scholarly journals Overexpression of Arabidopsis Ceramide Synthases Differentially Affects Growth, Sphingolipid Metabolism, Programmed Cell Death, and Mycotoxin Resistance

2015 ◽  
Vol 169 (2) ◽  
pp. 1108-1117 ◽  
Author(s):  
Kyle D. Luttgeharm ◽  
Ming Chen ◽  
Amit Mehra ◽  
Rebecca E. Cahoon ◽  
Jonathan E. Markham ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Sphingolipid Metabolism ◽  
Ceramide Synthases

scholarly journals Bax Inhibitor 1 (BI-1) as a conservative regulator of Programmed Cell Death

2019 ◽  
Vol 73 ◽  
pp. 681-702
Author(s):  
Mirosław Godlewski ◽  
Agnieszka Kobylińska
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Actin Polymerization ◽  
Functional Condition ◽  
Sphingolipid Metabolism ◽  
Antiapoptotic Proteins ◽  
Crop Tolerance ◽  
Cellular Processes ◽  
C Terminus ◽  
Suicidal Death

Programmed cell death (PCD) is a physiological process in which infected or unnecessary cells due to their suicidal death capability can be selectively eliminated. Pro- and antiapoptotic proteins play an important role in the induction or inhibition of this process. Presented article shows property of Bax-1 (BI-1) inhibitor which is one of the conservative protein associated with the endoplasmic reticulum (ER) as well as its cytoprotective role in the regulation of cellular processes. It was shown that: 1) BI-1 is a small protein consisting of 237 amino acids (human protein - 36 kDa) and has 6 (in animals) and 7 (in plants) α-helical transmembrane domains, 2) BI-1 is expressed in all organisms and in most tissues, moreover its level depends on the functional condition of cells and it is involved in the development or reaction to biotic and abiotic stresses, 3) BI-1 forms a pH-dependent Ca2+ channel enabling release of these ions from the ER, 4) cytoprotective effects of BI-1 requires a whole, unchanged C-terminus, 5) BI-1 can interact directly with numerous other proteins, BI-1 protein affects numerous cellular processes, including: counteracting ER stress, oxidative stress, loss of cellular Ca2+ homeostasis as well as this protein influences on sphingolipid metabolism, autophagy, actin polymerization, lysosomal activity and cell proliferation. Studies of BI-1 functions will allow understanding the mechanisms of anticancer therapy or increases the knowledge of crop tolerance to environmental stresses.

scholarly journals Ceramide synthases at the centre of sphingolipid metabolism and biology

2012 ◽  
Vol 441 (3) ◽  
pp. 789-802 ◽  
Author(s):  
Thomas D. Mullen ◽  
Yusuf A. Hannun ◽  
Lina M. Obeid
Keyword(s):  
Cell Death ◽  
De Novo ◽  
Acyl Chain ◽  
Sphingolipid Metabolism ◽  
Sphingoid Base ◽  
Salvage Pathway ◽  
Organismal Biology ◽  
Acyl Chain Length ◽  
Specific Manner ◽  
Ceramide Synthases

Sphingolipid metabolism in metazoan cells consists of a complex interconnected web of numerous enzymes, metabolites and modes of regulation. At the centre of sphingolipid metabolism reside CerSs (ceramide synthases), a group of enzymes that catalyse the formation of ceramides from sphingoid base and acyl-CoA substrates. From a metabolic perspective, these enzymes occupy a unique niche in that they simultaneously regulate de novo sphingolipid synthesis and the recycling of free sphingosine produced from the degradation of pre-formed sphingolipids (salvage pathway). Six mammalian CerSs (CerS1–CerS6) have been identified. Unique characteristics have been described for each of these enzymes, but perhaps the most notable is the ability of individual CerS isoforms to produce ceramides with characteristic acyl-chain distributions. Through this control of acyl-chain length and perhaps in a compartment-specific manner, CerSs appear to regulate multiple aspects of sphingolipid-mediated cell and organismal biology. In the present review, we discuss the function of CerSs as critical regulators of sphingolipid metabolism, highlight their unique characteristics and explore the emerging roles of CerSs in regulating programmed cell death, cancer and many other aspects of biology.

scholarly journals Sphingolipid-Induced Programmed Cell Death Is a Salicylic Acid and EDS1-Dependent Phenotype in Arabidopsis

2021 ◽  
Author(s):  
Stefanie Koenig ◽  
Jasmin Goemann ◽  
Agnieszka Zienkiewicz ◽  
Krzysztof Zienkiewicz ◽  
Dorothea Meldau ◽  
...  
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Programmed Cell Death ◽  
Sphingolipid Metabolism ◽  
Ceramide Synthase ◽  
Triple Mutant ◽  
A Cell ◽  
P Fraction ◽  
Chain Lengths ◽  
Cell Death Phenotype

Ceramides and long chain bases (LCBs) are plant sphingolipids involved in the induction of plant programmed cell death (PCD). The fatty acid hydroxylase mutant fah1 fah2 exhibits high ceramide levels and moderately elevated LCB levels. Salicylic acid (SA) is strongly induced in these mutants, but no cell death is visible. To determine the effect of ceramides with different chain lengths, fah1 fah2 was crossed with ceramide synthase mutants longevity assurance gene one homologue1-3 (loh1, loh2 and loh3). Surprisingly, only triple mutants with loh2 show a cell death phenotype under the selected conditions. Sphingolipid profiling revealed that the greatest differences between the triple mutant plants are in the LCB and LCB-phosphate (LCB-P) fraction. fah1 fah2 loh2 plants accumulate LCB d18:0 and LCB-P d18:0. Crossing fah1 fah2 loh2 with the SA synthesis mutant sid2-2, and with the SA signaling mutants enhanced disease susceptibility 1-2 (eds1-2) and phytoalexin deficient 4-1 (pad4-1), revealed that lesions are SA- and EDS1-dependent. These quadruple mutants also suggest that there may be a feedback loop between SA and sphingolipid metabolism as they accumulated less ceramides and LCBs. In conclusion, PCD in fah1 fah2 loh2 is a SA and EDS1-dependent phenotype, which is likely due to accumulation of LCB d18:0.

Programmed Cell Death Ligand 1 and Venous Thromboembolism in Patients with Primary Brain Tumors

2019 ◽  
Author(s):  
P. Seyed Mir ◽  
A.-S. Berghoff ◽  
M. Preusser ◽  
G. Ricken ◽  
J. Riedl ◽  
...  
Keyword(s):  
Cell Death ◽  
Venous Thromboembolism ◽  
Programmed Cell Death ◽  
Brain Tumors ◽  
Primary Brain Tumors

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

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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