P30 AR053495/AR/NIAMS NIH HHS/ -- P30AR053495/AR/NIAMS NIH HHS/ -- R01 AR063663/AR/NIAMS NIH HHS/ -- T32 GM007223/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Jul 26;487(7408):496-9. doi: 10.1038/nature11218.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Movement ; Cell Survival ; Cell Tracking ; Dermis/cytology ; Hair Follicle/*cytology ; Laser Therapy ; Mesoderm/cytology ; Mice ; Mice, Transgenic ; Microscopy, Fluorescence, Multiphoton ; Regeneration/*physiology ; Stem Cells/*cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    beta-Catenin activation regulates tissue growth non-cell autonomously in the hair stem cell niche (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-03-22
    Description: Wnt/beta-catenin signaling is critical for tissue regeneration. However, it is unclear how beta-catenin controls stem cell behaviors to coordinate organized growth. Using live imaging, we show that activation of beta-catenin specifically within mouse hair follicle stem cells generates new hair growth through oriented cell divisions and cellular displacement. beta-Catenin activation is sufficient to induce hair growth independently of mesenchymal dermal papilla niche signals normally required for hair regeneration. Wild-type cells are co-opted into new hair growths by beta-catenin mutant cells, which non-cell autonomously activate Wnt signaling within the neighboring wild-type cells via Wnt ligands. This study demonstrates a mechanism by which Wnt/beta-catenin signaling controls stem cell-dependent tissue growth non-cell autonomously and advances our understanding of the mechanisms that drive coordinated regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096864/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096864/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deschene, Elizabeth R -- Myung, Peggy -- Rompolas, Panteleimon -- Zito, Giovanni -- Sun, Thomas Yang -- Taketo, Makoto M -- Saotome, Ichiko -- Greco, Valentina -- 1R01AR063663-01/AR/NIAMS NIH HHS/ -- 2P50CA121974/CA/NCI NIH HHS/ -- 5P30 AR053495-07/AR/NIAMS NIH HHS/ -- K08 AR066790/AR/NIAMS NIH HHS/ -- P30 CA016359/CA/NCI NIH HHS/ -- P50 CA121974/CA/NCI NIH HHS/ -- R01 AR063663/AR/NIAMS NIH HHS/ -- T32 GM007223/GM/NIGMS NIH HHS/ -- TG32 GM007223/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1353-6. doi: 10.1126/science.1248373.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale Stem Cell Center, Yale Cancer Center, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24653033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Hair/*growth & development ; Hair Follicle/*cytology/*metabolism ; Ligands ; Mice ; Models, Biological ; Mutation ; Stem Cell Niche ; Stem Cells/cytology/*metabolism ; Tamoxifen/pharmacology ; Up-Regulation ; Wnt Proteins/genetics/metabolism ; *Wnt Signaling Pathway ; beta Catenin/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Dermal sheath contraction powers stem cell niche relocation during hair cycle regression (2019)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2019
    Description: 〈p〉Tissue homeostasis requires the balance of growth by cell production and regression through cell loss. In the hair cycle during follicle regression, the niche traverses the skin through an unknown mechanism to reach the stem cell reservoir and trigger new growth. Here we identify the dermal sheath that lines the follicle as the key driver of tissue regression and niche relocation via the smooth muscle contractile machinery that generates centripetal constriction force. We reveal that the calcium/calmodulin/myosin light chain kinase pathway controls sheath contraction. When this pathway is blocked, sheath contraction is inhibited, impeding follicle regression and niche relocation. Thus, our study identifies the dermal sheath as smooth muscle that drives follicle regression for reuniting niche and stem cells in order to regenerate tissue structure during homeostasis.〈/p〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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