scholarly journals Role of glial filaments in cells and tumors of glial origin: a review

1997 ◽  
Vol 3 (1) ◽  
pp. E2
Author(s):  
James T. Rutka ◽  
Masaji Murakami ◽  
Peter B. Dirks ◽  
Sherri Lynn Hubbard ◽  
Laurence E. Becker ◽  
...  
Keyword(s):  
Transgenic Animals ◽  
Cell Types ◽  
Specific Marker ◽  
Integrin Receptors ◽  
Cellular Space ◽  
Cellular Events ◽  
Supportive Role ◽  
Exact Function ◽  
Capillary Endothelial Cells

In the adult human brain, normal astrocytes constitute nearly 40% of the total central nervous system (CNS) cell population and may assume a star-shaped configuration resembling epithelial cells insofar as the astrocytes remain intimately associated, through their cytoplasmic extensions, with the basement membrane of the capillary endothelial cells and the basal lamina of the glial limitans externa. Although their exact function remains unknown, in the past, astrocytes were thought to subserve an important supportive role for neurons, providing a favorable ionic environment, modulating extracellular levels of neurotransmitters, and serving as spacers that organize neurons. In immunohistochemical preparations, normal, reactive, and neoplastic astrocytes may be positively identified and distinguished from other CNS cell types by the expression of the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). This GFAP is a 50-kD intracytoplasmic filamentous protein that constitutes a portion of, and is specific for, the cytoskeleton of the astrocyte. This protein has proved to be the most specific marker for cells of astrocytic origin under normal and pathological conditions. Interestingly, with increasing astrocytic malignancy, there is progressive loss of GFAP production. As the human gene for GFAP has now been cloned and sequenced, this review begins with a summary of the molecular biology of GFAP including the proven utility of the GFAP promoter in targeting genes of interest to the CNS in transgenic animals. Based on the data provided the authors argue cogently for an expanded role of GFAP in complex cellular events such as cytoskeletal reorganization, maintenance of myelination, cell adhesion, and signaling pathways. As such, GFAP may not represent a mere mechanical integrator of cellular space, as has been previously thought. Rather, GFAP may provide docking sites for important kinases that recognize key cellular substrates that enable GFAP to form a dynamic continuum with microfilaments, integrin receptors, and the extracellular matrix.

Role of glial filaments in cells and tumors of glial origin: a review

1997 ◽  
Vol 87 (3) ◽  
pp. 420-430 ◽  
Author(s):  
James T. Rutka ◽  
Masaji Murakami ◽  
Peter B. Dirks ◽  
Sherri Lynn Hubbard ◽  
Laurence E. Becker ◽  
...  
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Transgenic Animals ◽  
Cell Types ◽  
Acidic Protein ◽  
Specific Marker ◽  
Content Type ◽  
Supportive Role ◽  
Exact Function ◽  
Capillary Endothelial Cells

✓ In the adult human brain, normal astrocytes constitute nearly 40% of the total central nervous system (CNS) cell population and may assume a star-shaped configuration resembling epithelial cells insofar as the astrocytes remain intimately associated, through their cytoplasmic extensions, with the basement membrane of the capillary endothelial cells and the basal lamina of the glial limitans externa. Although their exact function remains unknown, in the past, astrocytes were thought to subserve an important supportive role for neurons, providing a favorable ionic environment, modulating extracellular levels of neurotransmitters, and serving as spacers that organize neurons. In immunohistochemical preparations, normal, reactive, and neoplastic astrocytes may be positively identified and distinguished from other CNS cell types by the expression of the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). Glial fibrillary acidic protein is a 50-kD intracytoplasmic filamentous protein that constitutes a portion of, and is specific for, the cytoskeleton of the astrocyte. This protein has proved to be the most specific marker for cells of astrocytic origin under normal and pathological conditions. Interestingly, with increasing astrocytic malignancy, there is progressive loss of GFAP production. As the human gene for GFAP has now been cloned and sequenced, this review begins with a summary of the molecular biology of GFAP including the proven utility of the GFAP promoter in targeting genes of interest to the CNS in transgenic animals. Based on the data provided the authors argue cogently for an expanded role of GFAP in complex cellular events such as cytoskeletal reorganization, maintenance of myelination, cell adhesion, and signaling pathways. As such, GFAP may not represent a mere mechanical integrator of cellular space, as has been previously thought. Rather, GFAP may provide docking sites for important kinases that recognize key cellular substrates that enable GFAP to form a dynamic continuum with microfilaments, integrin receptors, and the extracellular matrix.

Altering the cellular mechanical force balance results in integrated changes in cell, cytoskeletal and nuclear shape

1992 ◽  
Vol 103 (4) ◽  
pp. 1215-1222 ◽  
Author(s):  
J.R. Sims ◽  
S. Karp ◽  
D.E. Ingber
Keyword(s):  
Shape Control ◽  
Nuclear Shape ◽  
Force Balance ◽  
Dependent Manner ◽  
Integrin Receptors ◽  
Permeabilized Cells ◽  
Capillary Endothelial Cells ◽  
Shape Determination ◽  
Dose Dependent

Studies were carried out with capillary endothelial cells cultured on fibronectin (FN)-coated dishes in order to analyze the mechanism of cell and nuclear shape control by extracellular matrix (ECM). To examine the role of the cytoskeleton in shape determination independent of changes in transmembrane osmotic pressure, membranes of adherent cells were permeabilized with saponin (25 micrograms/ml) using a buffer that maintains the functional integrity of contractile microfilaments. Real-time videomicroscopic studies revealed that addition of 250 microM ATP resulted in time-dependent retraction and rounding of permeabilized cells and nuclei in a manner similar to that observed in intact living cells following detachment using trypsin-EDTA. Computerized image analysis confirmed that permeabilized cells remained essentially rigid in the absence of ATP and that retraction was stimulated in a dose-dependent manner as the concentration of ATP was raised from 10 to 250 microM. Maximal rounding occurred by 30 min with projected cell and nuclear areas being reduced by 69 and 41%, respectively. ATP-induced rounding was also accompanied by a redistribution of microfilaments resulting in formation of a dense net of F-actin surrounding retracted nuclei. Importantly, ATP-stimulated changes in cell, cytoskeletal, and nuclear form were prevented in permeabilized cells using a synthetic myosin peptide (IRICRKG) that has been previously shown to inhibit actomyosin filament sliding in muscle. In contrast, both the rate and extent of cell and nuclear rounding were increased in permeabilized cells exposed to ATP when the soluble FN peptide, GRGDSP, was used to dislodge immobilized FN from cell surface integrin receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Tribbles in normal and malignant haematopoiesis

2015 ◽  
Vol 43 (5) ◽  
pp. 1112-1115 ◽  
Author(s):  
Sarah J. Stein ◽  
Ethan A. Mack ◽  
Kelly S. Rome ◽  
Warren S. Pear
Keyword(s):  
E3 Ligase ◽  
Cell Types ◽  
Protein Family ◽  
Conserved Motifs ◽  
Tissue Specific ◽  
Cellular Events ◽  
Haematopoietic Cells ◽  
Evolutionarily Conserved ◽  
Multiple Cell

The tribbles protein family, an evolutionarily conserved group of pseudokinases, have been shown to regulate multiple cellular events including those involved in normal and malignant haematopoiesis. The three mammalian Tribbles homologues, Trib1, Trib2 and Trib3 are characterized by conserved motifs, including a pseudokinase domain and a C-terminal E3 ligase-binding domain. In this review, we focus on the role of Trib (mammalian Tribbles homologues) proteins in mammalian haematopoiesis and leukaemia. The Trib proteins show divergent expression in haematopoietic cells, probably indicating cell-specific functions. The roles of the Trib proteins in oncogenesis are also varied and appear to be tissue-specific. Finally, we discuss the potential mechanisms by which the Trib proteins preferentially regulate these processes in multiple cell types.

scholarly journals Ligand-Independent Antiapoptotic Function of Estrogen Receptor-β in Lung Cancer Cells

2010 ◽  
Vol 24 (9) ◽  
pp. 1737-1747 ◽  
Author(s):  
GuangFeng Zhang ◽  
Naveena Yanamala ◽  
Kira L. Lathrop ◽  
Lin Zhang ◽  
Judith Klein-Seetharaman ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Estrogen Receptor ◽  
Cell Types ◽  
Mitochondrial Fraction ◽  
Apoptotic Pathway ◽  
Independent Manner ◽  
Bh3 Domain ◽  
Exact Function ◽  
Apoptosis Inducing Agents

Abstract Recent studies have demonstrated the presence of estrogen receptor (ER)β in the mitochondria in various cell types and tissues, but the exact function of this localization remains unclear. In this study, we have examined the function of mitochondrial ERβ in non-small-cell lung cancer (NSCLC) cells. Down-regulation of ERβ by short hairpin RNA constructs sensitized NSCLC cells to various apoptosis-inducing agents such as cisplatin, taxol, and etoposide. The increased growth inhibition and induction of apoptosis in ERβ-knockdown cells was observed irrespective of estrogen treatment, suggesting a ligand-independent role of ERβ in regulating the intrinsic apoptotic pathway. Further, ERβ from the mitochondrial fraction physically interacted with the proapoptotic protein Bad, in a ligand-independent manner. Glutathione-S-transferase pull-down assays and molecular modeling studies revealed that the DNA-binding domain and hinge region of ERβ, and the BH3 domain of Bad were involved in these interactions. Further investigations revealed that ERβ inhibited Bad function by disrupting Bad-Bcl-XL and Bad-Bcl-2 interactions. Reintroduction of ERβ in the mitochondria of ERβ knockdown cells reversed their sensitivity to cisplatin. Overall, our results demonstrate a ligand-independent role of ERβ in regulating apoptosis, revealing a novel function for ERβ in the mitochondria.

scholarly journals Function of Astrocytes in Neuroprotection and Repair after Ischemic Stroke

2021 ◽  
pp. 1-9
Author(s):  
Shufen Zhang ◽  
Deshu Shang ◽  
Han Shi ◽  
Weiyu Teng ◽  
Li Tian
Keyword(s):  
Central Nervous System ◽  
Ischemic Stroke ◽  
Recent Literature ◽  
Current Knowledge ◽  
Cell Types ◽  
Exact Role ◽  
Exact Function ◽  
Numerous Cell ◽  
The Central Nervous System

<b><i>Background:</i></b> Astrocytes are the most numerous cell types within the central nervous system, and many efforts have been put into determining the exact role of astrocytes in neuroprotection and repair after ischemic stroke. Although numerous studies have been done in recent years, there is still no thorough understanding of the exact function of astrocytes in the whole course of the stroke. <b><i>Summary:</i></b> According to the recent literature, there are many structures and factors that play important roles in the process of ischemic stroke, among which blood-brain barrier, various growth factors, gap junctions, AQP4, and glial scars have been studied most comprehensively, and all these factors are closely related to astrocytes. The role of astrocytes in ischemic stroke, therefore, can be analyzed more comprehensively. <b><i>Key Message:</i></b> The present review mainly summarized the current knowledge about astrocytes and their potential roles after ischemic stroke.

Transgenic animal models of renal development and pathogenesis

1995 ◽  
Vol 269 (5) ◽  
pp. F601-F620 ◽  
Author(s):  
J. B. Kopp ◽  
P. E. Klotman
Keyword(s):  
Growth Factors ◽  
Renin Angiotensin System ◽  
Transgenic Animals ◽  
Cell Types ◽  
Pressure Control ◽  
Transgenic Animal ◽  
Renal Diseases ◽  
Renal Development

The use of transgenic animals represents a powerful tool with which to address the role of particular gene products in vivo. Recent technical and biological advances have simplified the process of creating both transgenic mice and null-mutation mice. Increasing numbers of genetic control elements are available to direct transgene expression to particular renal cell types and to enhance the consistency of expression. These approaches have contributed significantly to our understanding of renal development and pathogenesis, in particular in the following areas: the roles of various oncogenes, homeobox genes, and growth factors in renal development and the pathogenesis of cystic renal diseases; the contribution of systemic and local expression of the renin-angiotensin system to blood pressure control; the role of growth factors and cytokines in progressive glomerular disease; the role of viral proteins in the pathogenesis of glomerular and tubular disease; and mechanisms of immune-mediated renal disease.

scholarly journals Immunological identification of a new 14X10(3) Mr membrane-bound protein in Torpedo electric organ

1991 ◽  
Vol 98 (3) ◽  
pp. 351-361
Author(s):  
N. Morel ◽  
G. Brochier ◽  
M. Synguelakis ◽  
G. Le Gal La Salle
Keyword(s):  
External Surface ◽  
Electric Organ ◽  
Cell Types ◽  
Immunogold Labelling ◽  
Electron Microscope Level ◽  
Capillary Endothelial Cells ◽  
Membrane Bound ◽  
Torpedo Electric Organ ◽  
Immunological Identification

A series of monoclonal antibodies binding to different epitopes shared by a 14 × 10(3)Mr membrane-bound polypeptide has been obtained. By indirect immuno-fluorescence, it was shown that the 14 × 10(3)Mr antigen is present in various cell types in Torpedo electric organ and muscle, especially fibroblasts, capillary endothelial cells, axonal cuff cells and, to a lesser extent, Schwann cells. At the electron-microscope level, after immunogold labelling, the antigen was found associated with the external surface of the plasma membrane of these cells, with the exception of the axonal cuff cells where part of the labelling was intracellular. The possible biological role of this 14 × 10(3)Mr protein is unknown but preliminary experiments suggest that this antigen has affinity for other Torpedo electric organ membrane proteins.

Effect of Calcium on the Growth and Differentiation of Cultured Rat Esophageal Epithelial Cells

1982 ◽  
Vol 40 ◽  
pp. 132-133
Author(s):  
W.T. Gunning ◽  
M.R. Marino ◽  
M.S. Babcock ◽  
G.D. Stoner
Keyword(s):  
Epithelial Cells ◽  
Cell Types ◽  
Replication Rate ◽  
Enzymatic Dissociation ◽  
Growth Assay ◽  
Epidermal Growth ◽  
Fetal Bovine ◽  
Esophageal Epithelial Cells ◽  
Cellular Replication

The role of calcium in modulating cellular replication and differentiation has been described for various cell types. In the present study, the effects of Ca++ on the growth and differentiation of cultured rat esophageal epithelial cells was investigated.Epithelial cells were isolated from esophagi taken from 8 week-old male CDF rats by the enzymatic dissociation method of Kaighn. The cells were cultured in PFMR-4 medium supplemented with 0.25 mg/ml dialyzed fetal bovine serum, 5 ng/ml epidermal growth factor, 10-6 M hydrocortisone 10-6 M phosphoethanolamine, 10-6 M ethanolamine, 5 pg/ml insulin, 5 ng/ml transferrin, 10 ng/ml cholera toxin and 50 ng/ml garamycin at 36.5°C in a humidified atmosphere of 3% CO2 in air. At weekly intervals, the cells were subcultured with a solution containing 1% polyvinylpyrrolidone, 0.01% EGTA, and 0.05% trypsin. After various passages, the replication rate of the cells in PFMR-4 medium containing from 10-6 M to 10-3 M Ca++ was determined using a clonal growth assay.

Role of PKC isozymes in water transport in toad urinary bladder

1991 ◽  
Vol 49 ◽  
pp. 302-303
Author(s):  
A.J. Mia ◽  
L.X. Oakford ◽  
T. Yorio
Keyword(s):  
Urinary Bladder ◽  
Apical Membrane ◽  
Membrane Surface ◽  
Protein A ◽  
Cell Types ◽  
Leukemic Cells ◽  
Toad Urinary Bladder ◽  
Pkc Isozymes ◽  
Antibody Labeling

Protein kinase C (PKC) isozymes, when activated, are translocated to particulate membrane fractions for transport to the apical membrane surface in a variety of cell types. Evidence of PKC translocation was demonstrated in human megakaryoblastic leukemic cells, and in cardiac myocytes and fibroblasts, using FTTC immunofluorescent antibody labeling techniques. Recently, we reported immunogold localizations of PKC subtypes I and II in toad urinary bladder epithelia, following 60 min stimulation with Mezerein (MZ), a PKC activator, or antidiuretic hormone (ADH). Localization of isozyme subtypes I and n was carried out in separate grids using specific monoclonal antibodies with subsequent labeling with 20nm protein A-gold probes. Each PKC subtype was found to be distributed singularly and in discrete isolated patches in the cytosol as well as in the apical membrane domains. To determine if the PKC isozymes co-localized within the cell, a double immunogold labeling technique using single grids was utilized.

Role of the 807 C/T Polymorphism of the α2 Gene in Platelet GP Ia Collagen Receptor Expression and Function

1999 ◽  
Vol 81 (06) ◽  
pp. 951-956 ◽  
Author(s):  
J. Corral ◽  
R. González-Conejero ◽  
J. Rivera ◽  
F. Ortuño ◽  
P. Aparicio ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Cell Types ◽  
Receptor Expression ◽  
Case Control Studies ◽  
Platelet Surface ◽  
Vitro Analysis ◽  
And Function ◽  
In Vitro Analysis

SummaryThe variability of the platelet GP Ia/IIa density has been associated with the 807 C/T polymorphism (Phe 224) of the GP Ia gene in American Caucasian population. We have investigated the genotype and allelic frequencies of this polymorphism in Spanish Caucasians. The T allele was found in 35% of the 284 blood donors analyzed. We confirmed in 159 healthy subjects a significant association between the 807 C/T polymorphism and the platelet GP Ia density. The T allele correlated with high number of GP Ia molecules on platelet surface. In addition, we observed a similar association of this polymorphism with the expression of this protein in other blood cell types. The platelet responsiveness to collagen was determined by “in vitro” analysis of the platelet activation and aggregation response. We found no significant differences in these functional platelet parameters according to the 807 C/T genotype. Finally, results from 3 case/control studies involving 302 consecutive patients (101 with coronary heart disease, 104 with cerebrovascular disease and 97 with deep venous thrombosis) determined that the 807 C/T polymorphism of the GP Ia gene does not represent a risk factor for arterial or venous thrombosis.

Sign in / Sign up

Export Citation Format

Share Document