Cell surface area as a major parameter in the uptake of cadmium by unicellular green microalgae

1997 ◽  
Vol 65 (1) ◽  
pp. 13-19 ◽  
Author(s):  
A. Khoshmanesh ◽  
F. Lawson ◽  
I.G. Prince
Keyword(s):  
Cell Surface ◽  
Surface Area ◽  
Green Microalgae ◽  
Cell Surface Area ◽  
Major Parameter

scholarly journals MiR-26a-5p inhibits GSK3β expression and promotes cardiac hypertrophy in vitro

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10371
Author(s):  
Liqun Tang ◽  
Jianhong Xie ◽  
Xiaoqin Yu ◽  
Yangyang Zheng
Keyword(s):  
Cell Surface ◽  
Cardiac Hypertrophy ◽  
Surface Area ◽  
Myocardial Cell ◽  
Immunofluorescence Staining ◽  
Cell Surface Area ◽  
Direct Target

Background The role of miR-26a-5p expression in cardiac hypertrophy remains unclear. Herein, the effect of miR-26a-5p on cardiac hypertrophy was investigated using phenylephrine (PE)-induced cardiac hypertrophy in vitro and in a rat model of hypertension-induced hypertrophy in vivo. Methods The PE-induced cardiac hypertrophy models in vitro and vivo were established. To investigate the effect of miR-26a-5p activation on autophagy, the protein expression of autophagosome marker (LC3) and p62 was detected by western blot analysis. To explore the effect of miR-26a-5p activation on cardiac hypertrophy, the relative mRNA expression of cardiac hypertrophy related mark GSK3β was detected by qRT-PCR in vitro and vivo. In addition, immunofluorescence staining was used to detect cardiac hypertrophy related mark α-actinin. The cell surface area was measured by immunofluorescence staining. The direct target relationship between miR-26a-5p and GSK3β was confirmed by dual luciferase report. Results MiR-26a-5p was highly expressed in PE-induced cardiac hypertrophy. MiR-26a-5p promoted LC3II and decreased p62 expression in PE-induced cardiac hypertrophy in the presence or absence of lysosomal inhibitor. Furthermore, miR-26a-5p significantly inhibited GSK3β expression in vitro and in vivo. Dual luciferase report results confirmed that miR-26a-5p could directly target GSK3β. GSK3β overexpression significantly reversed the expression of cardiac hypertrophy-related markers including ANP, ACTA1 and MYH7. Immunofluorescence staining results demonstrated that miR-26a-5p promoted cardiac hypertrophy related protein α-actinin expression, and increased cell surface area in vitro and in vivo. Conclusion Our study revealed that miR-26a-5p promotes myocardial cell autophagy activation and cardiac hypertrophy by regulating GSK3β, which needs further research.

scholarly journals Ca2+-activated cleavage of ezrin visualised dynamically in living myeloid cells during cell surface area expansion

2020 ◽  
Vol 133 (5) ◽  
pp. jcs236968 ◽  
Author(s):  
Rhiannon E. Roberts ◽  
Marianne Martin ◽  
Sabrina Marion ◽  
Geetha L. Elumalai ◽  
Kimberly Lewis ◽  
...  
Keyword(s):  
Cell Surface ◽  
Surface Area ◽  
Myeloid Cells ◽  
Cell Surface Area ◽  
Area Expansion

scholarly journals Abnormalities in the mechanical properties of red blood cells caused by Plasmodium falciparum

Blood ◽  
1989 ◽  
Vol 74 (2) ◽  
pp. 855-861 ◽  
Author(s):  
GB Nash ◽  
E O'Brien ◽  
EC Gordon-Smith ◽  
JA Dormandy
Keyword(s):  
Mechanical Properties ◽  
Plasmodium Falciparum ◽  
Cell Surface ◽  
Surface Area ◽  
Volume Ratio ◽  
Great Difficulty ◽  
Cell Entry ◽  
Cell Surface Area ◽  
Entry Time ◽  
Main Factor

Abstract Although changes in the mechanical properties of infected red cells may contribute to the pathophysiology of malaria, such changes have not previously been described in detail. In this study, the physical properties of individual cells from both clinical and cultured samples infected with Plasmodium falciparum were tested using micropipette aspiration techniques. Cells containing ring forms took about 50% longer to enter 3 microns pipettes compared with nonparasitised cells, and there was a similar increase in the critical pressure required to induce cell entry. These abnormalities were similar in clinical and cultured samples. More mature cultured parasites (ie, trophozoites and schizonts containing pigment) caused much greater loss of deformability, with entry time and pressure increased four to sixfold. The decrease in deformability of the ring forms was attributable to a deficit in cell surface area/volume ratio (based on micropipette measurement of the surface area and volume of individual cells) and slight stiffening of the cell membrane (shear elastic modulus increased 13%, as measured by pipette aspiration of small membrane tongues). Measurement of the rate of cell shape recovery indicated that the membrane of parasitised cells was not more viscous. The main factor in the drastic loss of deformability of the trophozoites and schizonts was the presence of the large very resistant parasite itself. Otherwise, the cell surface area/volume deficit was slightly less and membrane rigidification slightly greater compared with ring forms. The above abnormalities should cause the trophozoites and schizonts to have great difficulty in traversing splenic or marrow sinuses and could contribute to microvascular occlusion and sequestration. On the other hand, the ring forms may be expected to circulate relatively unhindered.

scholarly journals Relationship between surface area and volume of the mastoid air cell system in adult humans

2011 ◽  
Vol 125 (6) ◽  
pp. 580-584 ◽  
Author(s):  
J D Swarts ◽  
B M Cullen Doyle ◽  
W J Doyle
Keyword(s):  
Cell Surface ◽  
Linear Function ◽  
Surface Area ◽  
Cell System ◽  
Cell Surface Area ◽  
Surface Areas ◽  
Wide Range ◽  
Computed Tomography Scanning ◽  
Cell Volumes ◽  
Area And Volume

AbstractIntroduction:The geometry of the adult human mastoid air cell system has not previously been described over a large range of mastoid air cell volumes.Methods:Twenty subjects with a wide range of mastoid air cell pneumatised areas, as determined by X-ray, underwent computed tomography scanning of the middle ear. Mastoid air cell surface areas and volumes were then reconstructed from serial imaging sections, using Image J software.Results:Mastoid air cell volumes varied from 0.7 to 21.4 ml, and were linearly related to the pneumatised area. Right and left mastoid air cell volumes and surface areas were highly correlated. The mastoid air cell surface area was a linear function of volume.Conclusion:The relationship between mastoid air cell surface area and volume is similar over a wide range of volumes. Given that the rate of gas exchange across the mastoid air cell mucosa is related to the mastoid air cell surface area, that rate will thus also be a direct linear function of the mastoid air cell volume.

Abstract 3770: Concentration-dependent Divergent Hypertrophic Effects of Estrogen in Adult Ventricular Myocytes

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ana Kilic ◽  
Sabzali A Javadov ◽  
Morris Karmazyn
Keyword(s):  
Cell Surface ◽  
Surface Area ◽  
Ventricular Remodeling ◽  
Specific Inhibitor ◽  
Left Ventricular ◽  
Synthetic Analog ◽  
Gene Markers ◽  
Low Concentration ◽  
Cell Surface Area ◽  
High Concentrations

High concentrations of estrogen have been shown to attenuate myocardial hypertrophy and left ventricular remodeling. However, the effects of low concentration of estrogen observed in postmenopausal women on cardiac hypertrophy have not been studied. In the present study we examined the effects of high (0.1 and 1 nM) and low (1 and 10 pM) concentration of the synthetic analog of estradiol, 17β-estradiol (E2) on adult cardiomyocytes (CMs). CMs were isolated from adult male and female Sprague-Dawley rats. The cells were used immediately after isolation to measure pH i or cultured to assess hypertrophic phenotype (cell surface area), gene markers (atrial natriuretic peptide, ANP), and protein activation. Low concentration of E2 (1 and 10 pM) increased cell surface area (females: 20%, P <0.05; males: 28%, P <0.05) and ANP expression (females: 394%, P <0.05; males: 497%, P <0.05) after 24 h. However, high concentrations (0.1 and 1 nM) of E2 did not induce cell hypertrophy but instead blocked the hypertrophic effect of the α 1 -agonist phenylephrinerophy. The pro-hypertrophic effect of low concentration of E2 was prevented by the sodium-hydrogen exchange isoform 1 (NHE-1) specific inhibitor AVE-4890 (AVE, 5 μM) suggesting involvement of NHE-1 in mediating the E2-induced hypertrophy. Fluorometric measurements with the pH i -sensitive dye BCECF demonstrated that a 1 pM E2 increased the pH i (females: +0.05 pH units; males +0.12 pH units, P <0.05) by a rapid non-genomic mechanism that was blocked by AVE. On the other hand, 1 nM E2 decreased the pH i (females: −0.24 pH units, P <0.05; males: −0.07 pH units, P <0.05) and this effect was also prevented by AVE. The NHE-1-mediated pro-hypertrophic effect of 1 pM E2 was dependent on phosphorylation of ERK1/2 MAPK since the effect was blocked with the ERK1/2 inhibitor PD98059 (10 μM) and there was no gender difference on ERK1/2 activation. E2 has a dual concentration-dependent role in adult CMs as manifested by a pro-hypertrophic effect at low concentrations (1 and 10 pM), and conversely, an anti-hypertrophic effect at high concentrations (0.1 and 1 nM). The pro-hypertrophic effect of E2 is mediated, at least in part, through ERK1/2/NHE-1 activation.

Analysis of hydrostatic pressure-induced changes in umbrella cell surface area

Methods ◽  
2003 ◽  
Vol 30 (3) ◽  
pp. 207-217 ◽  
Author(s):  
Edward Wang ◽  
Steven Truschel ◽  
Gerard Apodaca
Keyword(s):  
Hydrostatic Pressure ◽  
Cell Surface ◽  
Surface Area ◽  
Cell Surface Area ◽  
Umbrella Cell ◽  
Induced Changes

scholarly journals High level expression of transfected beta- and gamma-actin genes differentially impacts on myoblast cytoarchitecture

1992 ◽  
Vol 117 (4) ◽  
pp. 775-785 ◽  
Author(s):  
G Schevzov ◽  
C Lloyd ◽  
P Gunning
Keyword(s):  
Cell Surface ◽  
Surface Area ◽  
Mutant Form ◽  
Actin Gene ◽  
High Level Expression ◽  
Cell Surface Area ◽  
Actin Genes ◽  
Beta Actin ◽  
High Level ◽  
Actin Protein

The impact of the human beta- and gamma-actin genes on myoblast cytoarchitecture was examined by their stable transfection into mouse C2 myoblasts. Transfectant C2 clones expressing high levels of human beta-actin displayed increases in cell surface area. In contrast, C2 clones with high levels of human gamma-actin expression showed decreases in cell surface area. The changes in cell morphology were accompanied by changes in actin stress-fiber organization. The beta-actin transfectants displayed well-defined filamentous organization of actin; whereas the gamma-actin transfectants displayed a more diffuse organization of the actin cables. The role of the beta-actin protein in generating the enlarged cell phenotype was examined by transfecting a mutant form of the human beta-actin gene. Transfectant cells were shown to incorporate the aberrant actin protein into stress-fiber-like structures. High level expression of the mutant beta-actin produced decreases in cell surface area and disruption of the actin microfilament network similar to that seen with transfection of the gamma-actin gene. In contrast, transfection of another mutant form of the beta-actin gene which encodes an unstable protein had no impact on cell morphology or cytoarchitecture. These results strongly suggest that it is the nature of the encoded protein that determines the morphological response of the cell. We conclude that the relative gene expression of beta- and gamma-actin is of relevance to the control of myoblast cytoarchitecture. In particular, we conclude that the beta- and gamma-actin genes encode functionally distinct cytoarchitectural information.

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