Fibroblast progenitor cells of the embryonic chick limb

Development ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 191-200
Author(s):  
Stuart A. Newman
Keyword(s):  
Progenitor Cells ◽  
Cell Types ◽  
Mesenchymal Cells ◽  
The Other ◽  
Embryonic Chick ◽  
Similar Morphology ◽  
Level Characteristic ◽  
Fibroblast Progenitor Cells ◽  
Wing Tip ◽  
Mesodermal Lineage

A population of mesenchymal cells derived from the stage-25 chick wing tip gives rise to progeny of a similar morphology and to authentic fibroblasts when grown in low densityculture. Mixed clones containing both cell types are often observed. As the more rapidly proliferating fibroblasts begin to predominate in these cultures, collagen biosynthesisrises from the basal mesenchymal level to a level characteristic of mature fibroblasts. Thefibroblast progenitor is discussed relative to the other cell types of the mesodermal lineage of the developing limb.

scholarly journals Fetal erythropoiesis in steel mutant mice. III. Defect in differentiation from BFU-E to CFU-E during early development

Blood ◽  
1978 ◽  
Vol 51 (3) ◽  
pp. 539-547 ◽  
Author(s):  
DH Chui ◽  
SK Liao ◽  
K Walker
Keyword(s):  
Progenitor Cells ◽  
Early Development ◽  
The Other ◽  
Mutant Mice ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells ◽  
Other Hand ◽  
Colony Forming Units ◽  
Fetal Erythropoiesis

Abstract Erythroid progenitor cells in +/+ and Sl/Sld fetal livers manifested as burst-forming units-erythroid (BFU-E) and colony-forming units- erythroid (CFU-E) were assayed in vitro during early development. The proportion of BFU-E was higher as mutant than in normal fetal livers. On the other hand, the proportion of CFU-E was less in the mutant than in the normal. These results suggest that the defect in Sl/Sld fetal hepatic erythropoiesis is expressed at the steps of differentiation that effect the transition from BFU-E to CFU-E.

scholarly journals Fibroblast progenitor cells are recruited into the myocardium prior to the development of myocardial fibrosis

2012 ◽  
Vol 93 (2) ◽  
pp. 115-124 ◽  
Author(s):  
Mryanda Sopel ◽  
Alec Falkenham ◽  
Adam Oxner ◽  
Irene Ma ◽  
Timothy D.G. Lee ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Myocardial Fibrosis ◽  
Fibroblast Progenitor Cells

The influence of wing morphology and echolocation on the gleaning ability of the insectivorous bat Myotis tricolor

2004 ◽  
Vol 82 (12) ◽  
pp. 1854-1863 ◽  
Author(s):  
Samantha Stoffberg ◽  
David S Jacobs
Keyword(s):  
Discriminant Analysis ◽  
Foraging Behaviour ◽  
Myotis Lucifugus ◽  
The Other ◽  
Wing Morphology ◽  
Echolocation Calls ◽  
Narrow Bandwidth ◽  
Mole Crickets ◽  
Wing Tips ◽  
Wing Tip

On the basis of its external morphology, Myotis tricolor (Temminck, 1832) should be able to both aerial-feed and glean. Furthermore, this bat is known to use broadband calls of short duration, reinforcing the prediction that it gleans. However, results from this study indicate that M. tricolor does not commonly glean. This conclusion was reached after studying the foraging behaviour of M. tricolor in a flight room. We presented M. tricolor with mealworms, moths, mole crickets, beetles, and cicadas in a variety of ways that required either gleaning and (or) aerial feeding. Although M. tricolor readily took tethered prey, it did not take any of the variety of insects presented to it in a manner that required gleaning. We therefore compared its wing morphology and echolocation calls with those of several known gleaners, Nycteris thebaica E. Geoffroy, 1818, Myotis lucifugus (Le Conte, 1831), and Myotis septentrionalis (Trouessart, 1897), and an aerial forager, Neoromicia capensis (A. Smith, 1829). In a discriminant analysis wing-tip shape was the only variable to provide some degree of discrimination between species, with M. tricolor having more pointed wing tips than the known gleaners. Discriminant analysis of echolocation-call parameters grouped M. tricolor with the other Myotis species and separated it from N. capensis and N. thebaica. However, M. tricolor did not use harmonics as did the other Myotis species. The apparent failure of M. tricolor to glean might therefore be due to its relatively pointed wings and narrow-bandwidth echolocation calls, owing to the absence of harmonics in its calls.

scholarly journals Amino acid transport in normal and glutathione-deficient sheep erythrocytes

1976 ◽  
Vol 154 (1) ◽  
pp. 43-48 ◽  
Author(s):  
J D Young ◽  
J C Ellory ◽  
E M Tucker
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Amino Acid Transport ◽  
Cell Types ◽  
The Other ◽  
Acid Transport ◽  
Sheep Erythrocytes ◽  
Uptake Rates

1. Uptake rates for 23 amino acids were measured for both normal (high-GSH) and GSH-deficient (low-GSH) erythrocytes from Finnish Landrace sheep. 2. Compared with high-GSH cells, low-GSH cells had a markedly diminished permeability to D-alanine, L-alanine, α-amino-n-butyrate, valine, cysteine, serine, threonine, asparagine, lysine and ornithine. Smaller differences were observed for glycine and proline, whereas uptake of the other amino acids was not significantly different in the two cell types.

scholarly journals Multiple actins in drosophila melanogaster

1979 ◽  
Vol 82 (1) ◽  
pp. 86-92 ◽  
Author(s):  
SJ Horovitch ◽  
RV Storti ◽  
A Rich ◽  
ML Pardue
Keyword(s):  
Body Wall ◽  
Flight Muscle ◽  
Cell Types ◽  
Major Product ◽  
The Other ◽  
Stable Form ◽  
Larval Body ◽  
Drosophila Cell ◽  
Muscle Tissues ◽  
Adult Abdomen

The tissue and developmental specificities of the three Drosophila isoactins, originally identified in primary myogenic cultures and in the permanent Schneider L-2 cell line, have been investigated. Of these three isoactins (I, II, and III), actins I and II are stable and actin III is unstable. Two-dimensional polyacrylamide gel electrophoretic analyses of total cellular extracts after 1-h [(35)S]methionine pulses were performed on a large variety of embryonic, larval, and adult muscle and nonmuscle tissues. The results suggest that isoactins II and III are generalized cellular actins found in all drosophila cell types. Actin I, on the other hand, is muscle-associated and is found exclusively in supercontractile muscle (such as larval body wall and larval and adult viscera) including primary myogenic cell cultures. Although actin I synthesis is not detectable during very early embryogenesis, it is detectable by 25 h and actin I is a major stable actin in all larval muscle tissues. Actin I is synthesized in reduced amounts relative to the other actins in late third instar larvae but is again a major product of actin synthesis in the adult abdomen. A stable actin species with the same pI as actin III has been identified in the adult thorax and appears to be unique to flight muscle tissue. This new stable form of thoracic actin may be the result of a stabilization of the actin III found in other tissues or may be an entirely separate gene product.

Changes in Seryl-tRNA Formative in Developing Chick Muscle

1974 ◽  
Vol 52 (10) ◽  
pp. 838-844 ◽  
Author(s):  
Mark Nwagwu ◽  
John Lianga
Keyword(s):  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Deae Cellulose ◽  
The Other ◽  
Embryonic Chick ◽  
Qualitative And Quantitative ◽  
Embryonic Muscle ◽  
Quantitative Changes ◽  
The One

As a prelude to an analysis of the dependence of muscle protein synthesis on aminoacyl tRNA's, we have investigated the rates of seryl-tRNA formation, in vitro, by aminoacylating systems isolated from 11-, 14-, and 17-day chick embryonic muscle. The results show that the combination of 14-day tRNA and 14-day aminoacyl synthetase is the most efficient in seryl-tRNA formation. We have also studied the qualitative and quantitative changes in seryl-tRNA prepared from 11-, 14-, and 17-day embryonic chick muscle by chromatography of seryl-tRNA on benzoylated DEAE-cellulose columns. The results show that, although there are no qualitative differences in the chromatographic patterns of seryl-tRNA from the different ages, there are significant quantitative differences between the patterns for 11-day and 17-day seryl-tRNA on the one hand, and the pattern for 14-day seryl-tRNA on the other.

Abstract 305: Single Cell RNA Sequencing of Adult Cardiac c-kit+ Cells in a Murine Lineage Tracing Model

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Bryan D Maliken ◽  
Onur Kanisicak ◽  
Jeffery D Molkentin
Keyword(s):  
Single Cell ◽  
Progenitor Cells ◽  
Rna Sequencing ◽  
Cardiac Injury ◽  
Mesenchymal Cells ◽  
Lineage Tracing ◽  
Tyrosine Kinase Receptor ◽  
Early Differentiation ◽  
Gfp Reporter ◽  
Single Cell Rna Sequencing

A subset of adult cardiac resident cells defined by the stem cell factor tyrosine kinase receptor termed c-kit, are believed to have myogenic potential and are now being delivered via intracoronary infusion to presumably promote cardiac regeneration and improve ventricular function after ischemic cardiac injury. However, recent studies have shown that despite these benefits, c-kit+ progenitor cells in the adult murine heart are more inclined to take on an endothelial rather than cardiomyocyte lineage. To better define the factors involved in early differentiation of these resident cardiac progenitor cells and to distinguish distinct cell subpopulations, we performed single cell RNA sequencing on c-kit+ cells from Kit-Cre lineage traced GFP reporter mice versus total mesenchymal cells from the heart that were CD31- and CD45-. Cells were isolated by cardiac digestion and FACS was performed, positively sorting for the c-kit+ lineage while negatively sorting for CD31 and CD45 to eliminate endothelial and leukocyte progenitor contamination, respectively. Following this isolation, cells were examined to determine GFP reporter status and then submitted for single cell RNA sequencing using the Fluidigm A1 system. Clustering of 654 genes from this data identified 6 distinct subpopulations indicating various stages of early differentiation among CD31- and CD45-negative cardiac interstitial cells. Furthermore, comparison of GFP+ c-kit cells to the total non-GFP mesenchymal cells identified 75 differentially expressed transcripts. These unique gene signatures may help parse the genes that underlie cellular plasticity in the heart and define the best molecular lineages for transdifferentiation into cardiac myocytes.

The effect of pancreatic mesenchyme on the differentiation of endocrine cells from gastric endoderm

Development ◽  
1987 ◽  
Vol 100 (4) ◽  
pp. 661-671 ◽  
Author(s):  
B. Kramer ◽  
A. Andrew ◽  
B.B. Rawdon ◽  
P. Becker
Keyword(s):  
Endocrine Cell ◽  
Endocrine Cells ◽  
Cell Types ◽  
The Other ◽  
Chick Embryos ◽  
Cell Type ◽  
Pancreatic Insulin ◽  
Somatostatin Cells ◽  
Regional Specificity ◽  
Gut Endocrine Cells

To determine whether mesenchyme plays a part in the differentiation of gut endocrine cells, proventricular endoderm from 4- to 5-day chick or quail embryos was associated with mesenchyme from the dorsal pancreatic bud of chick embryos of the same age. The combinations were grown on the chorioallantoic membranes of host chick embryos until they reached a total incubation age of 21 days. Proventricular or pancreatic endoderm of the appropriate age and species reassociated with its own mesenchyme provided the controls. Morphogenesis in the experimental grafts corresponded closely to that in proventricular controls, i.e. the pancreatic mesenchyme supported the development of proventricular glands from proventricular endoderm. Insulin, glucagon and somatostatin cells and cells with pancreatic polypeptide-like immunoreactivity differentiated in the pancreatic controls. The latter three endocrine cell types, together with neurotensin and bombesin/gastrin-releasing polypeptide (GRP) cells, developed in proventricular controls and experimental grafts. The proportions of the major types common to proventriculus and pancreas (somatostatin and glucagon cells) were in general similar when experimental grafts were compared with proventricular controls but different when experimental and pancreatic control grafts were compared. Hence pancreatic mesenchyme did not materially affect the proportions of these three cell types in experimental grafts, induced no specific pancreatic (insulin) cell type and allowed the differentiation of the characteristic proventricular endocrine cell types, neurotensin and bombesin/GRP cells. However, an important finding was a significant reduction in the proportion of bombesin/GRP cells, attributable in part to a decrease in their number and in part to an increase in the numbers of endocrine cells of the other types. This indicates that mesenchyme may well play a part in determining the regional specificity of populations of gut endocrine cells.

Functional partitioning of beta1 integrins revealed by activating and inhibitory mAbs

1997 ◽  
Vol 110 (21) ◽  
pp. 2647-2659 ◽  
Author(s):  
M.T. Cruz ◽  
C.L. Dalgard ◽  
M.J. Ignatius
Keyword(s):  
Cell Surface ◽  
Actin Cytoskeleton ◽  
Dermal Fibroblasts ◽  
The Other ◽  
Embryonic Chick ◽  
Cell Surfaces ◽  
Double Labeling ◽  
Focal Contacts ◽  
Functional Partitioning ◽  
Discrete Populations

Integrins exist in different activation states on the surfaces of cells. Addition of the proper signal, ligand, or antibody can alter the activation state of these molecules. We report here the identification of two immunocytochemically distinct populations of beta1 integrins on fixed embryonic chick dermal fibroblasts. One population, recognized by the integrin activating mAb TASC, localizes to discrete regions of the cell, most likely focal contacts. These integrins co-localize with other proteins, such as vinculin and F-actin, and their retention at these sites is dependent on the actin cytoskeleton. The other population, identified with the inhibitory mAb W1B10, is more evenly distributed throughout the cell surface, and its pattern remains unchanged after disruption of the actin cytoskeleton. Double labeling experiments using Fab fragments of TASC alongside whole W1B10 IgG revealed non-overlapping staining patterns. These results show that it is possible to visualize and study discrete populations of integrins on cell surfaces using two different antibodies. We hypothesize that these antibodies report differences in the distribution of receptors in two different states. A model is proposed describing the ligand independent recruitment of integrins based on these findings and results from other labs.

scholarly journals Human leukemia mutations corrupt but do not abrogate GATA-2 function

2018 ◽  
Vol 115 (43) ◽  
pp. E10109-E10118 ◽  
Author(s):  
Koichi R. Katsumura ◽  
Charu Mehta ◽  
Kyle J. Hewitt ◽  
Alexandra A. Soukup ◽  
Isabela Fraga de Andrade ◽  
...  
Keyword(s):  
Dna Binding ◽  
Progenitor Cells ◽  
Zinc Finger ◽  
Erythroid Differentiation ◽  
Cell Types ◽  
Myeloid Differentiation ◽  
Human Leukemia ◽  
Hematopoietic Stem ◽  
Amino Terminal ◽  
Disease Mutations

By inducing the generation and function of hematopoietic stem and progenitor cells, the master regulator of hematopoiesis GATA-2 controls the production of all blood cell types. Heterozygous GATA2 mutations cause immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia. GATA2 disease mutations commonly disrupt amino acid residues that mediate DNA binding or cis-elements within a vital GATA2 intronic enhancer, suggesting a haploinsufficiency mechanism of pathogenesis. Mutations also occur in GATA2 coding regions distinct from the DNA-binding carboxyl-terminal zinc finger (C-finger), including the amino-terminal zinc finger (N-finger), and N-finger function is not established. Whether distinct mutations differentially impact GATA-2 mechanisms is unknown. Here, we demonstrate that N-finger mutations decreased GATA-2 chromatin occupancy and attenuated target gene regulation. We developed a genetic complementation assay to quantify GATA-2 function in myeloid progenitor cells from Gata2 −77 enhancer-mutant mice. GATA-2 complementation increased erythroid and myeloid differentiation. While GATA-2 disease mutants were not competent to induce erythroid differentiation of Lin−Kit+ myeloid progenitors, unexpectedly, they promoted myeloid differentiation and proliferation. As the myelopoiesis-promoting activity of GATA-2 mutants exceeded that of GATA-2, GATA2 disease mutations are not strictly inhibitory. Thus, we propose that the haploinsufficiency paradigm does not fully explain GATA-2–linked pathogenesis, and an amalgamation of qualitative and quantitative defects instigated by GATA2 mutations underlies the complex phenotypes of GATA-2–dependent pathologies.

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