scholarly journals Corneal endothelial cells changes in different stages of Keratoconus: a multi-Centre clinical study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ahmed Elmassry ◽  
Ahmed Osman ◽  
Moataz Sabry ◽  
Mohamed Elmassry ◽  
Mai Katkat ◽  
...  

Abstract Purpose To assess the corneal endothelial cells morphology and count in keratoconus patients and their correlation with different stages of keratoconus. Methods Prospective non randomized multi-centric clinical study included 150 eyes of 150 keratoconus patients. Four centers in Egypt participated in this study included: Departments of Ophthalmology in Alexandria University, Tanta University and Port Said University and Alex I-Care hospital. Pentacam (Wavelight Oculyzer II) and specular microscopy (Tomey EM-3000) were done to all eyes. Keratoconic eyes were classified according to Amsler classification into stage 1, 2 and 3. Stage 1 included 99 eyes, stage 2 included 32 eyes & stage 3 included 19 eyes. Results The mean age of keratoconus patients was 24.07 ± 6.154 years. Forty five cases were males (30%) and 105 cases were females (70%). There was statistically significant difference in endothelial cell density (p < 0.001) and coefficient of variation (p = 0.012) between different stages of keratoconus eyes. Regarding cell surface area, there was statistically significant difference in cell surface area between different stages of keratoconus eyes (p < 0.001). In addition, for cell morphology, there was statistically significant difference between different stages of keratoconus eyes (p < 0.001). Conclusions Qualitative and quantitative structural changes were seen in endothelial cells of keratoconus eyes by using specular microscopy. For stages 1 and 2, keratoconus may not affect the corneal endothelim significantly. The endothelium in stage 3 shows significant changes regarding polymegathism and pleomorphism.

2006 ◽  
Vol 290 (6) ◽  
pp. H2210-H2219 ◽  
Author(s):  
Susann Patschan ◽  
Hong Li ◽  
Sergey Brodsky ◽  
David Sullivan ◽  
Dino A. De Angelis ◽  
...  

Glycosylphosphatidylinositol (GPI)-anchored proteins have been shown to cluster in microdomains enriched in glycosphingolipids and cholesterol and represent a relatively selective marker of lipid rafts. In recent years, several attempts have been made to use fluorescent probes to nondisruptively label these domains in living cells. Here, we have transfected endothelial cells with a GPI-anchored thermotolerant green fluorescent protein (ttGFP) to show colocalization of this fluoroprobe with another marker of lipid rafts, urokinase-type plasminogen activator receptor-1. ttGFP was used to quantify the cell surface area occupied by lipid rafts and to examine the effect of various proatherogenic signals on lipid rafts. Exposure of endothelial cells to asymmetric dimethylarginine and oxidized LDL (oxLDL), as well as oxidant stress, reduced the cell surface area occupied by lipid rafts. Next, the property of ttGFP to undergo a shift in absorbance depending on the clustering of these molecules was utilized to perform proximity imaging (PRIM). PRIM showed that nitric oxide (NO) increased the distance between GPI-anchored ttGFP molecules clustered in lipid-rich microdomains. This “unclustering” of GPI-anchored ttGFP was not reproduced by prooxidant signals and was due to reduction in membrane-cytoskeletal constraints on the lipid rafts. These findings suggested that two fundamentally different mechanisms modulate lipid rafts: 1) substance regulation of lipid rafts involving modification of cholesterol and sphingolipids and 2) structural regulation of lipid rafts through disruption of membrane-cytoskeletal interactions, switching off the spatial confinement of lipid rafts.


PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10371
Author(s):  
Liqun Tang ◽  
Jianhong Xie ◽  
Xiaoqin Yu ◽  
Yangyang Zheng

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.


2018 ◽  
Vol 22 (2) ◽  
pp. 177-182
Author(s):  
Natàlia Coyo ◽  
Marta Leiva ◽  
Daniel Costa ◽  
Rafael Molina ◽  
Olga Nicolás ◽  
...  

2020 ◽  
Vol 133 (5) ◽  
pp. jcs236968 ◽  
Author(s):  
Rhiannon E. Roberts ◽  
Marianne Martin ◽  
Sabrina Marion ◽  
Geetha L. Elumalai ◽  
Kimberly Lewis ◽  
...  

Blood ◽  
1989 ◽  
Vol 74 (2) ◽  
pp. 855-861 ◽  
Author(s):  
GB Nash ◽  
E O'Brien ◽  
EC Gordon-Smith ◽  
JA Dormandy

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.


2011 ◽  
Vol 125 (6) ◽  
pp. 580-584 ◽  
Author(s):  
J D Swarts ◽  
B M Cullen Doyle ◽  
W J Doyle

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.


2018 ◽  
Vol 15 (2S) ◽  
pp. 145-152
Author(s):  
S. V. Shukhaev ◽  
E. V. Boiko

Purpose: to compare two types of phacoemulsification parameters (combination ultrasound and torsional US with IP) with estimating the number of postoperative complications caused by intraoperative trauma of corneal endothelial cells.Patients and methods. 72 patients underwent phacoemulsification with IOL implantation. Patients were randomly divided into two groups (main n = 33 and control n = 39). During the aspiration of lens fragments in the main group the combination ultrasound was used, while torsional US with IP was used in the control group. Endothelial cell counting and other examinations were performed 1 day, 1 week and 6 months after the surgery.Results. CDVA in the explored groups 1 week after the surgery was similar: the main group — 0.813 ± 0.228, the control group — 0.765 ± 0.250, There was also no statistically significant difference in the thickness of the cornea between the groups: the main group — 533.48 ± 12.41, the control group — 536.44 ± 10.92. At the same time, a statistically significant difference was found in the density of endothelial cells: the main group: 1871.30 ± 187.41 (after 1 week), 1865 ± 178.9 (after 6 months); control group: 1809.63 ± 225.43 (after 1 week), 1791 ± 230.82 (after 6 months). The percentage of cell loss was, respectively, lower in the main group at all times of observation: 3.90% (after 1 day), 4.54% (after 1 week), 4.9% (after 6 months). In the control group: 7.71% (after 1 day), 9.25% (after 1 week), 10.4% (after 6 months).Conclusions. Data obtained in this study has showed the advantages of combination ultrasound in comparison with torsional US with IP, when performing aspiration of dense lenses. Due to lower consumption of ultrasound energy and higher aspiration rate of the fragments, combination ultrasound can reduce the loss of corneal endothelial cells and decrease the number and severity of postoperative complications associated with it. 


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ana Kilic ◽  
Sabzali A Javadov ◽  
Morris Karmazyn

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.


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