scholarly journals Direct control of somatic stem cell proliferation by the Drosophila testis stem cell niche

2017 ◽  
Author(s):  
Eugene A. Albert ◽  
Olga A. Puretskaia ◽  
Nadezhda V. Terekhanova ◽  
Christian Bökel
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Cell Fate ◽  
Hippo Pathway ◽  
Tumour Suppressor Genes ◽  
Multiple Systems ◽  
Stem Cell Proliferation ◽  
Individual Aspect ◽  
Fate Decision

AbstractNiches have traditionally been characterized as signalling microenvironments that allow stem cells to maintain their fate. This definition implicitly assumes that the various niche signals are integrated towards a binary fate decision between stemness and differentiation. However, observations in multiple systems have demonstrated that stem cell properties such as proliferation and self renewal can be uncoupled at the level of niche signalling input, which is incompatible with this simplified view. We have studied the role of the transcriptional regulator Zfh1, a shared target of the Hedgehog and Jak/Stat niche signalling pathways, in the somatic stem cells of the Drosophila testis. We found that Zfh1 binds and downregulates salvador and kibra, two tumour suppressor genes of the Hippo/Wts/Yki pathway, thereby restricting Yki activation and proliferation to the Zfh1 positive stem cells. These observations provide an unbroken link from niche signal input to an individual aspect of stem cell behaviour that does not, at any step, involve a fate decision. We discuss the relevance of our observations and other reports in the literature for an overall concept of stemness and niche function.Summary statementWe demonstrate that the fly testis niche controls stem cell proliferation by repressing Hippo pathway genes independent of a binary cell fate decision between stemness and proliferation.

scholarly journals Mitochondria regulate intestinal stem cell proliferation and epithelial homeostasis through FOXO

2020 ◽  
Vol 31 (14) ◽  
pp. 1538-1549
Author(s):  
Fan Zhang ◽  
Mehdi Pirooznia ◽  
Hong Xu
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Stem Cell ◽  
Electron Transport Chain ◽  
Intestinal Stem Cell ◽  
Stem Cell Proliferation ◽  
Epithelial Homeostasis ◽  
Chain Complexes ◽  
Transport Chain

Deficiencies in electron transport chain complexes increase the activity of FOXO transcription factor in Drosophila midgut stem cells, which impairs stem cell proliferation and enterocyte specification.

EVALUATION OF HERBAL EXTRACTS SYNERGISTIC ACTIVITY USING TISSUE STEM CELLS

INDIAN DRUGS ◽  
2017 ◽  
Vol 54 (02) ◽  
pp. 73-75
Author(s):  
S. Priya ◽  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Stem Cell ◽  
System Analysis ◽  
Cultured Cells ◽  
Well Being ◽  
Ocimum Sanctum ◽  
Synergistic Activity ◽  
Stem Cell Proliferation ◽  
Cell Proliferation And Differentiation

Herbal stem cell therapy promotes endogenous stem cell proliferation and differentiation and is ued in the treatment of various human diseases. At present, recommendations are warranted to support the consumption of foods rich in bioactive components. Stem cells and progenitor cells from organs form the basis for well-being of the mammalian system. Analysis based on these cultured cells would form a viable alternative to stem cell transplantation, and would facilitate to design approaches that stimulate endogenous stem cells through diet to promote healing and regeneration. In the present study, synergistic activity of selected herbs such as Phyllanthus amarus, Myristica fragrans, Ocimum sanctum and Withania somnifera were analysed for their stem cell proliferation enhancing activity using goat bone marrow derived stem cells.

scholarly journals Microfluidic Enrichment of Mouse Epidermal Stem Cells and Validation of Stem Cell Proliferation In Vitro

2013 ◽  
Vol 19 (10) ◽  
pp. 765-773 ◽  
Author(s):  
Beili Zhu ◽  
James Smith ◽  
Martin L. Yarmush ◽  
Yaakov Nahmias ◽  
Brian J. Kirby ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Epidermal Stem Cells ◽  
Stem Cell Proliferation ◽  
Proliferation In Vitro

Excessive Hematopoietic Stem Cell Proliferation Leads to Chromosomal Instability

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4772-4772
Author(s):  
Liliana Souza ◽  
Natalyn Hawk ◽  
Sweta Sengupta ◽  
Carlos Cabrera ◽  
Morgan L. McLemore
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Chromosomal Instability ◽  
Wild Type ◽  
Dna Breaks ◽  
Hematopoietic Stem ◽  
Stem Cell Proliferation ◽  
Double Stranded Dna

Abstract Truncation mutations in the granulocyte colony stimulating factor receptor (G-CSFR), common in severe congenital neutropenia (SCN), lead to excessive stem cell proliferation in response to G-CSF. These G-CSFR mutants are (at least indirectly) implicated in the progression of these patients to acute leukemia. Since SCN patients require continuous G-CSF treatment throughout their lifespan, we hypothesize that excessive stem cell proliferation can lead to DNA damage. Stem cells are relatively quiescent and rarely enter the cell cycle under normal conditions. During the cell cycle cells generate approximately 5000 single strand DNA lesions per nucleus (Vilenchik and Knudson, 2003). Approximately 1% of these lesions are ultimately converted to double strand DNA breaks (DSBs). Hematopoietic stem cells are found within the Sca+ ckit+ Lin- (KLS) population. Wild type and mice bearing a mutant G-CSFR similar to that found in patients with SCN were treated with G-CSF. After 21 days of treatment with G-CSF (10 ug/kg/day), the KLS population in the bone marrow increased four-fold in wild type mice and eight-fold in mutant mice. We isolated Lin-Sca+ bone marrow cells from these G-CSF treated mice and evaluated for the presence of double stranded DNA breaks by staining with anti-phospho-H2AX by immunofluorescence. H2AX is a histone whose phosphorylated form localizes to the site of double stranded DNA breaks. The results showed that there is an 8-fold increase in the DSB in wild type Lin-Sca+ and 10-fold in mutant Lin-Sca+ when compared to cells from untreated mice. This data suggests that excessive proliferation can contribute to an increase in DSBs in hematopoietic stem cells. Investigation of potential mechanisms contributing to DSB formation are ongoing. Understanding the causes and trends of chromosomal instability would improve our understanding of leukemogenesis and potentially reveal novel treatment strategies.

scholarly journals Interleukin-3-stimulated haemopoietic stem cell proliferation. Evidence for activation of protein kinase C and Na+/H+ exchange without inositol lipid hydrolysis

1988 ◽  
Vol 256 (2) ◽  
pp. 585-592 ◽  
Author(s):  
A D Whetton ◽  
S J Vallance ◽  
P N Monk ◽  
E J Cragoe ◽  
T M Dexter ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Intracellular Ph ◽  
Stem Cell Proliferation ◽  
Interleukin 3 ◽  
Haemopoietic Stem Cell ◽  
Kinase C

Interleukin 3 (IL-3) is an important regulator of haemopoietic stem cell proliferation both in vivo and in vitro. Little is known about the possible mechanisms whereby this growth factor acts on stem cells to stimulate cell survival and proliferation. Here we have investigated the role of intracellular pH and the Na+/H+ antiport in stem cell proliferation using the multipotential IL-3-dependent stem cell line, FDCP-Mix 1. Evidence is presented that IL-3 can stimulate the activation of an amiloride-sensitive Na+/H+ exchange via protein kinase C activation. IL-3-mediated activation of the Na+/H+ exchange is not observed in FDCP-Mix 1 cells where protein kinase C levels have been down-modulated by treatment with phorbol esters. Also the protein kinase C inhibitor H7 can inhibit IL-3-mediated increases in intracellular pH. This activation of Na+/H+ exchange via protein kinase C has been shown to occur with no measurable effects of IL-3 on inositol lipid hydrolysis or on cytosolic Ca2+ levels. Evidence is also presented that this IL-3-stimulated alkalinization acts as a signal for cellular proliferation in stem cells.

scholarly journals The Hippo pathway regulates intestinal stem cell proliferation during Drosophila adult midgut regeneration

Development ◽  
2010 ◽  
Vol 137 (24) ◽  
pp. 4147-4158 ◽  
Author(s):  
R. L. Shaw ◽  
A. Kohlmaier ◽  
C. Polesello ◽  
C. Veelken ◽  
B. A. Edgar ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Hippo Pathway ◽  
Intestinal Stem Cell ◽  
Stem Cell Proliferation ◽  
The Hippo Pathway

scholarly journals TRiC activates the unfolded protein response and protects starved stem cells by modulating energy and lipid metabolism during planarian regeneration

2019 ◽  
Author(s):  
Óscar Gutiérrez-Gutiérrez ◽  
Daniel A. Felix ◽  
Alessandra Salvetti ◽  
Anne Thems ◽  
Stefan Pietsch ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Lipid Metabolism ◽  
Unfolded Protein Response ◽  
Stem Cell Proliferation ◽  
Unfolded Protein ◽  
Cell Genome ◽  
The Unfolded Protein Response ◽  
Protein Response

SummaryFasting protects stem cells and increases stem cell functionality through mechanisms which are not fully understood. Planarians are not only able to regenerate their bodies, but also to stand long periods of starvation by shrinking in size. This adaptation is possible because of a large population of adult stem cells which indefinitely self-renew even under starved conditions and thus confer planarians with immortality. How starved planarians are able to maintain healthy stem cells and to fuel stem cell proliferation allowing regeneration is unknown. Here we found the TCP-1 ring complex (TRiC) to be upregulated in starved stem cells. Down-regulation of TRiC impairs planarian regenerative response by inducing stem cell genome instability, mitotic defects and stem cell death which translates into stem cell exhaustion. This regulation is specific of starvation since feeding planarians prevents the phenotype. Importantly we found that TRiC activates the unfolded protein response (UPR) which allows a convergent regulation of cellular energy and lipid metabolism in starved planarians thus permitting the high energy demanding regenerative mitotic response. We identified a novel mechanism through which starvation protects the somatic stem cell genome allowing for unlimited stem cell proliferation and regeneration.

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