Active Control of Epithelial Cell-Density Gradients Grown Along the Channel of an Organic Electrochemical Transistor

2009 ◽  
Vol 21 (43) ◽  
pp. 4379-4382 ◽  
Author(s):  
Maria H. Bolin ◽  
Karl Svennersten ◽  
David Nilsson ◽  
Anurak Sawatdee ◽  
Edwin W. H. Jager ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Density ◽  
Active Control ◽  
Density Gradients ◽  
Electrochemical Transistor

Dendritic competition in the developing retina: Ganglion cell density gradients and laterally displaced dendrites

1993 ◽  
Vol 10 (2) ◽  
pp. 313-324 ◽  
Author(s):  
Rafael Linden
Keyword(s):  
Density Gradient ◽  
Cell Density ◽  
Time Course ◽  
Ganglion Cells ◽  
Lateral Displacement ◽  
Optic Tract ◽  
Density Gradients ◽  
Temporal Asymmetry ◽  
Dendritic Arbors ◽  
Contralateral Eye

AbstractDendrites of retinal ganglion cells (RGCs) tend to be distributed preferentially toward areas of reduced RGC density. This, however, does not occur in the retina of normal pigmented rats, in which it has been suggested that the centro-peripheral gradient of RGC density is too shallow to provide directional guidance to growing dendrites. In this study, laterally displaced dendrites of RGCs retrogradely labeled with horseradish peroxidase were related to cell density gradients induced experimentally in the rat retina. Neonatal unilateral lesions of the optic tract produced retrograde degeneration of contralaterally projecting RGCs, but spared ipsilaterally projecting neurons in the same retina. These lesions created an anomalous temporal to nasal gradient of cell density across the decussation line, opposite to the nasal to temporal gradient found along the same axis in either normal rats or rats that had the contralateral eye removed at birth. RGCs in rats that received optic tract lesions had their dendrites displaced laterally toward the depleted nasal retina, while in either normal or enucleated rats there was no naso-temporal asymmetry. The lateral displacement affected both primary dendrites and higher-order branches. However, the gradient of cell density after optic tract lesions was less steep than the gradient in either normal or enucleated rats. To test for the presence of steeper gradients at early stages of development, RGC density gradients were also examined at postnatal day 5 (P5). In normal rats, the RGCs were homogeneously distributed throughout the retina, while rats given optic tract lesions at birth already showed a temporo-nasal density gradient at P5. Still, this anomalous gradient was less steep than that found in normal adults. It is concluded that the time course, rather than the steepness of the RGC density gradient, is the major determinant of the lateral displacement of dendritic arbors with respect to the soma in developing RGCs. The data are consistent with the idea that the overall shape of dendritic arbors depends in part on dendritic competition during retinal development.

Pattern formation of vascular smooth muscle cells subject to nonuniform fluid shear stress: role of PDGF-β receptor and Src

2003 ◽  
Vol 285 (3) ◽  
pp. H1081-H1090 ◽  
Author(s):  
Shu Q. Liu ◽  
Christopher Tieche ◽  
Dalin Tang ◽  
Paul Alkema
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Cell Density ◽  
Fluid Shear Stress ◽  
Density Gradients ◽  
Dependent Manner ◽  
Fluid Shear ◽  
Polymer Implants ◽  
Β Receptor

Blood vessels are subject to fluid shear stress, a hemodynamic factor that inhibits the mitogenic activities of vascular cells. The presence of nonuniform shear stress has been shown to exert graded suppression of cell proliferation and induces the formation of cell density gradients, which in turn regulate the direction of smooth muscle cell (SMC) migration and alignment. Here, we investigated the role of platelet-derived growth factor (PDGF)-β receptor and Src in the regulation of such processes. In experimental models with vascular polymer implants, SMCs migrated from the vessel media into the neointima of the implant under defined fluid shear stress. In a nonuniform shear model, blood shear stress suppressed the expression of PDGF-β receptor and the phosphorylation of Src in a shear level-dependent manner, resulting in the formation of mitogen gradients, which were consistent with the gradient of cell density as well as the alignment of SMCs. In contrast, uniform shear stress in a control model elicited an even influence on the activity of mitogenic molecules without modulating the uniformity of cell density and did not significantly influence the direction of SMC alignment. The suppression of the PDGF-β receptor tyrosine kinase and Src with pharmacological substances diminished the gradients of mitogens and cell density and reduced the influence of nonuniform shear stress on SMC alignment. These observations suggest that PDGF-β receptor and Src possibly serve as mediating factors in nonuniform shear-induced formation of cell density gradients and alignment of SMCs in the neointima of vascular polymer implants.

Histologic Changes in Human Vocal Folds Correlated with Aging: A Histomorphometric Study

2003 ◽  
Vol 112 (10) ◽  
pp. 894-898 ◽  
Author(s):  
João Aragão Ximenes Filho ◽  
Paulo Hilário Saldiva do Nascimento ◽  
Domingos Hiroshi Tsuji ◽  
Luiz Ubirajara Sennes
Keyword(s):  
Epithelial Cell ◽  
Cell Density ◽  
Lamina Propria ◽  
Vocal Folds ◽  
The Elderly ◽  
Histomorphometric Analysis ◽  
Younger Adults ◽  
Histomorphometric Study ◽  
The Voice ◽  
Histologic Changes

The voice of aged persons is usually different from that of younger adults — a fact indicating that aging induces changes in the human larynx. The aim of this study was to perform a histomorphometric analysis of the vocal fold and of a fragment of skin in order to determine the modifications related to aging and possible differences between genders. Twenty cadavers, 10 men and 10 women, were studied. Stereological methods were used for histologic analysis. In the vocal folds, we observed a reduction of the lamina propria thickness (p < .001) and of epithelial cell density (p < .001) as a function of age. In the skin, there was a reduction of chorion thickness (p = .02) and of epithelial cell density (p = .01). The decrease in the thickness of the lamina propria of the vocal folds with aging may contribute to the vocal pattern present in the elderly. These changes were more evident in men.

Biphasic effect of the mitotoxin bFGF-saporin on bovine lens epithelial cell growth: Effect of cell density and extracellular matrix

1992 ◽  
Vol 153 (3) ◽  
pp. 483-490 ◽  
Author(s):  
Thierry David ◽  
Jacqueline Tassin ◽  
Douglas A. Lappi ◽  
Andrew Baird ◽  
Yves Courtois
Keyword(s):  
Extracellular Matrix ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Cell Density ◽  
Lens Epithelial Cell ◽  
Growth Effect ◽  
Bovine Lens ◽  
Biphasic Effect

Determinants of Sickle Cell Density Distribution: A Study of Benin Twins.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1244-1244
Author(s):  
Mary E. Fabry ◽  
Anne C. Rybicki ◽  
Sandra M. Suzuka ◽  
M. Cherif Rahimy ◽  
Rajagopal Krishnamoorthy ◽  
...  
Keyword(s):  
Density Distribution ◽  
Cell Density ◽  
Sickle Cell ◽  
Dna Analysis ◽  
Complex Mixture ◽  
Density Gradients ◽  
Red Cell ◽  
Alpha Thalassemia ◽  
Gardos Channel ◽  
One Year

Abstract Red cell density distribution affects both hemolysis and vaso-occlusion; however, currently recognized factors cannot account for all of the variation seen. We hypothesized that a range of genetically controlled factors contributes to red cell density distribution and hemolysis, which has recently received a great deal of attention from Gladwin et al for its role in sickle cell anemia (SCA) and its impact on NO metabolism. Our previous studies have demonstrated that although RBC density distribution varies significantly from patient to patient, the pattern for individual patients is stable in the absence of disease. Some genetically determined factors that affect red cell density distribution have been defined, such as alpha-thalassemia and % HbF (Fabry et al, Blood, 1982); however, neither of these factors completely predicts density distribution. The study of identical twins offers the unique opportunity to minimize some of the genetic variability between individuals that may not be relevant to RBC density while allowing the remaining differences to be detected. Because SCA patients from the US have a complex mixture of Caucasian, other ethnicities, and genes from all parts of Africa including all of the sickle haplotypes, we have chosen to recruit our population from Benin that has a single beta-globin haplotype, thus further minimizing differences arising from admixture from inside and outside of Africa. We have collected samples from six sets of monozygous twins from Benin and validated their monozygosity by DNA analysis. Of the 6 twin sets analyzed to date, 4 have alpha-thalassemia. We compared density gradients on two separate occasions, approximately one year apart, for these twins and found that density gradients for both members of all twin sets without medical complications (malaria, painful crisis) were indistinguishable. This is not true for pairs of randomly chosen individuals even after their % HbF and alpha-thalassemia status has been determined and matched. After elimination of WBCs, we were able to isolate sufficient RNA to obtain microarray data without amplification. We compared subjects with a low % dense cells vs a high % dense cells. In the combinations that were analyzed, we found a consistent pattern of up- and down-regulated genes. Down-regulated genes included the Gardos channel (KCNN4), K-Cl cotransporter (KCC1), NOS3, CAIV, and PKC. Up-regulated genes included ferritin heavy chain (probably in mitochondria that are present in reticulocytes) and 2,3-bisphosphomutase that was elevated in twins with higher MCHC (density). The latter is consistent with our previous observations and those of Poillon et al that DPG can affect polymer formation and RBC density. We conclude that the study of twins demonstrates that there is a strong genetic component in the control of sickle cell density distribution and that a better understanding of factors controlling density distribution may lead to new forms of treatment.

Electrical control of cell density gradients on a conducting polymer surface

2009 ◽  
pp. 5278 ◽  
Author(s):  
Alwin M. D. Wan ◽  
Daniel J. Brooks ◽  
Abdurrahman Gumus ◽  
Claudia Fischbach ◽  
George G. Malliaras
Keyword(s):  
Cell Density ◽  
Conducting Polymer ◽  
Polymer Surface ◽  
Density Gradients ◽  
Electrical Control

scholarly journals The ZO-1–associated Y-box factor ZONAB regulates epithelial cell proliferation and cell density

2003 ◽  
Vol 160 (3) ◽  
pp. 423-432 ◽  
Author(s):  
Maria S. Balda ◽  
Michelle D. Garrett ◽  
Karl Matter
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Tight Junctions ◽  
Cell Density ◽  
Mdck Cells ◽  
Nuclear Accumulation ◽  
Regulation Of Transcription ◽  
Epithelial Cell Proliferation ◽  
Nucleic Acid Binding ◽  
Nucleic Acid Binding Proteins

Epithelial tight junctions regulate paracellular permeability, restrict apical/basolateral intramembrane diffusion of lipids, and have been proposed to participate in the control of epithelial cell proliferation and differentiation. Previously, we have identified ZO-1–associated nucleic acid binding proteins (ZONAB), a Y-box transcription factor whose nuclear localization and transcriptional activity is regulated by the tight junction–associated candidate tumor suppressor ZO-1. Now, we found that reduction of ZONAB expression using an antisense approach or by RNA interference strongly reduced proliferation of MDCK cells. Transfection of wild-type or ZONAB-binding fragments of ZO-1 reduced proliferation as well as nuclear ZONAB pools, indicating that promotion of proliferation by ZONAB requires its nuclear accumulation. Overexpression of ZONAB resulted in increased cell density in mature monolayers, and depletion of ZONAB or overexpression of ZO-1 reduced cell density. ZONAB was found to associate with cell division kinase (CDK) 4, and reduction of nuclear ZONAB levels resulted in reduced nuclear CDK4. Thus, our data indicate that tight junctions can regulate epithelial cell proliferation and cell density via a ZONAB/ZO-1–based pathway. Although this regulatory process may also involve regulation of transcription by ZONAB, our data suggest that one mechanism by which ZONAB and ZO-1 influence proliferation is by regulating the nuclear accumulation of CDK4.

scholarly journals A novel role of PRL in regulating epithelial cell density by inducing apoptosis at confluence

2021 ◽  
Author(s):  
Sweksha Lohani ◽  
Yosuke Funato ◽  
Yuki Akieda ◽  
Kiyohito Mizutani ◽  
Yoshimi Takai ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Density ◽  
Mdck Cells ◽  
Zebrafish Embryos ◽  
Developmental Defect ◽  
Convergent Extension ◽  
Regenerating Liver ◽  
Phosphatase Of Regenerating Liver ◽  
Multicellular Organisms

Maintaining proper epithelial cell density is essential for the survival of multicellular organisms. While regulation of cell density through apoptosis is well known, its mechanistic details remain elusive. Here, we report the involvement of membrane-anchored phosphatase of regenerating liver (PRL), originally known for its role in cancer malignancy, in this process. In epithelial MDCK cells, upon confluence, doxycycline-induced expression of PRL upregulated apoptosis, reducing the cell density. This could be circumvented by artificially reducing the cell density via stretching the cell-seeded silicon chamber. Moreover, siRNA-mediated knockdown of endogenous PRL blocked apoptosis, leading to greater cell density. Mechanistically, PRL promoted apoptosis by upregulating the translation of E-cadherin and activating TGF-β pathway. Morpholino-mediated inhibition of PRL expression in zebrafish embryos caused developmental defect with reduced apoptosis and increased epithelial cell density during convergent extension. This study revealed a novel role of PRL in regulating density-dependent apoptosis in vertebrate epithelium.

Sign in / Sign up

Export Citation Format

Share Document