Placental apoptosis in pre-eclampsia

The objective was to determine the presence and severity of placental apoptosis in pre-eclampsia. The study included 31 patients. All patients were divided into 2 groups: group I (treatment) included 11 pregnant women with preeclampsia, group II (control) - 20 healthy patients. Gene expression was evaluated with qPCR assay, and placental apoptosis was assessed by the TUNEL method. It was found that the level of placental apoptosis in preeclampsia patients was significantly higher compared to that of apparently healthy females, and in some cases stem villi are destroyed due to programmed cell death in the villous stroma and syncytiotrophoblast. In preeclampsia, oxidative stress leads to increased levels of apoptosis in placental villi. Both trophoblast cells and, in certain cases, cells of the villous stroma are subject to apoptosis.

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Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

Ecology and Noospherology ◽

10.15421/032001 ◽

2020 ◽

Vol 31 (1) ◽

pp. 3-10

Author(s):

V. S. Nedzvetsky ◽

V. Ya. Gasso ◽

A. M. Hahut ◽

I. A. Hasso

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Programmed Cell Death ◽

Oxidative Damage ◽

Cadmium Chloride ◽

Glioma Cells ◽

Low Doses ◽

Genotoxic Effects ◽

Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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Programmed cell death 4 and BCR-ABL fusion gene expression are negatively correlated in chronic myeloid leukemia

Oncology Letters ◽

10.3892/ol.2016.4942 ◽

2016 ◽

Vol 12 (4) ◽

pp. 2976-2981 ◽

Cited By ~ 2

Author(s):

Xia Zhang ◽

Riming Liu ◽

Baohua Huang ◽

Xiaolu Zhang ◽

Weijuan Yu ◽

...

Keyword(s):

Gene Expression ◽

Cell Death ◽

Chronic Myeloid Leukemia ◽

Programmed Cell Death ◽

Myeloid Leukemia ◽

Fusion Gene ◽

Programmed Cell Death 4

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Macrophage Autophagy and Oxidative Stress: An Ultrastructural and Immunoelectron Microscopical Study

Oxidative Medicine and Cellular Longevity ◽

10.1155/2011/282739 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 12

Author(s):

Ida Perrotta ◽

Valentina Carito ◽

Emilio Russo ◽

Sandro Tripepi ◽

Saveria Aquila ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Programmed Cell Death ◽

Defense Mechanisms ◽

Ultrastructural Localization ◽

Microscopical Study ◽

Beclin 1 ◽

Cell Organelles ◽

A Cell ◽

First Time

The word autophagy broadly refers to the cellular catabolic processes that lead to the removal of damaged cytosolic proteins or cell organelles through lysosomes. Although autophagy is often observed during programmed cell death, it may also serve as a cell survival mechanism. Accumulation of reactive oxygen species within tissues and cells induces various defense mechanisms or programmed cell death. It has been shown that, besides inducing apoptosis, oxidative stress can also induce autophagy. To date, however, the regulation of autophagy in response to oxidative stress remains largely elusive and poorly understood. Therefore, the present study was designed to examine the ratio between oxidative stress and autophagy in macrophages after oxidant exposure (AAPH) and to investigate the ultrastructural localization of beclin-1, a protein essential for autophagy, under basal and stressful conditions. Our data provide evidence that oxidative stress induces autophagy in macrophages. We demonstrate, for the first time by immunoelectron microscopy, the subcellular localization of beclin-1 in autophagic cells.

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Delayed administration of zingerone mitigates the behavioral and histological alteration via repression of oxidative stress and intrinsic programmed cell death in focal transient ischemic rats

Pharmacology Biochemistry and Behavior ◽

10.1016/j.pbb.2013.10.008 ◽

2013 ◽

Vol 113 ◽

pp. 53-62 ◽

Cited By ~ 22

Author(s):

Kumar Vaibhav ◽

Pallavi Shrivastava ◽

Rizwana Tabassum ◽

Andleeb Khan ◽

Hayate Javed ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Programmed Cell Death ◽

Histological Alteration

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Mk 886 Functions As A Radiomimetic Agent: Genomic Responses Related to Oxidative Stress, The Cell Cycle, Proliferation and Programmed Cell Death in Panc-1 Cells

Advances in Experimental Medicine and Biology - Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 5 ◽

10.1007/978-1-4615-0193-0_70 ◽

2002 ◽

pp. 451-456 ◽

Cited By ~ 2

Author(s):

Ken M. Anderson ◽

Waddah Alrefai ◽

Colin Anderson ◽

Philip Bonomi ◽

Jules Harris

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Cell Death ◽

Programmed Cell Death

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Programmed Cell Death-1: Programmed Cell Death-Ligand 1 Interaction Protects Human Cardiomyocytes Against T-Cell Mediated Inflammation and Apoptosis Response In Vitro

International Journal of Molecular Sciences ◽

10.3390/ijms21072399 ◽

2020 ◽

Vol 21 (7) ◽

pp. 2399

Author(s):

Woan Ting Tay ◽

Yi-Hsien Fang ◽

Suet Theng Beh ◽

Yen-Wen Liu ◽

Ling-Wei Hsu ◽

...

Keyword(s):

Gene Expression ◽

Cell Death ◽

T Cell ◽

T Lymphocytes ◽

Programmed Cell Death ◽

T Cell Response ◽

Tumor Bearing ◽

Cd8 T Lymphocytes ◽

Programmed Cell Death 1

Aim: Immunological checkpoint therapy is considered a powerful method for cancer therapy and acts by re-activating autologous T cells to kill the cancer cell. Myocarditis cases have been reported in cancer patients after immunological therapy; for example, nivolumab treatment is a monoclonal antibody that blocks programmed cell death-1/programmed cell death ligand-1 ligand interaction. This project provided insight into the inflammatory response as a benchmark to investigate the potential cardiotoxic effect of T cell response to the programmed cell death-1 (PD-1)/programmed cell death ligand-1 (PD-L1) axis in regulating cardiomyocyte injury in vitro. Methods and Results: We investigated cardiomyopathy resulted from the PD-1/PD-L1 axis blockade using the anti-PD-1 antibody in Rockefeller University embryonic stem cells-derived cardiomyocytes (RUES2-CMs) and a melanoma tumor-bearing murine model. We found that nivolumab alone did not induce inflammatory-related proteins, including PD-L1 expression, and did not induce apoptosis, which was contrary to doxorubicin, a cardiotoxic chemotherapy drug. However, nivolumab was able to exacerbate the immune response by increasing cytokine and inflammatory gene expression in RUES2-CMs when co-cultured with CD4+ T lymphocytes and induced apoptosis. This effect was not observed when RUES2-CMs were co-cultured with CD8+ T lymphocytes. The in vivo model showed that the heart function of tumor-bearing mice was decreased after treatment with anti-PD-1 antibody and demonstrated a dilated left ventricle histological examination. The dilated left ventricle was associated with an infiltration of CD4+ and CD8+ T lymphocytes into the myocardium. PD-L1 and inflammatory-associated gene expression were significantly increased in anti-PD-1-treated tumor-bearing mice. Cleaved caspase-3 and mouse plasma cardiac troponin I expressions were increased significantly. Conclusion: PD-L1 expression on cardiomyocytes suppressed T-cell function. Blockade of PD-1 by nivolumab enhanced cardiomyocyte inflammation and apoptosis through the enhancement of T-cell response towards cardiomyocytes.

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The Protective Effect of Static Magnetic Fields with Different Magnetic Inductions against Fluoride Toxicity Is Related to the NRF2 Signaling Pathway

Applied Sciences ◽

10.3390/app10186509 ◽

2020 ◽

Vol 10 (18) ◽

pp. 6509

Author(s):

Magdalena Kimsa-Dudek ◽

Agata Krawczyk ◽

Agnieszka Synowiec-Wojtarowicz

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Programmed Cell Death ◽

Protective Effect ◽

Signaling Pathway ◽

Magnetic Induction ◽

Redox Homeostasis ◽

Fluoride Toxicity ◽

Static Magnetic Fields ◽

Nrf2 Signaling Pathway

A redox imbalance disrupts the cellcycle and the proliferation process, and contributes to the initiation of programmed cell death. One of the pathways that are important for redox homeostasis is the Nrf2-ARE signaling pathway. Fluoride as well as static magnetic fields (SMF) are associated with the concepts of oxidative stress, and thus programmed cell death. Therefore, this study aimed to assess the connection between oxidative stress and apoptosis in human cells co-exposed to fluoride and a SMF with a different magnetic induction and to determine whether the Nrf2-signaling pathway is involved in these effects. The research was realized using normal human dermal fibroblasts that had been co-exposed to fluoride (0.3 mmol/L) and a SMF with a different magnetic induction (0.45 T, 0.55 T, 0.65 T) for 12 h. The mRNA levels of the cellular antioxidant system-related genes and apoptosis-related genes were assessed using the quantitative reverse transcription polymerase chain reaction (RT-qPCR) method. Our results indicated that the increased activity of antioxidant enzymes (SOD1 (superoxide dismutase 1), SOD2 and GSR (glutathione reductase)) suggests the restoration of the cell redox homeostasis that had been disturbed by fluoride, and also that the genes whose expression is associated with the induction of apoptosis are down regulated as a result of exposure to a SMF. The SMF with a 0.65 T flux density had the strongest effect on the fibroblasts. Moreover, our findings demonstrated that the Nrf2 transcription factor plays a crucial role in the protective effect of a SMF against fluoride toxicity in human cells. The results of these studies can form the basis for developing therapeutic strategies for apoptosis and oxidative stress-related diseases.

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Hepatocyte nuclear factor-1 beta protects endometriotic cells against apoptotic cell death by up-regulating the expression of antiapoptotic genes†

Biology of Reproduction ◽

10.1093/biolre/ioz127 ◽

2019 ◽

Vol 101 (4) ◽

pp. 686-694 ◽

Cited By ~ 1

Author(s):

Umma Hafsa Preya ◽

Jeong-Hwa Woo ◽

Youn Seok Choi ◽

Jung-Hye Choi

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Cell Death ◽

Apoptotic Cell ◽

Apoptotic Cell Death ◽

Nuclear Factor ◽

Hepatocyte Nuclear Factor ◽

Antiapoptotic Gene ◽

Nuclear Factor 1 ◽

Hes Cells

Abstract The overexpression of hepatocyte nuclear factor-1 beta (HNF1β) in endometriotic lesion has been demonstrated. However, the role of HNF1β in endometriosis remains largely unknown. Human endometriotic 12Z cells showed higher level of HNF1β when compared with normal endometrial HES cells. In human endometriotic 12Z cells, HNF1β knockdown increased susceptibility to apoptotic cell death by oxidative stress, while HNF1β overexpression suppressed apoptosis. In addition, HNF1β knockdown and overexpression significantly decreased and increased, respectively, the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-dependent antiapoptotic genes. Knockdown of the antiapoptotic genes significantly reduced the HNF1β-induced resistance against oxidative stress in 12Z cells. Furthermore, HNF1β regulated the transcriptional activity of NF-κB, and an NF-κB inhibitor suppressed the HNF1β-enhanced NF-κB-dependent antiapoptotic gene expression and the resistance of the 12Z cells against cell death. Taken together, these data suggest that HNF1β overexpression may protect endometriotic cells against oxidative damage by augmenting antiapoptotic gene expression.

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