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mBio ◽  
2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Setsu Kato ◽  
Kenta Suzuki ◽  
Taiki Kenjo ◽  
Junya Kato ◽  
Yoshiteru Aoi ◽  
...  

Cells display various behaviors even though they originate from a clonal population. Such diversity is also observed in cell survival in the stationary phase of Saccharomyces cerevisiae .


Antibiotics ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1359
Author(s):  
Ibrahim Alfarrayeh ◽  
Edit Pollák ◽  
Árpád Czéh ◽  
András Vida ◽  
Sourav Das ◽  
...  

This study investigated the effect of CAPE on planktonic growth, biofilm-forming abilities, mature biofilms, and cell death of C. albicans, C. tropicalis, C. glabrata, and C. parapsilosis strains. Our results showed a strain- and dose-dependent effect of CAPE on Candida, and the MIC values were between 12.5 and 100 µg/mL. Similarly, the MBIC values of CAPE ranging between 50 and 100 µg/mL highlighted the inhibition of the biofilm-forming abilities in a dose-dependent manner, as well. However, CAPE showed a weak to moderate biofilm eradication ability (19-49%) on different Candida strains mature biofilms. Both caspase-dependent and caspase-independent apoptosis after CAPE treatment were observed in certain tested Candida strains. Our study has displayed typical apoptotic hallmarks of CAPE-induced chromatin margination, nuclear blebs, nuclear condensation, plasma membrane detachment, enlarged lysosomes, cytoplasm fragmentation, cell wall distortion, whole-cell shrinkage, and necrosis. In conclusion, CAPE has a concentration and strain-dependent inhibitory activity on viability, biofilm formation ability, and cell death response in the different Candida species.


2021 ◽  
Author(s):  
Shuyi Xu ◽  
Shiyi Lu ◽  
Haichao Wang ◽  
Sisi Li ◽  
Jie Feng

Abstract Background: Hyperosmotic stress resulting from lumen contents is a big challenge to the normal function of the intestinal epithelium. Betaine is a potent organic osmolyte, but it is mostly studied in kidney. The purpose of this study was to gain insight into the osmoprotectant role of betaine in intestinal epithelium of piglets and intestinal porcine epithelial cells (IPEC-J2 cells) under hyperosmotic condition.Results: The result showed that the osmolarity of intestinal chyme was much higher than that of plasma (P < 0.05), indicating a natural hyperosmotic environment of intestinal lumen and subsequently leading to hyperosmotic stress to intestinal epithelium. Meanwhile, hyperosmolarity corresponding to intestinal environment was simulated by 150 mmol/L NaCl in vitro and caused a significant decrease of cell viability (P < 0.05). It was found that betaine could remarkably decrease hyperosmolarity-induced reactive oxygen species (ROS) of intestinal epithelium in vivo and vitro (P < 0.05) with the significant restoration of cell shrinkage (P < 0.05). Furthermore, since hyperosmolarity caused mitochondrial-related apoptosis with the remarkable increase of cleaved Caspase3, cleaved PARP-1, cytoplasm cytochrome c as well as obvious decrease of Bcl-2 in protein level (P < 0.05), betaine prevented mitochondria from membrane collapse and alleviated apoptosis (P < 0.05) in vivo and vitro. Meanwhile, it was also confirmed that betaine reduced hyperosmotic stress-induced apoptotic incidence in IPEC-J2 cells via fluorescence microscope and flow cytometry (P < 0.05). In addition, betaine supplementation significantly suppressed hyperosmotic stress-induced elevated expression of LC3 II and reduced expression of p62 (P < 0.05). indicating that betaine ameliorated autophagy of porcine intestinal epithelium caused by hyperosmolarity in vivo and vitro. Autophagic flux determined by mRFP-GFP-LC3B system in IPEC-J2 cells was in agreement with the result of western blotting as well (P < 0.05). Conclusions: Betaine could alleviate hyperosmotic stress-induced cell shrinkage, ROS accumulation as well as ameliorate subsequently apoptosis and autophagy in small intestinal epithelium of piglets and IPEC-J2 cells.


Author(s):  
Hüseyin İzgördü ◽  
Canan Vejselova Sezer ◽  
Kadir Bayçelebi ◽  
Murat Baloğlu ◽  
Hatice Mehtap Kutlu

Background: Cancer is a complex disease that is derived from the uncontrolled proliferation of cells. Bone cancer is a type of prevalent cancer that occurs both in youngsters and adults. Bone cancer is mostly common in the long bones of the pelvis, arms, and legs. Statistically, more than 200 cases of osteosarcoma have been reported annually in our country. Classical treatment with chemotherapeutics remains ineffective for the cure of this cancer. Recent studies have shown that ceramide induces apoptosis due to its increased levels in the cells. Thus, many studies have been conducted for the accumulation of ceramide molecules in the cell by different ways to induce apoptosis. NOE (N-oleoylethanolamine) is a specific inhibitor of ceramidase enzymes that hydrolyse intracellular ceramides and prevent apoptosis. Objective: This study investigates the cytotoxic and apoptosis-inducing activities of NOE on human osteosarcoma Saos-2 cells. Methods: Cytotoxic effects were investigated by MTT colorimetric assay. For the detection of morphological and ultrastructural indicators of apoptosis, confocal and TEM techniques were used, respectively. Results: Our finding indicated that NOE is effective in the inhibition of the growth of Saos-2 cells. Confocal and TEM findings showed morphological and ultrastructural changes as chromatin condensation, fragmentations of nuclei and mitochondria, as well as damaged cytoskeleton and cell shrinkage. Conclusion: The results revealed that NOE exhibits its cytotoxicity on Saos-2 cells by changing the ultrastructure and morphology of cells with clear apoptotic sparks.


2021 ◽  
Vol 55 (S1) ◽  
pp. 119-134

BACKGROUND/AIMS: Arginine vasopressin (AVP) neurons play an important role for sensing a change in the plasma osmolarity and thereby responding with regulated AVP secretion in order to maintain the body fluid homeostasis. The osmo-sensing processes in magnocellular neurosecretory cells (MNCs) including AVP and oxytocin (OXT) neurons of the hypothalamus were reported to be coupled to sustained osmotic shrinkage or swelling without exhibiting discernible cell volume regulation. Since increasing evidence has shown some important differences in properties between AVP and OXT neurons, osmotic volume responses are to be reexamined with distinguishing these cell types from each other. We previously reported that AVP neurons identified by transgenic expression of enhanced green fluorescence protein (eGFP) possess the ability of regulatory volume decrease (RVD) after hypoosmotic cell swelling. Thus, in the present study, we examined the ability of regulatory volume increase (RVI) after hyperosmotic cell shrinkage in AVP neurons. METHODS: Here, we used eGFP-identified AVP neurons acutely dissociated from AVP-eGFP transgenic rats. We performed single-cell size measurements, cytosolic RT-PCR analysis, AVP secretion measurements, and patch-clamp studies. RESULTS: The AVP neurons were found to respond to a hyperosmotic challenge with physiological cell shrinkage caused by massive secretion of AVP, called a secretory volume decrease (SVD), superimposed onto physical osmotic cell shrinkage, and also to exhibit the ability of RVI coping with osmotic and secretory cell shrinkage. Furthermore, our pharmacological and molecular examinations indicated that AVP secretion and its associated SVD event are triggered by activation of T-type Ca2+ channels, and the RVI event is attained by parallel operation of Na+/H+ exchanger and Cl-/HCO3- anion exchanger. CONCLUSION: Thus, it is concluded that AVP neurons respond to hyperosmotic stimulation with the regulatory volume increase and the secretory volume increase by activating ion transporters and Ca2+ channels, respectively.


2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Ali Reza Zangeneh ◽  
Mohammad Ali Takhshid ◽  
Reza Ranjbaran ◽  
Mahsa Maleknia ◽  
Mohammad Hassan Meshkibaf

Purpose. The role of oxidative stress in Aluminum (Al)-induced apoptotic effects has been investigated and suicidal death of erythrocytes, eryptosis, is characterized by cell shrinkage and phosphatidylserine externalization (PSE) at the surface of the erythrocyte cell membrane. Eryptosis is stimulated by an increase in cytosolic Ca2+ concentration and reactive oxygen species (ROS). This ex vivo study was conducted to evaluate the effect of well-known antioxidants including vitamin C (vit C) and N-acetylcysteine (NAC), against Al-induced hemolysis and eryptosis. Methods. Isolated erythrocytes from the healthy volunteers were partitioned into various groups (6 replicates/group) and treated by various concentrations of Al (3–100 µM) in the presence and absence of vit C (0.6 mM) and NAC (1 mM). After 24 hours of treatment, hemolysis was determined from hemoglobin levels in the supernatant. Flowcytometric methods were applied to measure PSE, cell shrinkage, Ca2+ content, and ROS abundance using annexin V-binding, forward scatter, Fluo3-fluorescence, and DCFDA dependent fluorescence, respectively. Reduced glutathione (GSH) was measured by the ELISA method. Results. The results showed that a 24 hours’ exposure of the erythrocytes to Al (10–100 µM) significantly increased hemolysis in a dose and Ca2+dependent manner. Al also dramatically decreased forward scatter. The percentage of PSE cells, Fluo3-fluorescence, and DCFDA fluorescence were increased by Al. Furthermore, cotreatment with NAC inhibited the effect of Al on hemolysis, eryptosis, and ROS production. Vit C decreased Al-induced ROS production. However, increased Al-induced eryptosis. There were no significant changes in glutathione after the ALCL3 treatment. Conclusions. Al-induced eryptosis and hemolysis through triggering oxidative stress, while NAC could diverse this effect. In contrast, vit C might intensify Al-induced eryptosis at particular doses through a less known mechanism.


Author(s):  
Carl D. Bortner ◽  
John A. Cidlowski

The movement of water across the cell membrane is a natural biological process that occurs during growth, cell division, and cell death. Many cells are known to regulate changes in their cell volume through inherent compensatory regulatory mechanisms. Cells can sense an increase or decrease in their cell volume, and compensate through mechanisms known as a regulatory volume increase (RVI) or decrease (RVD) response, respectively. The transport of sodium, potassium along with other ions and osmolytes allows the movement of water in and out of the cell. These compensatory volume regulatory mechanisms maintain a cell at near constant volume. A hallmark of the physiological cell death process known as apoptosis is the loss of cell volume or cell shrinkage. This loss of cell volume is in stark contrast to what occurs during the accidental cell death process known as necrosis. During necrosis, cells swell or gain water, eventually resulting in cell lysis. Thus, whether a cell gains or loses water after injury is a defining feature of the specific mode of cell death. Cell shrinkage or the loss of cell volume during apoptosis has been termed apoptotic volume decrease or AVD. Over the years, this distinguishing feature of apoptosis has been largely ignored and thought to be a passive occurrence or simply a consequence of the cell death process. However, studies on AVD have defined an underlying movement of ions that result in not only the loss of cell volume, but also the activation and execution of the apoptotic process. This review explores the role ions play in controlling not only the movement of water, but the regulation of apoptosis. We will focus on what is known about specific ion channels and transporters identified to be involved in AVD, and how the movement of ions and water change the intracellular environment leading to stages of cell shrinkage and associated apoptotic characteristics. Finally, we will discuss these concepts as they apply to different cell types such as neurons, cardiomyocytes, and corneal epithelial cells.


Author(s):  
François Bouteau ◽  
David Reboutier ◽  
Daniel Tran ◽  
Patrick Laurenti

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