scholarly journals Direct control of somatic stem cell proliferation factors by theDrosophilatestis stem cell niche

Development ◽  
2018 ◽  
Vol 145 (17) ◽  
pp. dev156315 ◽  
Author(s):  
Eugene A. Albert ◽  
Olga A. Puretskaia ◽  
Nadezhda V. Terekhanova ◽  
Anastasia Labudina ◽  
Christian Bökel
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Stem Cell Niche ◽  
Somatic Stem Cell ◽  
Direct Control ◽  
Stem Cell Proliferation ◽  
Cell Niche

scholarly journals Wolbachia Enhance Drosophila Stem Cell Proliferation and Target the Germline Stem Cell Niche

Science ◽  
2011 ◽  
Vol 334 (6058) ◽  
pp. 990-992 ◽  
Author(s):  
E. M. Fast ◽  
M. E. Toomey ◽  
K. Panaram ◽  
D. Desjardins ◽  
E. D. Kolaczyk ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Stem Cell Niche ◽  
Germline Stem Cell ◽  
Stem Cell Proliferation ◽  
Cell Niche ◽  
Germline Stem Cell Niche

Does primary myelofibrosis involve a defective stem cell niche? From concept to evidence

Blood ◽  
2008 ◽  
Vol 112 (8) ◽  
pp. 3026-3035 ◽  
Author(s):  
Jean-Jacques Lataillade ◽  
Olivier Pierre-Louis ◽  
Hans Carl Hasselbalch ◽  
Georges Uzan ◽  
Claude Jasmin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Hematopoietic Stem Cells ◽  
Stem Cell Niche ◽  
Primary Myelofibrosis ◽  
Hematopoietic Stem ◽  
Stem Cell Proliferation ◽  
Cell Niche

Abstract Primary myelofibrosis (PMF) is the rarest and the most severe Philadelphia-negative chronic myeloproliferative syndrome. By associating a clonal proliferation and a mobilization of hematopoietic stem cells from bone marrow to spleen with profound alterations of the stroma, PMF is a remarkable model in which deregulation of the stem cell niche is of utmost importance for the disease development. This paper reviews key data suggesting that an imbalance between endosteal and vascular niches participates in the development of clonal stem cell proliferation. Mechanisms by which bone marrow niches are altered with ensuing mobilization and homing of neoplastic hematopoietic stem cells in new or reinitialized niches in the spleen and liver are examined. Differences between signals delivered by both endosteal and vascular niches in the bone marrow and spleen of patients as well as the responsiveness of PMF stem cells to their specific signals are discussed. A proposal for integrating a potential role for the JAK2 mutation in their altered sensitivity is made. A better understanding of the cross talk between stem cells and their niche should imply new therapeutic strategies targeting not only intrinsic defects in stem cell signaling but also regulatory hematopoietic niche–derived signals and, consequently, stem cell proliferation.

Analysis of GPI-anchored proteins involved in germline stem cell proliferation in the Caenorhabditis elegans germline stem cell niche

2020 ◽  
Vol 168 (6) ◽  
pp. 589-602
Author(s):  
Marika Rikitake ◽  
Ayako Matsuda ◽  
Daisuke Murata ◽  
Katsufumi Dejima ◽  
Kazuko H Nomura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Caenorhabditis Elegans ◽  
Lipid Rafts ◽  
Stem Cell Niche ◽  
Germline Stem Cell ◽  
Self Renewal ◽  
Stem Cell Proliferation ◽  
Cell Niche ◽  
Germline Stem Cell Niche

Abstract Stem cells divide and undergo self-renewal depending on the signals received from the stem cell niche. This phenomenon is indispensable to maintain tissues and organs in individuals. However, not all the molecular factors and mechanisms of self-renewal are known. In our previous study, we reported that glycosylphosphatidylinositol (GPI)-anchored proteins (GPI-APs) synthesized in the distal tip cells (DTCs; the stem cell niche) are essential for germline stem cell proliferation in Caenorhabditis elegans. Here, we characterized the GPI-APs required for proliferation. We selected and verified the candidate GPI-APs synthesized in DTCs by RNA interference screening and found that F57F4.3 (GFI-1), F57F4.4 and F54E2.1 are necessary for germline proliferation. These proteins are likely involved in the same pathway for proliferation and activated by the transcription factor PQM-1. We further provided evidence suggesting that these GPI-APs act through fatty acid remodelling of the GPI anchor, which is essential for association with lipid rafts. These findings demonstrated that GPI-APs, particularly F57F4.3/4 and F54E2.1, synthesized in the germline stem cell niche are located in lipid rafts and involved in promoting germline stem cell proliferation in C. elegans. The findings may thus shed light on the mechanisms by which GPI-APs regulate stem cell self-renewal.

scholarly journals Epimorphin regulates the intestinal stem cell niche via effects on the stromal microenvironment

2018 ◽  
Vol 315 (2) ◽  
pp. G185-G194 ◽  
Author(s):  
Courtney E. Vishy ◽  
Elzbieta A. Swietlicki ◽  
Vered Gazit ◽  
Suneetha Amara ◽  
Gabriela Heslop ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Surface Area ◽  
Stem Cell Niche ◽  
Cell Secretion ◽  
Small Bowel Length ◽  
Stem Cell Proliferation ◽  
Cell Niche

Stem cell therapy is a potential therapeutic approach for disorders characterized by intestinal injury or loss of functional surface area. Stem cell function and proliferation are mediated by the stem cell niche. Stromal cells such as intestinal subepithelial myofibroblasts (ISEMFs) are important but poorly studied components of the stem cell niche. To examine the role of ISEMFs, we have previously generated mice with deletion of epimorphin ( Epim), an ISEMF protein and member of the syntaxin family of intracellular vesicle docking proteins that regulate cell secretion. Herein we explore the mechanisms for previous observations that Epim deletion increases gut crypt cell proliferation, crypt fission, and small bowel length in vivo. Stem cell-derived crypt culture techniques were used to explore the interaction between enteroids and myofibroblasts from Epim−/− and WT mice. Enteroids cocultured with ISEMFS had increased growth and crypt-like budding compared with enteroids cultured without stromal support. Epim deletion in ISEMFs resulted in increased enteroid budding and surface area compared with cocultures with wild-type (WT) ISEMFs. In primary crypt cultures, Epim−/− enteroids had significantly increased surface area and budding compared with WTs. However, stem cell assays comparing the number of Epim−/− vs. WT colony-forming units after first passage showed no differences in the absence of ISEMF support. Epim−/− vs. WT ISEMFs had increased Wnt4 expression, and addition of Wnt4 to WT cocultures enhanced budding. We conclude that ISEMFs play an important role in the stem cell niche. Epim regulates stem cell proliferation and differentiation via stromal contributions to the niche microenvironment. NEW & NOTEWORTHY The role of subepithelial intestinal myofibroblasts (ISEMFs) in the gut stem cell niche is controversial. We provide novel evidence supporting ISEMFs as important niche contributors. We show that the in vivo intestinal effects of deletion of myofibroblast Epim can be recapitulated in crypt stem cell cultures in vitro. ISEMFs support cocultured stem cell proliferation and enteroid growth, and these effects are augmented by deletion of Epim, a syntaxin that regulates myofibroblast cell secretion.

scholarly journals miR-34a is a microRNA safeguard for Citrobacter-induced inflammatory colon oncogenesis

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Lihua Wang ◽  
Ergang Wang ◽  
Yi Wang ◽  
Robert Mines ◽  
Kun Xiang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Th17 Cell ◽  
Stem Cell Niche ◽  
Orphan Receptor ◽  
Interleukin 17 ◽  
T Helper 17 ◽  
Stem Cell Proliferation ◽  
Cell Niche ◽  
Interleukin 23

Inflammation often induces regeneration to repair the tissue damage. However, chronic inflammation can transform temporary hyperplasia into a fertile ground for tumorigenesis. Here, we demonstrate that the microRNA miR-34a acts as a central safeguard to protect the inflammatory stem cell niche and reparative regeneration. Although playing little role in regular homeostasis, miR-34a deficiency leads to colon tumorigenesis after Citrobacter rodentium infection. miR-34a targets both immune and epithelial cells to restrain inflammation-induced stem cell proliferation. miR-34a targets Interleukin six receptor (IL-6R) and Interleukin 23 receptor (IL-23R) to suppress T helper 17 (Th17) cell differentiation and expansion, targets chemokine CCL22 to hinder Th17 cell recruitment to the colon epithelium, and targets an orphan receptor Interleukin 17 receptor D (IL-17RD) to inhibit IL-17-induced stem cell proliferation. Our study highlights the importance of microRNAs in protecting the stem cell niche during inflammation despite their lack of function in regular tissue homeostasis.

scholarly journals Multiscale analysis reveals that diet-dependent midgut plasticity emerges from alterations in both stem cell niche coupling and enterocyte size

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Alessandro Bonfini ◽  
Adam J Dobson ◽  
David Duneau ◽  
Jonathan Revah ◽  
Xi Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Multiscale Analysis ◽  
Stem Cell Niche ◽  
Tor Signaling ◽  
Cell Numbers ◽  
Stem Cell Proliferation ◽  
Dietary Variation ◽  
Cell Niche ◽  
Complex Relationships

The gut is the primary interface between an animal and food, but how it adapts to qualitative dietary variation is poorly defined. We find that the Drosophila midgut plastically resizes following changes in dietary composition. A panel of nutrients collectively promote gut growth, which sugar opposes. Diet influences absolute and relative levels of enterocyte loss and stem cell proliferation, which together determine cell numbers. Diet also influences enterocyte size. A high sugar diet inhibits translation and uncouples intestinal stem cell proliferation from expression of niche-derived signals, but, surprisingly, rescuing these effects genetically was not sufficient to modify diet’s impact on midgut size. However, when stem cell proliferation was deficient, diet’s impact on enterocyte size was enhanced, and reducing enterocyte-autonomous TOR signaling was sufficient to attenuate diet-dependent midgut resizing. These data clarify the complex relationships between nutrition, epithelial dynamics, and cell size, and reveal a new mode of plastic, diet-dependent organ resizing.

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