Integrin-dependent anchoring of a stem-cell niche

Tanentzapf, Guy; Devenport, Danelle; Godt, Dorothea; Brown, Nicholas H.

doi:10.1038/ncb1660

Cited by 200 publications

(245 citation statements)

References 29 publications

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“…In this, they may be analogous to the hub cells present in the Drosophila gonadal niches where cell-cell interaction between hub and stem cell are required to maintain the latter in an undifferentiated state, in the SEZ providing signals that cannot be transmitted via the basal process [18,19]. However, our observations do not argue against conclusions from recent experimental work that the vasculature plays a critical role in supporting stem/ precursor cell proliferation [4][5][6].…”

Section: Kazanis and Ffrench-constantcontrasting

confidence: 56%

The Number of Stem Cells in the Subependymal Zone of the Adult Rodent Brain is Correlated with the Number of Ependymal Cells and Not with the Volume of the Niche

Kazanis

ffrench‐Constant

2012

Stem Cells and Development

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2The mammalian subependymal zone (SEZ; often called subventricular) situated at the lateral walls of the lateral ventricles of the brain contains a pool of relatively quiescent adult neural stem cells whose neurogenic activity persists throughout life. These stem cells are positioned in close proximity both to the ependymal cells that provide the cerebrospinal fluid interface and to the blood vessel endothelial cells, but the relative contribution of these 2 cell types to stem cell regulation remains undetermined. Here, we address this question by analyzing a naturally occurring example of volumetric scaling of the SEZ in a comparison of the mouse SEZ with the larger rat SEZ. Our analysis reveals that the number of stem cells in the SEZ niche is correlated with the number of ependymal cells rather than with the volume, thereby indicating the importance of ependymal-derived factors in the formation and function of the SEZ. The elucidation of the factors generated by ependymal cells that regulate stem cell numbers within the SEZ is, therefore, of importance for stem cell biology and regenerative neuroscience.

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Section: Kazanis and Ffrench-constantcontrasting

confidence: 56%

The Number of Stem Cells in the Subependymal Zone of the Adult Rodent Brain is Correlated with the Number of Ependymal Cells and Not with the Volume of the Niche

Kazanis

ffrench‐Constant

2012

Stem Cells and Development

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“…46 Fourth, lack of ␤1 integrin in Drosophila melanogaster gonad stem cells damages the stem cell niche. 47 Our study also showed decreased expression of several other stem cell markers (cytokeratin 15 and ␣6 integrin) in KS skin. Taken together, the data raise the possibility that defective or absent FFH1 may be linked to an epidermal stem cell defect.…”

Section: Discussionmentioning

confidence: 63%

Loss-of-Function FERMT1 Mutations in Kindler Syndrome Implicate a Role for Fermitin Family Homolog-1 in Integrin Activation

Lai-Cheong

Parsons

Tanaka

et al. 2009

The American Journal of Pathology

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Kindler syndrome is an autosomal recessive disorder characterized by skin atrophy and blistering. It results from loss-of-function mutations in the FERMT1 gene encoding the focal adhesion protein, fermitin family homolog-1. How and why deficiency of fermitin family homolog-1 results in skin atrophy and blistering are unclear. In this study, we investigated the epidermal basement membrane and keratinocyte biology abnormalities in Kindler syndrome. We identified altered distribution of several basement membrane proteins, including types IV, VII, and XVII collagens and laminin-332 in Kindler syndrome skin. In addition, reduced immunolabeling intensity of epidermal cell markers such as ␤1 and ␣6 integrins and cytokeratin 15 was noted. At the cellular level, there was loss of ␤4 integrin immunolocalization and random distribution of laminin-332 in Kindler syndrome keratinocytes. Of note, active ␤1 integrin was reduced but overexpression of fermitin family homolog-1 restored integrin activation and partially rescued the Kindler syndrome cellular phenotype. This study provides evidence that fermitin family homolog-1 is implicated in integrin activation and demonstrates that lack of this protein leads to pathological changes be- Kindler syndrome (KS; OMIM 173650) is a rare autosomal recessive disorder characterized by trauma-induced skin blistering, skin atrophy, and poikiloderma.1 KS results from pathogenic mutations in the FERMT1 (formerly KIND1 or C20orf42) gene that encodes fermitin family homolog-1 (FFH1) (formerly kindlin-1 or kindlerin), an actin cytoskeleton and focal adhesion-associated molecule.2,3 FFH1 is mainly expressed in basal keratinocytes. [3][4][5][6] In KS, however, there is often a complete absence of FFH1 protein expression, although some variability may occur. 6 Thus far, 37 different loss-of-function FERMT1 mutations have been identified. 7-9 The mechanism by which these pathogenic FERMT1 mutations result in skin atrophy and blistering, however, remains unclear. Indeed, insight from studies on KS skin and FFH1 has been limited. Ultrastructural and immunohistochemical studies on KS skin have revealed a disrupted and reduplicated cutaneous basement membrane, 4,10 -16 and silencing of FFH1 in HaCaT cells results in reduced cell adhesion, proliferation, and spreading. 17 In addition, cultured KS keratinocytes display decreased cell adhesion and proliferation and exhibit multiple cell polarities

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“…In monolayer, provision of a free surface may act as an injury response to initiate cell division, whereas 3D culture might provide equivalent signals on all cell surfaces. β 1 -Integrin signals are important for maintaining the architecture of the niche and also for establishing the orientation of cell division [28,42,43]. Asymmetric divisions are important to control maintenance or exit from the niche, and it is likely that monolayer culture provides an exit signal while 3D provides a maintenance signal.…”

Section: Discussionmentioning

confidence: 99%

Modeling the Prostate Stem Cell Niche: An Evaluation of Stem Cell Survival and Expansion In Vitro

Lang

Anderson

Fordham

et al. 2010

Stem Cells and Development

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Integrin-dependent anchoring of a stem-cell niche

Cited by 200 publications

References 29 publications

The Number of Stem Cells in the Subependymal Zone of the Adult Rodent Brain is Correlated with the Number of Ependymal Cells and Not with the Volume of the Niche

The Number of Stem Cells in the Subependymal Zone of the Adult Rodent Brain is Correlated with the Number of Ependymal Cells and Not with the Volume of the Niche

Loss-of-Function FERMT1 Mutations in Kindler Syndrome Implicate a Role for Fermitin Family Homolog-1 in Integrin Activation

Modeling the Prostate Stem Cell Niche: An Evaluation of Stem Cell Survival and Expansion In Vitro

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