Special issue: The intersection of stem/progenitor cell biology and hypoxic–ischemic cerebral injury/stroke

2006 ◽  
Vol 199 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Evan Y. Snyder
2012 ◽  
Vol 196 (5) ◽  
pp. 553-562 ◽  
Author(s):  
Ryan S. King ◽  
Phillip A. Newmark

Regeneration of complex structures after injury requires dramatic changes in cellular behavior. Regenerating tissues initiate a program that includes diverse processes such as wound healing, cell death, dedifferentiation, and stem (or progenitor) cell proliferation; furthermore, newly regenerated tissues must integrate polarity and positional identity cues with preexisting body structures. Gene knockdown approaches and transgenesis-based lineage and functional analyses have been instrumental in deciphering various aspects of regenerative processes in diverse animal models for studying regeneration.


2006 ◽  
Vol 84 (4) ◽  
pp. 515-522 ◽  
Author(s):  
Preetinder K. Dhanoa ◽  
Alison M. Sinclair ◽  
Robert T. Mullen ◽  
Jaideep Mathur

The discovery and development of multicoloured fluorescent proteins has led to the exciting possibility of observing a remarkable array of subcellular structures and dynamics in living cells. This minireview highlights a number of the more common fluorescent protein probes in plants and is a testimonial to the fact that the plant cell has not lagged behind during the live-imaging revolution and is ready for even more in-depth exploration.


2009 ◽  
Vol 104 (8) ◽  
pp. 969-977 ◽  
Author(s):  
Sang-Mo Kwon ◽  
Takahiro Suzuki ◽  
Atsuhiko Kawamoto ◽  
Masaaki Ii ◽  
Masamichi Eguchi ◽  
...  

2017 ◽  
Vol 26 (144) ◽  
pp. 170054 ◽  
Author(s):  
Carla F. Kim

The use of stem cell biology approaches to study adult lung progenitor cells and lung cancer has brought a variety of new techniques to the field of lung biology and has elucidated new pathways that may be therapeutic targets in lung cancer. Recent results have begun to identify the ways in which different cell populations interact to regulate progenitor activity, and this has implications for the interventions that are possible in cancer and in a variety of lung diseases. Today's better understanding of the mechanisms that regulate lung progenitor cell self-renewal and differentiation, including understanding how multiple epigenetic factors affect lung injury repair, holds the promise for future better treatments for lung cancer and for optimising the response to therapy in lung cancer. Working between platforms in sophisticated organoid culture techniques, genetically engineered mouse models of injury and cancer, and human cell lines and specimens, lung progenitor cell studies can begin with basic biology, progress to translational research and finally lead to the beginnings of clinical trials.


2019 ◽  
Vol 63 (8-9-10) ◽  
pp. 317-320 ◽  
Author(s):  
Ricardo Escalante ◽  
Elena Cardenal-Muñoz

When we set out to organize this Special Issue, we faced the difficult task of gathering together a large variety of topics with the unique commonality of having been studied in a single model organism, Dictyostelium discoideum. This apparent setback turned into a wonderful opportunity to learn about an organism as a whole, which provides a more complete understanding of life processes, their natural meaning and their changes during evolution. From studies dedicated almost exclusively to cell motility, differentiation and patterning, the versatility of D. discoideum has allowed in recent years the expansion of our knowledge to other areas, including cell biology and many others related to human diseases. The present collection of papers can be considered as a journey throughout the mechanisms of life, where D. discoideum acts as a very special tourist guide.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1194-1194
Author(s):  
Fang Tan ◽  
Robert Thomas ◽  
Flaubert Mbeunkui ◽  
Solomon F. Ofori-Acquah

Abstract Regulation of hematopoietic progenitor cell lineage-commitment, proliferation and differentiation by cell-cell adhesion mechanisms is poorly understood. Activated leukocyte cell adhesion molecule (ALCAM) is a member of the immunoglobulin super family. It is expressed by human hematopoietic stem cells, bone marrow stromal cells, endothelial cells and osteoblasts. Monoclonal anti-ALCAM antibodies inhibit myeloid but not erythroid colony formation, which suggest a lineage-specific role for ALCAM in hematopoiesis. To explore this hypothesis, ALCAM mRNA and protein expression was quantified in human hematopoietic cell lines of myeloid, lymphoid, erythroid, and megakaryocytic lineages by real-time quantitative PCR and western blot analyses. No ALCAM transcripts were detected in K562 and MEG-01 cells, the level of ALCAM mRNA was 2-fold more abundant in HL-60 and THP-1 cells than in U937 and Jurkat cells. This expression pattern was confirmed at the protein level as none of the megakaryocyte-erythroid progenitor cell lines (K562, MEG-01 and HEL) expressed ALCAM. On the contrary, ALCAM was abundantly expressed in THP-1 and HL-60 cells and moderately in U937 and Jurkat cells. GATA-1 was abundantly expressed in megakaryocyte-erythroid progenitor cell lines but not in any of the myeloid cell lines. Thus, there is an inverse relationship between expression of ALCAM and GATA-1 in hematopoietic cells. To test the hypothesis that GATA-1 is involved in silencing ALCAM gene expression, multiple ALCAM-promoter luciferase constructs were studied. A negative regulatory region was identified in the ALCAM promoter containing an inverted GATA-1 cis element at −850 upstream of the translational start site. GATA-1 occupied this canonical element in vivo as determined by chromatin immunoprecipitation experiments. A two-base pair mutation of the −850 GATA-1 cis element increased ALCAM promoter activity 3-fold in K562 and MEG-01 cells, providing direct evidence of GATA-1’s negative regulatory role in ALCAM promoter activity. To test the hypothesis that ALCAM silencing is essential for megakaryocyte-erythroid progenitor cell biology, stable lines of K562 cells were established forcibly expressing ALCAM-GFP or a control GFP. Live cell imaging demonstrated recruitment of ALCAM to sites of cell-cell adhesion in ALCAM-GFP-K562 cells, whereas GFP remained distributed in the cell cytosol in control cells. ALCAM-GFP-K562 cells formed markedly more clusters consisting of significantly more cells than control GFP-K562 cells. Finally, the number of ALCAM-GFP-K562 cells at log-phase growth was significantly higher than GFP-K562 cells over the same time period. Our findings demonstrate for the first time lineage-specific silencing of the cell adhesion molecule ALCAM in megakaryocyte-erythroid progenitor cells, mediated at least in part by GATA-1. That ectopic expression of ALCAM increased proliferation of K562 cells suggests that GATA-1-mediated silencing of ALCAM is essential in slowing down expansion of megakaryocyte-erythroid progenitor cells. Indeed, preliminary studies show an excessive number of erythroid and megakaryocytic cells in the adult spleen of ALCAM-null mice. This model is being used in ongoing studies to confirm our findings in vivo.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4160-4160
Author(s):  
David Traver ◽  
Julien Bertrand ◽  
Albert Kim ◽  
Jennifer Cisson ◽  
Emily Violette

Abstract Over the past decade, the development of forward genetic approaches in the zebrafish system has provided unprecedented power in understanding the molecular basis of vertebrate blood development. Establishment of cellular and hematological approaches to better understand the biology of resulting blood mutants, however, has lagged behind these efforts. We have recently developed the means to identify zebrafish hematopoietic stem cells (HSCs), transgenic lines to mark hematopoietic precursors and their progeny, and the assays to test these populations functionally. Like other vertebrates, zebrafish demonstrate differential waves of hematopoiesis during embryogenesis. These waves can be visualized directly by fluorescent transgenesis in living embryos. The earliest blood-forming cells in the zebrafish embryo express the scl and lmo2 genes. By directing expression of GFP to early blood precursors using the lmo2 promoter, we have isolated early hematopoietic cells by flow cytometry and tested them functionally by transplantation. Transplantation of lmo2::GFP+ cells isolated from embryos at 14 hours post-fertilization (hpf) resulted in only transient reconstitution of erythrocytes, suggesting that the earliest identifiable blood-forming cells are committed to the erythroid lineage. Later in embryogenesis, lmo2:GFP+ GATA-1:dsRED+ cells are found in the posterior blood island (PBI) from approximately 30–60 hpf. Molecular and functional characterization of these cells suggests that they possess limited myeloid and erythroid, but not lymphoid differentiation potentials. This suggests that committed progenitors with definitive hematopoietic potential arise in the embryo before HSCs can be identified. Additional studies have suggested that the first multipotent HSCs are born later in the zebrafish aorta/gonad/mesonephros (AGM) region. We have visualized putative HSCs in the AGM by their expression of the lmo2 and cd41 transgenes. Using confocal timelapse imaging in living embryos, lmo2::GFP+ cells have been observed to emigrate from the AGM region into circulation. Transplantation studies are underway to test putative HSC populations for repopulation activity. Taken together, our findings suggest that at least three independent waves of blood cell precursors are formed during zebrafish embryogenesis.


Sign in / Sign up

Export Citation Format

Share Document