Stenocalcic properties in the serpentine-endemic plant Alyssum inflatum Nyárády

2015 ◽  
Vol 63 (2) ◽  
pp. 31 ◽  
Author(s):  
Rasoul Ghasemi ◽  
Zohreh Zare Chavoshi ◽  
Seyed Majid Ghaderian
Keyword(s):  
Cell Death ◽  
Solution Culture ◽  
Nadh Oxidation ◽  
Blue Staining ◽  
Endemic Plant ◽  
High Concentration ◽  
Oxidation Activity ◽  
Root Cells ◽  
Protein Leakage ◽  
Whole Plant

Serpentine-endemic plants need to grow in substrates with low calcium (Ca). To test this hypothesis, we compared some of the survival-related physiological responses to different concentrations of Ca in Alyssum inflatum (serpentine endemic) and A. lanceolatum (non-serpentine plant). Accordingly, we grew the plants by using solution culture, and the death of root cells was estimated by using Evan’s blue staining. The electrolyte and protein leakage from roots and NADH oxidation activity in the leaked contents were measured as indices of cell death. The results showed that despite the higher growth of shoots in serpentine plants, the high concentration of Ca caused less root growth. Meanwhile, we observed root-cell death, whole-plant death, more electrolyte and protein leakage from roots and a greater NADH oxidation activity in Ca-treated serpentine plants. In non-serpentine plants, both root and shoot showed more growth, whereas no evidence of cell death in the roots was observed. On the basis of the responses to different concentrations of Ca, we introduce the serpentine plant A. inflatum as a stenocalcic that has to live in substrates with a narrow range of Ca concentrations so that it could prevent lethal Ca toxicity. The results demonstrated the reason behind the uneven distribution of the plant on serpentine patches in its habitat.

Programmed cell death during Drosophila embryogenesis

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 29-43 ◽  
Author(s):  
J.M. Abrams ◽  
K. White ◽  
L.I. Fessler ◽  
H. Steller
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Acridine Orange ◽  
Nile Blue ◽  
Molecular Genetic ◽  
Blue Staining ◽  
Nuclear Condensation ◽  
The Central Nervous System ◽  
Ultrastructural Appearance ◽  
Dying Cells

The deliberate and orderly removal of cells by programmed cell death is a common phenomenon during the development of metazoan animals. We have examined the distribution and ultrastructural appearance of cell deaths that occur during embryogenesis in Drosophila melanogaster. A large number of cells die during embryonic development in Drosophila. These cells display ultrastructural features that resemble apoptosis observed in vertebrate systems, including nuclear condensation, fragmentation and engulfment by macrophages. Programmed cell deaths can be rapidly and reliably visualized in living wild-type and mutant Drosophila embryos using the vital dyes acridine orange or nile blue. Acridine orange appears to selectively stain apoptotic forms of death in these preparations, since cells undergoing necrotic deaths were not significantly labelled. Likewise, toluidine blue staining of fixed tissues resulted in highly specific labelling of apoptotic cells, indicating that apoptosis leads to specific biochemical changes responsible for the selective affinity to these dyes. Cell death begins at stage 11 (approximately 7 hours) of embryogenesis and thereafter becomes widespread, affecting many different tissues and regions of the embryo. Although the distribution of dying cells changes drastically over time, the overall pattern of cell death is highly reproducible for any given developmental stage. Detailed analysis of cell death in the central nervous system of stage 16 embryos (13-16 hours) revealed asymmetries in the exact number and position of dying cells on either side of the midline, suggesting that the decision to die may not be strictly predetermined at this stage. This work provides the basis for further molecular genetic studies on the control and execution of programmed cell death in Drosophila.

Abstract 146: Biphasic Effect Of Cyclic Amp Axis On Cardiomyocyte Survival

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Morihiko Aoyama ◽  
Yasuko K Bando ◽  
Haruya Kawase ◽  
Akio Monji ◽  
Toyoaki Murohara
Keyword(s):  
Cell Death ◽  
Cyclic Amp ◽  
Pressure Overload ◽  
Myocardial Cell ◽  
Threshold Concentration ◽  
High Concentration ◽  
Neonatal Cardiomyocytes ◽  
Myocardial Apoptosis ◽  
Vitro Analysis

Background: Persistent cardiac hypertrophy in response to pathological stimuli is results in maladaptive myocardial remodeling and cell death. Clinical evidence revealed that one of the most significantly beneficial medications for targeting heart failure with pathologic myocardial hypertrophy is beta1-adrenergic receptor (β1R) blockers. The molecular pathway of β1R is mediated by the second messenger cyclic AMP (cAMP). However, there are some debate regarding the role of cAMP in myocardial survival. We hypothesized whether there may be threshold concentration of cAMP in cell susceptibility to cardiomyocyte cell death. Methods: Male 14-week-old C57BL6 mice were subjected to the surgery of thoracic aortic constriction (TAC) to induce pressure overload. Changes in apoptosis were evaluated in each heart section and in vitro culture of neonatal cardiomyocytes using TUNEL. To elucidate the concentration-dependent distinct effect of cAMP on myocardial cell death, we tested the different concentration of cell-permeable cAMP (8-br-cAMP) at low (60 μM) and high concentration (6 mM), and receptor-mediated cAMP-stimulators (Ex4; exendin-4, ISO; isoproterenol). Results: In vitro analysis revealed that the high-cAMP and ISO exhibited marked increase in TUNEL-positivity (15.46%±3.09% for high-cAMP versus 6.71%±0.33% for ISO), which was reversed by Rp-cAMP (1.80%±0.17% and 2.05%±0.25%, respectively). Unexpectedly, the 8-p-Methoxyphenylthon-2-O-methyl-cAMP (pMe-cAMP, 50 μM), the specific activator of another cAMP-sensitive target Epac, reversed the high-cAMP-induced cell death even at a less extent compared to that observed by PKA-inhibitor Rp-cAMP (3.73%±0.70%). Serum depletion induced 3.22±0.24% of TUNEL-positive cell count of NRVM, which was reversed by pMe-cAMP, (50 μM) and Ex4 (1.74±0.18%, n=6, P<0.01), which was insensitive to PKA inhibition by Rp-cAMP (100 μM). TAC increased myocardial apoptosis. TAC-CON heart exhibited 1.66-fold decrease in cardiac cAMP concentration compared to sham-CON. Ex4 ameliorated the TAC-induced cardiac dysfunction and apoptosis by increase in cAMP. Conclusions: The cAMP-related cell death was mediated by PKA activation, which were reversed by Epac activation.

Overexpressed LncRNA ADAMTS9-AS2 inhibited gastric cancer (GC) development and sensitized chemoresistant GC cells to cisplatin by regulating miR-223-3p/NLRP3 axis

2020 ◽  
Author(s):  
Niansheng Ren ◽  
Tao Jiang ◽  
Chengbo Wang ◽  
Shilin Xie ◽  
Yanwei Xing ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cell Viability ◽  
Pearson Correlation ◽  
Luciferase Reporter ◽  
Blue Staining ◽  
Luciferase Reporter Gene ◽  
Kaplan Meier ◽  
Cisplatin Sensitivity ◽  
Cancer Tissues

Abstract Background The role of LncRNA ADAMTS9-AS2 in the regulation of pathogenesis and chemoresistance of gastric cancer (GC) is largely unkonwn, and this study aimed to solve this problem. Methods Real-Time qPCR was used to examine LncRNA ADAMTS9-AS2 and miR-223-3p expressions, and pearson correlation analysis was conducted to analyse their correlations. Kaplan-Meier survival analysis was performed to evaluate prognosis of GC patients. Dual-luciferase reporter gene system and pull-down assay were employed to validate the target sites of LncRNA ADAMTS9-AS2, miR-223-3p and NLRP3 mRNA. Cell viability was evaluated by CCK-8 assay, trypan blue staining and colony formation assay. Cell apoptosis ratio was detected by FCM and TUNEL assay. Transwell assay for cell migration and Western Blot for protein expressions. ELISA was used to measure cytokines secretion. FISH was conducted to examine LncRNA ADAMTS9-AS2 expressions and localization in mice cancer tissues. Results LncRNA ADAMTS9-AS2 was low-expressed in GC tissues and cells compared to their normal counterparts. Besides, LncRNA ADAMTS9-AS2 inhibited miR-223-3p expressions in GC cells by acting as competing endogenous RNA, and the levels of LncRNA ADAMTS9-AS2 and miR-223-3p showed negative correlations in GC tissues. Of note, overexpression of LncRNA ADAMTS9-AS2 inhibited GC cell viability and motility by sponging miR-223-3p. In addition, the levels of LncRNA ADAMTS9-AS2 were lower, and miR-223-3p was higher in cisplatin-resistant GC (CR-GC) cells than their parental cisplatin-sensitive GC (CS-GC) cells. LncRNA ADAMTS9-AS2 overexpression enhanced the cytotoxic effects of cisplatin on CR-GC cells, which were reversed by overexpressing miR-223-3p. Furthermore, LncRNA ADAMTS9-AS2 increased NLRP3 expressions by targeting miR-223-3p, and upregulation of LncRNA ADAMTS9-AS2 triggered pyroptotic cell death in cisplatin treated CR-GC cells by activating NLRP3 inflammasome through downregulating miR-223-3p. Finally, the promoting effects of LncRNA ADAMTS9-AS2 overexpression on CR-GC cell death were abrogated by pyroptosis inhibitor NSA.Conclusions LncRNA ADAMTS9-AS2 acted as a tumor suppressor and enhanced cisplatin sensitivity in GC cells by regulating miR-223-3p/NLRP3 axis mediated pyroptosis.

scholarly journals (+)-Spectaline and Iso-6-Spectaline Induce a Possible Cross-Talk between Autophagy and Apoptosis in Trypanosoma brucei rhodesiense

2019 ◽  
Vol 4 (3) ◽  
pp. 98
Author(s):  
Kah Tee Lim ◽  
Chiann Ying Yeoh ◽  
Zafarina Zainuddin ◽  
Mohd. Ilham Adenan
Keyword(s):  
Cell Death ◽  
Cross Talk ◽  
Piperidine Alkaloids ◽  
High Concentration ◽  
Trypanosoma Brucei Rhodesiense ◽  
Morphological Alterations ◽  
L6 Cells ◽  
Senna Spectabilis ◽  
Late Apoptosis ◽  
Potential Use

In our previous study, two known piperidine alkaloids (+)-spectaline (1) and iso-6-spectaline (2) were isolated from the leaves of Senna spectabilis and showed no toxic effect on L6 cells. In view of the potential use of piperidine alkaloids in S. spectabilis for the treatment of sleeping sickness, further investigation on the cell death actions of the parasite after treatment with compound 1 and 2 suggested that the treated parasites died by a process of autophagy based on the characteristic morphological alterations observed in intracellular T. b. rhodesiense. In search for apoptosis, interestingly, trypanosomes treated with high concentration of compound 1 and 2 after 72 h significantly induced an early apoptosis-like programmed cell death (PCD) such as phosphatidylserine (PS) exposure, loss of mitochondrial membrane potential and caspases activation. No DNA laddering discriminated late apoptosis event. Taken together, these findings demonstrated the potential of compound 1 and 2 as a natural chemotherapeutic capable of inducing a possible cross-talk between autophagy and apoptosis in T. b. rhodesiense.

Gauging Turfgrass Salinity Responses in Whole‐Plant Microculture and Solution Culture

Crop Science ◽  
1993 ◽  
Vol 33 (3) ◽  
pp. 566-572 ◽  
Author(s):  
Mary Ann L. Smith ◽  
Jeffrey E. Meyer ◽  
Sharon L. Knight ◽  
G. Stanley Chen
Keyword(s):  
Solution Culture ◽  
Whole Plant

scholarly journals Increased Lysosomal Membrane Permeabilization in Oxidant-exposed Macrophages of Human Fibrotic Lungs

2013 ◽  
Vol 6 ◽  
pp. JCD.S13271 ◽  
Author(s):  
Hans L Persson ◽  
Linda K. Vainikka
Keyword(s):  
Cell Death ◽  
Lung Fibrosis ◽  
Reduced Glutathione ◽  
Atomic Absorption Spectrophotometry ◽  
Membrane Permeabilization ◽  
Lysosomal Membrane ◽  
Blue Staining ◽  
Green Fluorescence ◽  
Lysosomal Membrane Permeabilization ◽  
Typical Morphology

A disrupted balance of reduced glutathione (GSH) and iron (Fe) and subsequent enhanced susceptibility of lysosomes of lung macrophages (LMs) to oxidants may play a role in lung fibrogenesis. We assessed cellular Fe/GSH, lysosomal membrane permeabilization (LMP), and cell death in cultures of oxidant exposed LMs. LMs from 7 lung fibrosis patients and healthy subjects were exposed to a physiologic concentration of H2O2 for 1 h. LMP was assessed with acridine orange green fluorescence, apoptosis/necrosis were estimated by apoptotic DNA and typical morphology, Fe was assessed with Prussian blue staining/atomic absorption spectrophotometry, and GSH was evaluated using a GSH assay kit. Oxidant-induced LMP and cell death were more pronounced in cultures of LMs from patients with lung fibrosis, and these cells contained less GSH and more cytochemically stained Fe. These observations indicate that LMP may be involved in fibrosis development, possibly through activation of the inflammasome complex. Further studies are warranted for a detailed understanding.

The interaction of QDs with RAW264.7 cells: nanoparticle quantification, uptake kinetics and immune responses study

RSC Advances ◽  
2015 ◽  
Vol 5 (53) ◽  
pp. 42250-42258 ◽  
Author(s):  
O. Gladkovskaya ◽  
V. A. Gerard ◽  
M. Nosov ◽  
Y. K. Gun'ko ◽  
G. M. O'Connor ◽  
...  
Keyword(s):  
Cell Culture ◽  
Cell Death ◽  
Immune Responses ◽  
Cell Population ◽  
Uptake Kinetics ◽  
Raw264.7 Cells ◽  
High Concentration ◽  
Apoptosis And Necrosis

Exposure to small QDs in high concentration in continuous cell culture results in cell death by apoptosis and necrosis co-existing within the same cell population.

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