scholarly journals Isolation and Culture of Dental Epithelial Stem Cells from the Adult Mouse Incisor

10.3791/51266 ◽  
2014 ◽  
Author(s):  
Miquella G. Chavez ◽  
Jimmy Hu ◽  
Kerstin Seidel ◽  
Chunying Li ◽  
Andrew Jheon ◽  
...  
Keyword(s):  
Stem Cells ◽  
Adult Mouse ◽  
Epithelial Stem Cells ◽  
Mouse Incisor

Notch signalling is required for the survival of epithelial stem cells in the continuously growing mouse incisor

2010 ◽  
Vol 80 (4-5) ◽  
pp. 241-248 ◽  
Author(s):  
Szabolcs Felszeghy ◽  
Marika Suomalainen ◽  
Irma Thesleff
Keyword(s):  
Stem Cells ◽  
Notch Signalling ◽  
Epithelial Stem Cells ◽  
Mouse Incisor

scholarly journals Characterization of Dental Epithelial Stem Cells from the Mouse Incisor with Two-Dimensional and Three-Dimensional Platforms

2013 ◽  
Vol 19 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Miquella G. Chavez ◽  
Wenli Yu ◽  
Brian Biehs ◽  
Hidemitsu Harada ◽  
Malcolm L. Snead ◽  
...  
Keyword(s):  
Stem Cells ◽  
Three Dimensional ◽  
Two Dimensional ◽  
Epithelial Stem Cells ◽  
Mouse Incisor

scholarly journals Resolving stem and progenitor cells in the adult mouse incisor through gene co-expression analysis

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Kerstin Seidel ◽  
Pauline Marangoni ◽  
Cynthia Tang ◽  
Bahar Houshmand ◽  
Wen Du ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Expression Analysis ◽  
Adult Mouse ◽  
Deep Understanding ◽  
Lineage Tracing ◽  
Differentiated Cells ◽  
Mouse Incisor ◽  
Stem Cell Niches

Investigations into stem cell-fueled renewal of an organ benefit from an inventory of cell type-specific markers and a deep understanding of the cellular diversity within stem cell niches. Using the adult mouse incisor as a model for a continuously renewing organ, we performed an unbiased analysis of gene co-expression relationships to identify modules of co-expressed genes that represent differentiated cells, transit-amplifying cells, and residents of stem cell niches. Through in vivo lineage tracing, we demonstrated the power of this approach by showing that co-expression module members Lrig1 and Igfbp5 define populations of incisor epithelial and mesenchymal stem cells. We further discovered that two adjacent mesenchymal tissues, the periodontium and dental pulp, are maintained by distinct pools of stem cells. These findings reveal novel mechanisms of incisor renewal and illustrate how gene co-expression analysis of intact biological systems can provide insights into the transcriptional basis of cellular identity.

scholarly journals Localization of Putative Stem Cells in Dental Epithelium and Their Association with Notch and Fgf Signaling

1999 ◽  
Vol 147 (1) ◽  
pp. 105-120 ◽  
Author(s):  
Hidemitsu Harada ◽  
Päivi Kettunen ◽  
Han-Sung Jung ◽  
Tuija Mustonen ◽  
Y. Alan Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Cell Lineage ◽  
Fgf Signaling ◽  
Epithelial Stem Cells ◽  
Lunatic Fringe ◽  
Reticulum Cells ◽  
Stellate Reticulum ◽  
Mouse Incisor ◽  
Basal Epithelial Cells

The continuously growing mouse incisor is an excellent model to analyze the mechanisms for stem cell lineage. We designed an organ culture method for the apical end of the incisor and analyzed the epithelial cell lineage by 5-bromo-2′-deoxyuridine and DiI labeling. Our results indicate that stem cells reside in the cervical loop epithelium consisting of a central core of stellate reticulum cells surrounded by a layer of basal epithelial cells, and that they give rise to transit-amplifying progeny differentiating into enamel forming ameloblasts. We identified slowly dividing cells among the Notch1-expressing stellate reticulum cells in specific locations near the basal epithelial cells expressing lunatic fringe, a secretory molecule modulating Notch signaling. It is known from tissue recombination studies that in the mouse incisor the mesenchyme regulates the continuous growth of epithelium. Expression of Fgf-3 and Fgf-10 were restricted to the mesenchyme underlying the basal epithelial cells and the transit-amplifying cells expressing their receptors Fgfr1b and Fgfr2b. When FGF-10 protein was applied with beads on the cultured cervical loop epithelium it stimulated cell proliferation as well as expression of lunatic fringe. We present a model in which FGF signaling from the mesenchyme regulates the Notch pathway in dental epithelial stem cells via stimulation of lunatic fringe expression and, thereby, has a central role in coupling the mitogenesis and fate decision of stem cells.

scholarly journals Senescence of alveolar stem cells drives progressive pulmonary fibrosis

2019 ◽  
Author(s):  
Changfu Yao ◽  
Xiangrong Guan ◽  
Gianni Carraro ◽  
Tanyalak Parimon ◽  
Xue Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Chronic Disease ◽  
Pulmonary Fibrosis ◽  
Cellular Senescence ◽  
Adult Mouse ◽  
Alveolar Type ◽  
Epithelial Stem Cells ◽  
Organ Function ◽  
P53 Activation

AbstractTissue fibrosis is a common pathological outcome of chronic disease that markedly impairs organ function leading to morbidity and mortality. In the lung, idiopathic pulmonary fibrosis (IPF) is an insidious and fatal interstitial lung disease associated with declining pulmonary function. Here, we show that alveolar type 2 (AT2) stem cells isolated from IPF lung tissue exhibit characteristic transcriptomic features of cellular senescence. We used conditional loss of Sin3a in adult mouse AT2 cells to initiate a program of p53-dependent cellular senescence, AT2 cell depletion, and spontaneous, progressive pulmonary fibrosis. We establish that senescence rather than loss of epithelial stem cells serves as a proximal driver of Tgfβ activation and progressive fibrosis and show that either genetic or pharmacologic interventions targeting p53 activation, senescence, or downstream Tgfβ activation, block fibrogenesis.

scholarly journals In vivo administration of dental epithelial stem cells at the apical end of the mouse incisor

2015 ◽  
Vol 6 ◽  
Author(s):  
Giovanna Orsini ◽  
Lucia Jimenez-Rojo ◽  
Despoina Natsiou ◽  
Angelo Putignano ◽  
Thimios A. Mitsiadis
Keyword(s):  
Stem Cells ◽  
Epithelial Stem Cells ◽  
Mouse Incisor ◽  
In Vivo Administration

scholarly journals E-cadherin regulates the behavior and fate of epithelial stem cells and their progeny in the mouse incisor

2012 ◽  
Vol 366 (2) ◽  
pp. 357-366 ◽  
Author(s):  
Chun-Ying Li ◽  
Wanghee Cha ◽  
Hans-Ulrich Luder ◽  
Roch-Philippe Charles ◽  
Martin McMahon ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Stem Cells ◽  
Mouse Incisor ◽  
E Cadherin

scholarly journals Arid1a regulates cell cycle exit of transit-amplifying cells by inhibiting the Aurka-Cdk1 axis in mouse incisor

Development ◽  
2021 ◽  
Vol 148 (8) ◽  
Author(s):  
Jiahui Du ◽  
Junjun Jing ◽  
Shuo Chen ◽  
Yuan Yuan ◽  
Jifan Feng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adult Mouse ◽  
Cell Types ◽  
Tissue Homeostasis ◽  
Cell Cycle Exit ◽  
Core Component ◽  
Mouse Incisor

ABSTRACT Stem cells self-renew or give rise to transit-amplifying cells (TACs) that differentiate into specific functional cell types. The fate determination of stem cells to TACs and their transition to fully differentiated progeny is precisely regulated to maintain tissue homeostasis. Arid1a, a core component of the switch/sucrose nonfermentable complex, performs epigenetic regulation of stage- and tissue-specific genes that is indispensable for stem cell homeostasis and differentiation. However, the functional mechanism of Arid1a in the fate commitment of mesenchymal stem cells (MSCs) and their progeny is not clear. Using the continuously growing adult mouse incisor model, we show that Arid1a maintains tissue homeostasis through limiting proliferation, promoting cell cycle exit and differentiation of TACs by inhibiting the Aurka-Cdk1 axis. Loss of Arid1a overactivates the Aurka-Cdk1 axis, leading to expansion of the mitotic TAC population but compromising their differentiation ability. Furthermore, the defective homeostasis after loss of Arid1a ultimately leads to reduction of the MSC population. These findings reveal the functional significance of Arid1a in regulating the fate of TACs and their interaction with MSCs to maintain tissue homeostasis.

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