Faculty Opinions recommendation of Inflammatory memory sensitizes skin epithelial stem cells to tissue damage.

2017 ◽  
Author(s):  
Suzanne Watt
Keyword(s):  
Stem Cells ◽  
Tissue Damage ◽  
Epithelial Stem Cells

scholarly journals Type 3 innate lymphoid cells maintain intestinal epithelial stem cells after tissue damage

2015 ◽  
Vol 212 (11) ◽  
pp. 1783-1791 ◽  
Author(s):  
Patricia Aparicio-Domingo ◽  
Monica Romera-Hernandez ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
Natalie Papazian ◽  
...  
Keyword(s):  
Stem Cells ◽  
Tissue Damage ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Intestinal Damage ◽  
Intestinal Epithelial ◽  
Epithelial Stem Cells ◽  
Intestinal Tissue ◽  
Mucosal Surfaces ◽  
Type 3

Disruption of the intestinal epithelial barrier allows bacterial translocation and predisposes to destructive inflammation. To ensure proper barrier composition, crypt-residing stem cells continuously proliferate and replenish all intestinal epithelial cells within days. As a consequence of this high mitotic activity, mucosal surfaces are frequently targeted by anticancer therapies, leading to dose-limiting side effects. The cellular mechanisms that control tissue protection and mucosal healing in response to intestinal damage remain poorly understood. Type 3 innate lymphoid cells (ILC3s) are regulators of homeostasis and tissue responses to infection at mucosal surfaces. We now demonstrate that ILC3s are required for epithelial activation and proliferation in response to small intestinal tissue damage induced by the chemotherapeutic agent methotrexate. Multiple subsets of ILC3s are activated after intestinal tissue damage, and in the absence of ILC3s, epithelial activation is lost, correlating with increased pathology and severe damage to the intestinal crypts. Using ILC3-deficient Lgr5 reporter mice, we show that maintenance of intestinal stem cells after damage is severely impaired in the absence of ILC3s or the ILC3 signature cytokine IL-22. These data unveil a novel function of ILC3s in limiting tissue damage by preserving tissue-specific stem cells.

scholarly journals Type 3 innate lymphoid cells maintain intestinal epithelial stem cells after tissue damage

2015 ◽  
Vol 210 (7) ◽  
pp. 2107OIA193
Author(s):  
Patricia Aparicio-Domingo ◽  
Monica Romera-Hernandez ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
Natalie Papazian ◽  
...  
Keyword(s):  
Stem Cells ◽  
Tissue Damage ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Intestinal Epithelial ◽  
Epithelial Stem Cells ◽  
Type 3

scholarly journals YAP and TAZ in epithelial stem cells: A sensor for cell polarity, mechanical forces and tissue damage

BioEssays ◽  
2016 ◽  
Vol 38 (7) ◽  
pp. 644-653 ◽  
Author(s):  
Ahmed Elbediwy ◽  
Zoé I. Vincent‐Mistiaen ◽  
Barry J. Thompson
Keyword(s):  
Stem Cells ◽  
Cell Polarity ◽  
Tissue Damage ◽  
Mechanical Forces ◽  
Epithelial Stem Cells

scholarly journals Author Correction: Inflammatory memory sensitizes skin epithelial stem cells to tissue damage

Nature ◽  
2018 ◽  
Vol 560 (7716) ◽  
pp. E2-E2 ◽  
Author(s):  
Shruti Naik ◽  
Samantha B. Larsen ◽  
Nicholas C. Gomez ◽  
Kirill Alaverdyan ◽  
Ataman Sendoel ◽  
...  
Keyword(s):  
Stem Cells ◽  
Tissue Damage ◽  
Epithelial Stem Cells

scholarly journals Inflammatory memory sensitizes skin epithelial stem cells to tissue damage

Nature ◽  
2017 ◽  
Vol 550 (7677) ◽  
pp. 475-480 ◽  
Author(s):  
Shruti Naik ◽  
Samantha B. Larsen ◽  
Nicholas C. Gomez ◽  
Kirill Alaverdyan ◽  
Ataman Sendoel ◽  
...  
Keyword(s):  
Stem Cells ◽  
Tissue Damage ◽  
Epithelial Stem Cells

A common mechanism links activities of butyrate in the colon

2017 ◽  
Author(s):  
Mohit S. Verma ◽  
Michael J. Fink ◽  
Gabriel L Salmon ◽  
Nadine Fornelos ◽  
Takahiro E. Ohara ◽  
...  
Keyword(s):  
Stem Cells ◽  
Histone Deacetylases ◽  
Biological Activities ◽  
Short Chain Fatty Acids ◽  
Common Mechanism ◽  
Epithelial Stem Cells ◽  
Degree Of Unsaturation ◽  
Structure Activity ◽  
Starting Point ◽  
New Compounds

Two biological activities of butyrate in the colon (suppression of proliferation of colonic epithelial stem cells and inflammation) correlate with inhibition of histone deacetylases. Cellular and biochemical studies of molecules similar in structure to butyrate, but different in molecular details (functional groups, chain-length, deuteration, oxidation level, fluorination, or degree of unsaturation) demonstrated that these activities were sensitive to molecular structure, and were compatible with the hypothesis that butyrate acts by binding to the Zn<sup>2+</sup> in the catalytic site of histone deacetylases. Structure-activity relationships drawn from a set of 36 compounds offer a starting point for the design of new compounds targeting the inhibition of histone deacetylases. The observation that butyrate was more potent than other short-chain fatty acids is compatible with the hypothesis that crypts evolved (at least in part), to separate stem cells at the base of crypts from butyrate produced by commensal bacteria.

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