scholarly journals Autophagy attenuates high glucose-induced oxidative injury to lens epithelial cells

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Xiaomin Liu ◽  
Xiaowen Zhao ◽  
Rong Cheng ◽  
Yusen Huang
Keyword(s):  
Oxidative Stress ◽  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Epithelial Cells ◽  
High Glucose ◽  
Lens Epithelial Cells ◽  
Ros Generation ◽  
Diabetic Mice ◽  
Transmission Electron ◽  
And Oxidative Stress

Abstract Purpose: Autophagic dysfunction and abnormal oxidative stress are associated with cataract. The purpose of the present study was to investigate the changes of cellular autophagy and oxidative stress and their association in lens epithelial cells (LECs) upon exposure to high glucose. Methods: Autophagy and oxidative stress-related changes were detected in streptozotocin-induced Type 1 diabetic mice and normal mouse LECs incubated in high glucose conditions. Rapamycin at a concentration of 100 nm/l or 50 μM chloroquine was combined for analysis of the relationship between autophagy and oxidative stress. The morphology of LECs during autophagy was observed by transmission electron microscopy. The expressions of autophagy markers (LC3B and p62) were identified, as well as the key factors of oxidative stress (SOD2 and CAT) and mitochondrial reactive oxygen species (ROS) generation. Results: Transmission electron microscopy indicated an altered autophagy activity in diabetic mouse lens tissues with larger autophagosomes and multiple mitochondria. Regarding the expressions, LC3B was elevated, p62 was decreased first and then increased, and SOD2 and CAT were increased before a decrease during 4 months of follow-up in diabetic mice and 72 h of culture under high glucose for mouse LECs. Furthermore, rapamycin promoted the expressions of autophagy markers but alleviated those of oxidative stress markers, whereas chloroquine antagonized autophagy but enhanced oxidative stress by elevating ROS generation in LECs exposed to high glucose. Conclusions: The changes in autophagy and oxidative stress were fluctuating in the mouse LECs under constant high glucose conditions. Autophagy might attenuate high glucose-induced oxidative injury to LECs.

Oviducal structure in four species of gekkonid lizard differing in parity mode and eggshell structure

1998 ◽  
Vol 10 (2) ◽  
pp. 139 ◽  
Author(s):  
J. E. Girling ◽  
A. Cree ◽  
L. J. Guillette, Jr
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Epithelial Cells ◽  
Uterine Tube ◽  
Hemidactylus Turcicus ◽  
Transmission Electron ◽  
Eggshell Structure ◽  
Scanning Electron ◽  
Parity Mode

Oviducal structure was analysed in vitellogenic females from four species of gekkonid lizard exhibiting variation in parity mode and eggshell structure: Hemidactylus turcicus (oviparous) which produces a hard, calcareous eggshell; Saltuarius wyberba (oviparous) which produces a soft, parchment-like eggshell; and Hoplodactylus maculatus and Hoplodactylus duvaucelii (both viviparous). Oviducts were analysed by light, scanning electron and transmission electron microscopy. The uterus exhibited differences among species that were directly attributable to parity mode. H. turcicus and S. wyberba (oviparous) had numerous uterine shell glands; H. maculatus and H. duvaucelii(viviparous) had very few. The uterus also exhibited differences between the two oviparous species (H. turcicusand S. wyberba) which may be related to the type of eggshell produced. Variations were noted in the staining properties of the uterine glandular and epithelial cells. The structure of the infundibulum, uterine tube, isthmus and vagina also differed among species, but differences could not be directly related to parity mode or eggshell structure. Instead, the differences may be related to how prepared the oviduct is for ovulation in individuals analysed from the different species. This study confirms, in the Gekkonidae, aspects of oviducal structure that have been associated with parity mode in other squamate taxa.

scholarly journals Investigation of Cytotoxicity, Apoptosis, and Oxidative Stress Response of Fe3O4-RGO Nanocomposites in Human Liver HepG2 cells

Materials ◽  
2020 ◽  
Vol 13 (3) ◽  
pp. 660 ◽  
Author(s):  
Maqusood Ahamed ◽  
Mohd Javed Akhtar ◽  
M. A. Majeed Khan
Keyword(s):  
Oxidative Stress ◽  
Electron Microscopy ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Molecular Level ◽  
Biological Response ◽  
Cycle Arrest ◽  
Transmission Electron ◽  
Mitochondrial Membrane Potential Loss ◽  
And Oxidative Stress

Iron oxide–reduced graphene oxide (Fe3O4-RGO) nanocomposites have attracted enormous interest in the biomedical field. However, studies on biological response of Fe3O4-RGO nanocomposites at the cellular and molecular level are scarce. This study was designed to synthesize, characterize, and explore the cytotoxicity of Fe3O4-RGO nanocomposites in human liver (HepG2) cells. Potential mechanisms of cytotoxicity of Fe3O4-RGO nanocomposites were further explored through oxidative stress. Prepared samples were characterized by UV-visible spectrophotometer, X-ray diffraction, scanning electron microscopy, transmission electron microscopy, and energy dispersive spectroscopy. The results demonstrated that RGO induce dose-dependent cytotoxicity in HepG2 cells. However, Fe3O4-RGO nanocomposites were not toxic. We further noted that RGO induce apoptosis in HepG2 cells, as evidenced by mitochondrial membrane potential loss, higher caspase-3 enzyme activity, and cell cycle arrest. On the other hand, Fe3O4-RGO nanocomposites did not alter these apoptotic parameters. Moreover, we observed that RGO increases intracellular reactive oxygen species and hydrogen peroxide while decrease antioxidant glutathione. Again, Fe3O4-RGO nanocomposites did not exert oxidative stress. Altogether, we found that RGO significantly induced cytotoxicity, apoptosis and oxidative stress. However, Fe3O4-RGO nanocomposites showed good biocompatibility to HepG2 cells. This study warrants further research to investigate the biological response of Fe3O4-RGO nanocomposites at the gene and molecular level.

scholarly journals Effect of thioltransferase on oxidative stress induced by high glucose and advanced glycation end products in human lens epithelial cells

2021 ◽  
Vol 14 (7) ◽  
pp. 965-972
Author(s):  
Qing Liu ◽  
◽  
Hong Yan ◽  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Advanced Glycation End Products ◽  
High Glucose ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Advanced Glycation ◽  
Human Lens Epithelial Cells ◽  
Glycation End Products ◽  
End Products

AIM: To study the effect of thioltransferase (TTase) on oxidative stress in human lens epithelial cells (HLECs) induced by high glucose and advanced glycation end products (AGEs). METHODS: HLECs were treated with 35.5 mmol/L glucose or 1.5 mg/mL AGEs modified bovine serum albumin (AGEs-BSA) as the experimental groups, respectively. Cells were collected at the time point of 1, 2, 3, and 4d. The TTase activity were measured accordingly. TTase mRNA levels were detected by quantitative reverse transcription polymerase chain response (qRT-RCR) and its protein level was detected by Western blot. The siRNA was used to knock down the expression of TTase. The activity of catalase (CAT) and superoxide dismutase (SOD), the content of reactive oxygen species (ROS) and the ratio of oxidized glutathione/total glutathione (GSSG/T-GSH) were assessed in different groups, respectively. RESULTS: The level of TTase mRNA gradually increased and reached the top at 2d, then it decreased to the normal level at 4d, and the TTase activity increased from 2 to 3d in both high glucose and AGEs-BSA groups. The TTase expression elevated from 2d in high glucose group, and it began to rise from 3d in AGEs-BSA group. The activity of CAT and SOD showed a decrease and the content of ROS and the ratio of GSSG/T-GSH showed an increase in high glucose and AGEs-BSA group. These biochemical alterations were more prominent in the groups with TTase siRNA. CONCLUSION: High glucose and AGEs can increase ROS content in HLECs; therefore, it induces oxidative stress. This may result in the decreased GSH and increased GSSG content, impaired activity of SOD and CAT. The up-regulated TTase likely provides oxidation damage repair induced by high glucose and AGEs in the early stage.

Angiotensin II-mediated oxidative stress promotes myocardial tissue remodeling in the transgenic (mRen2) 27 Ren2 rat

2007 ◽  
Vol 293 (1) ◽  
pp. E355-E363 ◽  
Author(s):  
Adam Whaley-Connell ◽  
Gurushankar Govindarajan ◽  
Javad Habibi ◽  
Melvin R. Hayden ◽  
Shawna A. Cooper ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Heart Tissue ◽  
Left Ventricular ◽  
Cine Mri ◽  
Ang Ii ◽  
Transmission Electron

Angiotensin II (ANG II) contributes to cardiac remodeling, hypertrophy, and left ventricular dysfunction. ANG II stimulation of the ANG type 1 receptor (AT1R) generates reactive oxygen species via NADPH oxidase, which facilitates this hypertrophy and remodeling. This investigation sought to determine whether cardiac oxidative stress and cellular remodeling could be attenuated by in vivo AT1R blockade (AT1B) (valsartan) or superoxide dismutase/catalase mimetic (tempol) treatment in a rodent model of chronically elevated tissue levels of ANG II, the transgenic (mRen2) 27 rat (Ren2). Ren2 rats overexpress the mouse renin transgene with resultant hypertension, insulin resistance, proteinuria, and cardiovascular damage. Young (6–7 wk old) male Ren2 and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Heart tissue NADPH oxidase (NOX) activity and immunohistochemical analysis of subunits NOX2, Rac1, and p22phox, heart tissue malondialdehyde, and insulin-stimulated protein kinase B (Akt) activation were measured. Structural changes were assessed with cine MRI, transmission electron microscopy, and light microscopy. Increases in septal wall thickness and altered systolic function (cine MRI) were associated with perivascular fibrosis and increased mitochondria in Ren2 on light and transmission electron microscopy ( P < 0.05). AT1B, but not tempol, reduced blood pressure ( P < 0.05); significant improvements were seen with both AT1B and tempol on NOX activity, subunit expression, malondialdehyde, and insulin-mediated activation/phosphorylation of Akt (each P < 0.05). Collectively, these data suggest cardiac oxidative stress-induced structural and functional changes are driven, in part, by AT1R-mediated increases in NADPH oxidase activity.

Cdc20 protects cells from Ara-c-induced apoptosis in AML via targeting  autophagy

2021 ◽  
Author(s):  
Shumin Ding ◽  
Jinyao Kan ◽  
Yan Wang ◽  
Siyuan Cui ◽  
Jingyi Wang ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Cell Viability ◽  
Western Blotting ◽  
Ros Generation ◽  
Apoptosis Rate ◽  
Rate Expression ◽  
Transmission Electron ◽  
Induced Apoptosis

Abstract ObjectiveThis study aims to explore the role and mechanism of Cdc20 on Ara-c chemosensitivity of AML cells.MethodsEvaluation experiments of effects of Cdc20 on Ara-c chemosensitivity were performed with AML cell transfected with constructs overexpressing Cdc20 or AML cell transfected with Cdc20 shRNA through observing cell viability, apoptosis rate,expression of apoptosis protein.The level of autophagy was assessed by transmission electron microscopy and western blotting.ResultsAfter exposure to Ara-c, Cdc20 expression is down-regulated. Intracellular Cdc20 expression inhibited Ara-c-induced apoptosis as shown by increasing cell viability and decreasing expression of cleaved caspase3.The expression of LC3B was mediated by Cdc20 expression,which further inhibits autophagy. Moreover, Cdc20 mediated LC3B-decreasing promotes the expression of P-Akt and P-ERK and inhibits ROS generation.ConclusionIt was determined that Cdc20 promoted the degradation of LC3B, thereby inhibiting autophagy and decreasing Ara-c-induced apoptosis in AML cells.

scholarly journals Ultrastructure of the Epithelial Cells Associated with Tooth Biomineralization in the Chiton Acanthopleura hirtosa

2009 ◽  
Vol 15 (2) ◽  
pp. 154-165 ◽  
Author(s):  
Jeremy A. Shaw ◽  
David J. Macey ◽  
Lesley R. Brooker ◽  
Edward J. Stockdale ◽  
Martin Saunders ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Epithelial Cells ◽  
Light Microscopy ◽  
Mineralization Process ◽  
Conventional Transmission Electron Microscopy ◽  
Physiological Conditions ◽  
Microwave Assisted ◽  
Transmission Electron ◽  
Extracellular Compartment

AbstractThe cusp epithelium is a specialized branch of the superior epithelium that surrounds the developing teeth of chitons and is responsible for delivering the elements required for the formation of biominerals within the major lateral teeth. These biominerals are deposited within specific regions of the tooth in sequence, making it possible to conduct a row by row examination of cell development in the cusp epithelium as the teeth progress from the unmineralized to the mineralized state. Cusp epithelium from the chiton Acanthopleura hirtosa was prepared using conventional chemical and microwave assisted tissue processing, for observation by light microscopy, conventional transmission electron microscopy (TEM) and energy filtered TEM. The onset of iron mineralization within the teeth, initiated at row 13, is associated with a number of dramatic changes in the ultrastructure of the apical cusp cell epithelium. Specifically, the presence of ferritin containing siderosomes, the position and number of mitochondria, and the structure of the cell microvilli are each linked to aspects of the mineralization process. These changes in tissue development are discussed in context with their influence over the physiological conditions within both the cells and extracellular compartment of the tooth at the onset of iron mineralization.

scholarly journals Mesenchymal stem cell-derived exosomes inhibit the VEGF-A expression in human retinal vascular endothelial cells induced by high glucose

2021 ◽  
Vol 14 (12) ◽  
pp. 1820-1827
Author(s):  
Guang-Hui He ◽  
◽  
Meng Dong ◽  
Song Chen ◽  
Yu-Chuan Wang ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Endothelial Cells ◽  
High Glucose ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Nanoparticle Tracking Analysis ◽  
Transmission Electron ◽  
Group B ◽  
Group D

AIM: To determine the effect of exosomes derived from human umbilical cord blood mesenchymal stem cells (hUCMSCs) on the expression of vascular endothelial growth factor A (VEGF-A) in human retinal vascular endothelial cells (HRECs). METHODS: Exosomes were isolated from hUCMSCs using cryogenic ultracentrifugation and characterized by transmission electron microscopy, Western blotting and nanoparticle tracking analysis. HRECs were randomly divided into a normal control group (group A), a high glucose model group (group B), a high glucose group with 25 μg/mL (group C), 50 μg/mL (group D), and 100 μg/mL exosomes (group E). Twenty-four hours after coculture, the cell proliferation rate was detected using flow cytometry, and the VEGF-A level was detected using immunofluorescence. After coculture 8, 16, and 24h, the expression levels of VEGF-A in each group were detected using PCR and Western blots. RESULTS: The characteristic morphology (membrane structured vesicles) and size (diameter between 50 and 200 nm) were observed under transmission electron microscopy. The average diameter of 122.7 nm was discovered by nanoparticle tracking analysis (NTA). The exosomal markers CD9, CD63, and HSP70 were strongly detected. The proliferation rate of the cells in group B increased after 24h of coculture. Immunofluorescence analyses revealed that the upregulation of VEGF-A expression in HRECs stimulated by high glucose could be downregulated by cocultured hUCMSC-derived exosomes (F=39.03, P<0.01). The upregulation of VEGF-A protein (group C: F=7.96; group D: F=17.29; group E: F=11.89; 8h: F=9.45; 16h: F=12.86; 24h: F=42.28, P<0.05) and mRNA (group C: F=4.137; group D: F=13.64; group E: F=22.19; 8h: F=7.253; 16h: F=16.98; 24h: F=22.62, P<0.05) in HRECs stimulated by high glucose was downregulated by cocultured hUCMSC-derived exosomes (P<0.05). CONCLUSION: hUCMSC-derived exosomes downregulate VEGF-A expression in HRECs stimulated by high glucose in time and concentration dependent manner.

Extracellular potassium modifies the structure of kidney epithelial cells in culture

1985 ◽  
Vol 249 (1) ◽  
pp. C105-C110 ◽  
Author(s):  
S. Waack ◽  
M. M. Walsh-Reitz ◽  
F. G. Toback
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Epithelial Cells ◽  
Unit Surface Area ◽  
Scanning Electron Micrographs ◽  
Membrane Function ◽  
Transmission Electron ◽  
Kidney Epithelial Cells ◽  
K Concentration ◽  
Low K

In animals fed a K-deficient diet, alterations in kidney cell structure and function occur in association with changes in the ionic composition of the extracellular fluid. The hypothesis that the extracellular K concentration mediates these changes in renal tissue was tested in cultures of monkey kidney epithelial cells (BSC-1 line) by reducing the K concentration of the culture medium from the control value of 5.4 to 3.2 mM. Exposure of BSC-1 cells to low-K medium raised the maximal rate of uptake for L-glutamic acid by 39% without a change in apparent Km. To determine whether this alteration in plasma membrane function had a structural correlate, studies of the cell surface were performed using scanning and transmission electron microscopy. Morphometric analysis of scanning electron micrographs revealed that the number of microvilli per cell per unit surface area was 45% greater in cells exposed to low-K medium for 3 min than those exposed to control medium. This observation was confirmed by transmission electron microscopy. The results indicate that an alteration in the extracellular K concentration per se can modify specific structural and functional characteristics of kidney epithelial cells.

Sign in / Sign up

Export Citation Format

Share Document