scholarly journals Evaluation of programmed cell death processes on the lens epithelium of older dogs with diabetic and hypermature cataracts

2018 ◽  
Vol 55 (2) ◽  
pp. e133668
Author(s):  
Ana Paula Franco do Amaral Hvenegaard ◽  
Paulo Sergio De Moraes Barros ◽  
Angélica Mendonça Vaz Safatle ◽  
Michelle Barbosa Pereira Braga-Sá ◽  
Luana Vicente Melo ◽  
...  
Keyword(s):  
Cell Death ◽  
Cataract Surgery ◽  
Trypan Blue ◽  
Caspase 3 ◽  
Posterior Capsule Opacification ◽  
Beclin 1 ◽  
Cellular Damage ◽  
Lens Epithelial Cells ◽  
Future Studies ◽  
Proliferation And Differentiation

It is well known that posterior capsule opacification (PCO), one of the most common late postoperative complications of cataract surgery, is mainly caused by proliferation and differentiation of remaining lens epithelial cells (LECs) on the posterior lens capsule. Many authors suggest that alterations induced by the pathophysiology of cataracts, its metabolism and the use of 0.1% trypan blue (TB) must cause some degree of cellular damage on these cells, wicht would help to prevent and/or reduce the incidence of PCO after cataract surgery in humans. Therefore, the aim of this study was to evaluate the expression of cell death markers on LECs of older dogs with diabetic and hypermature cataracts, after capsulorhexis, both using 0.1% TB. Twenty samples collected from 13 dogs of different breeds, with ages varying from 8 to 12 years-old, with diabetic and hypermature cataracts, which had been subjected to phacoemulsification surgery (Phaco) using 0.1% TB for staining were studied. Animals were classified as dogs with diabetic (DC) and hypermature cataracts (HC), and expression of molecular markers for apoptosis and autophagy (caspase-3 and beclin-1) on LECs were obtained by immunofluorescence technique. The expression of caspase-3 and beclin-1 was observed in every studied sample and did not differ between groups. In conclusion, our findings suggest that apoptosis and autophagy processes occur to LECs in older dogs presenting diabetic and hypermature cataracts after Phaco utilizing 0.1% TB. Our results may be helpful to future studies of PCO in post-phacoemulsification surgery patients.

Surface modification of intraocular lenses with hyaluronic acid and lysozyme for the prevention of endophthalmitis and posterior capsule opacification

RSC Advances ◽  
2015 ◽  
Vol 5 (5) ◽  
pp. 3597-3604 ◽  
Author(s):  
Bailiang Wang ◽  
Quankui Lin ◽  
Tingwei Jin ◽  
Chenghui Shen ◽  
Junmei Tang ◽  
...  
Keyword(s):  
Surface Modification ◽  
Hyaluronic Acid ◽  
Epithelial Cells ◽  
Cataract Surgery ◽  
Posterior Capsule Opacification ◽  
Intraocular Lenses ◽  
Posterior Capsule ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Human Lens Epithelial Cells

Posterior capsule opacification is one of the complications of cataract surgery caused by the adhesion and reproduction of residual human lens epithelial cells (HLECs) on the posterior capsule.

scholarly journals In Vitro Growth of Lens Epithelial Cells from Cataract Patients - Association with Possible Risk Factors for Posterior Capsule Opacification

2014 ◽  
Vol 8 (1) ◽  
pp. 19-23 ◽  
Author(s):  
Karin Sundelin ◽  
Anne Petersen ◽  
Yalda Soltanpour ◽  
Madeleine Zetterberg
Keyword(s):  
Risk Factors ◽  
Epithelial Cells ◽  
Cataract Surgery ◽  
Calf Serum ◽  
Posterior Capsule Opacification ◽  
Posterior Capsule ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Proliferative Capacity

Aim : Inter-individual differences in intrinsic proliferative capacity of lens epithelial cells may have importance for the risk of developing posterior capsule opacification (PCO) after cataract surgery. The purpose of the present study was to determine growth of human lens epithelial cells (HLEC) in culture and investigate possible associations with clinical characteristics of the donors, such as age, sex, pseudoexfoliation, uveitis and diabetes. Methods : Pieces of lens capsule and adhering lens epithelial cells were obtained through capsulorhexis at cataract surgery. Specimens were cultured in a humidified CO2-incubator using standard culture medium and 5% fetal calf serum for two weeks after which cultured cells were stained with carboxy-fluorescein diacetate succinimidyl ester. Image processing software was used to determine the area of the confluent epithelial cell layer in relation to the size of the original capsule specimen. Results : The increase in area of confluent HLEC showed a negative correlation with diabetes at the first week after surgery. Lower age and female sex showed border-line significant associations with a higher rate of cell proliferation. The presence of pseudoexfoliation in vivo did not significantly affect cell growth in culture postoperatively. Nor did installation of xylocain in the anterior chamber during surgery. Conclusion : Diabetes is associated with lower rate of proliferation of lens epithelial cells in culture. The lack of strong correlations between in vitro growth and known risk factors for PCO in the donors suggest that other factors than the proliferative capacity of the cells per se are important for PCO formation.

scholarly journals Induction of Necrosis and DNA Fragmentation during Hypothermic Preservation of Hepatocytes in UW, HTK, and Celsior Solutions

2003 ◽  
Vol 12 (1) ◽  
pp. 59-68 ◽  
Author(s):  
Salomon L. Abrahamse ◽  
Pieter Van Runnard Heimel ◽  
Robin J. Hartman ◽  
Rob A. F. M. Chamuleau ◽  
Thomas M. Van Gulik
Keyword(s):  
Cell Death ◽  
Cell Viability ◽  
Dna Fragmentation ◽  
Trypan Blue ◽  
Caspase 3 ◽  
Trypan Blue Exclusion ◽  
Hypothermic Preservation ◽  
Mtt Reduction ◽  
Ldh Release ◽  
Porcine Hepatocytes

Donor cells can be preserved in University of Wisconsin (UW), histidine-tryptophan-ketoglutarate (HTK), or Celsior solution. However, differences in efficacy and mode of action in preventing hypothermia-induced cell injury have not been unequivocally clarified. Therefore, we investigated and compared necrotic and apoptotic cell death of freshly isolated primary porcine hepatocytes after hypothermic preservation in UW, HTK, and Celsior solutions and subsequent normothermic culturing. Hepatocytes were isolated from porcine livers, divided in fractions, and hypothermically (4°C) stored in phosphate-buffered saline (PBS), UW, HTK, or Celsior solution. Cell necrosis and apoptosis were assessed after 24- and 48-h hypothermic storage and after 24-h normothermic culturing following the hypothermic preservation periods. Necrosis was assessed by trypan blue exclusion, lactate dehydrogenase (LDH) release, and mitochondrial 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) reduction. Apoptosis was assessed by the induction of histone-associated DNA fragments and cellular caspase-3 activity. Trypan blue exclusion, LDH release, and MTT reduction of hypothermically preserved hepatocytes showed a decrease in cell viability of more than 50% during the first 24 h of hypothermic preservation. Cell viability was further decreased after 48-h preservation. DNA fragmentation was slightly enhanced in hepatocytes after preservation in all solutions, but caspase-3 activity was not significantly increased in these cells. Normothermic culturing of hypothermically preserved cells further decreased cell viability as assessed by LDH release and MTT reduction. Normothermic culturing of hypothermically preserved hepatocytes induced DNA fragmentation, but caspase-3 activity was not enhanced in these cells. Trypan blue exclusion, LDH leakage, and MTT reduction demonstrated the highest cell viability after storage in Celsior, and DNA fragmentation was the lowest in cells that had been stored in PBS and UW solutions. None of the preservation solutions tested in this study was capable of adequately preventing cell death of isolated porcine hepatocytes after 24-h hypothermic preservation and subsequent 24-h normothermic culturing. Culturing of isolated and hypothermically preserved hepatocytes induces DNA fragmentation, but does not lead to caspase-3 activation. With respect to necrosis and DNA fragmentation of hypothermically preserved cells, UW and Celsior were superior to PBS and HTK solutions in this model of isolated porcine hepatocyte preservation.

scholarly journals Beclin 1 Interacts With Active Caspase-3 and Bax in Oocytes From Atretic Follicles in the Rat Ovary

2019 ◽  
Vol 67 (12) ◽  
pp. 873-889 ◽  
Author(s):  
María L. Escobar ◽  
Olga M. Echeverria ◽  
Sebastián Palacios-Martínez ◽  
Silvia Juárez-Chavero ◽  
Luis Sánchez-Sánchez ◽  
...  
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Beclin 1 ◽  
Follicular Atresia ◽  
Different Types ◽  
Old Rats ◽  
Rat Ovary ◽  
Apoptotic Proteins ◽  
Autophagic Proteins ◽  
Active Caspase

Oocyte cell death is a normal process in the mammalian ovary during follicular growth. Recent reports have demonstrated the presence of pro-apoptotic and pro-autophagic proteins during oocyte elimination. The goal of this study was to identify the interactions between proteins involved in different types of programmed cell death in the same oocyte during follicular atresia. We evaluated the presence of Beclin 1 and its interaction with the pro-apoptotic proteins active caspase-3, Bax, and Bak by means of histochemical observations, ultrastructural immunodetection, and immunoprecipitation techniques in ovaries from prepubertal (28- and 33-day-old), juvenile (40-day-old), and young adult (90-day-old) rats. In this study, we identified that oocyte elimination occurred with a high quantity of pro-autophagic protein Beclin 1 and increased the presence of the pro-apoptotic proteins active caspase-3, Bax, and Bak. Conversely, the antiapoptotic protein Bcl-2 was reduced in oocytes from atretic follicles. In addition, Beclin 1 was shown to interact with active caspase-3 and Bax. Our results suggest that the increase in Beclin 1 is directly related to the rise of pro-apoptotic proteins, which could promote the apoptotic process during oocyte elimination.

The P-MAPA immunomodulator partially prevents apoptosis induced by Zika virus infection in THP-1 cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Morganna C. Lima ◽  
Elisa A. N. Azevedo ◽  
Clarice N. L. de Morais ◽  
Larissa I. O. de Sousa ◽  
Bruno M. Carvalho ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Virus Infection ◽  
Virus Replication ◽  
Zika Virus ◽  
Mammalian Cells ◽  
Caspase 3 ◽  
Neurological Complications ◽  
Zika Virus Infection

Background: Zika virus is an emerging arbovirus of global importance. ZIKV infection is associated with a range of neurological complications such as the Congenital Zika Syndrome and Guillain Barré Syndrome. Despite the magnitude of recent outbreaks, there is no specific therapy to prevent or to alleviate disease pathology. Objective: To investigate the role of P-MAPA immunomodulator in Zika-infected THP-1 cells. Methods: THP-1 cells were subjected at Zika virus infection (Multiplicity of Infection = 0.5) followed by treatment with P-MAPA for until 96 hours post-infection. After that, the cell death was analyzed by annexin+/ PI+ and caspase 3/ 7+ staining by flow cytometry. In addition, the virus replication and cell proliferation were accessed by RT-qPCR and Ki67 staining, respectively. Results: We demonstrate that P-MAPA in vitro treatment significantly reduces Zika virus-induced cell death and caspase-3/7 activation on THP-1 infected cells, albeit it has no role in virus replication and cell proliferation. Conclusions: Our study reveals that P-MAPA seems to be a satisfactory alternative to inhibits the effects of Zika virus infection in mammalian cells.

scholarly journals Transcriptome Analysis Reveals HgCl2 Induces Apoptotic Cell Death in Human Lung Carcinoma H1299 Cells through Caspase-3-Independent Pathway

2021 ◽  
Vol 22 (4) ◽  
pp. 2006
Author(s):  
Mi Jin Kim ◽  
Jinhong Park ◽  
Jinho Kim ◽  
Ji-Young Kim ◽  
Mi-Jin An ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Transcriptome Analysis ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Expression Patterns ◽  
Nitrogen Compound ◽  
Apoptotic Cell Death ◽  
Mercury Chloride ◽  
Rna Seq

Mercury is one of the detrimental toxicants that can be found in the environment and exists naturally in different forms; inorganic and organic. Human exposure to inorganic mercury, such as mercury chloride, occurs through air pollution, absorption of food or water, and personal care products. This study aimed to investigate the effect of HgCl2 on cell viability, cell cycle, apoptotic pathway, and alters of the transcriptome profiles in human non-small cell lung cancer cells, H1299. Our data show that HgCl2 treatment causes inhibition of cell growth via cell cycle arrest at G0/G1- and S-phase. In addition, HgCl2 induces apoptotic cell death through the caspase-3-independent pathway. Comprehensive transcriptome analysis using RNA-seq indicated that cellular nitrogen compound metabolic process, cellular metabolism, and translation for biological processes-related gene sets were significantly up- and downregulated by HgCl2 treatment. Interestingly, comparative gene expression patterns by RNA-seq indicated that mitochondrial ribosomal proteins were markedly altered by low-dose of HgCl2 treatment. Altogether, these data show that HgCl2 induces apoptotic cell death through the dysfunction of mitochondria.

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