scholarly journals Characterization of dual effects induced by antimicrobial peptides: Regulated cell death or membrane disruption

2012 ◽  
Vol 1820 (7) ◽  
pp. 1062-1072 ◽  
Author(s):  
Edgar J. Paredes-Gamero ◽  
Marta N.C. Martins ◽  
Fábio A.M. Cappabianco ◽  
Jaime S. Ide ◽  
Antonio Miranda
Keyword(s):  
Cell Death ◽  
Antimicrobial Peptides ◽  
Membrane Disruption ◽  
Regulated Cell Death

scholarly journals Mode-of-Action of Antimicrobial Peptides: Membrane Disruption vs. Intracellular Mechanisms

2020 ◽  
Vol 2 ◽  
Author(s):  
Aurélie H. Benfield ◽  
Sónia Troeira Henriques
Keyword(s):  
Antimicrobial Peptides ◽  
Physicochemical Properties ◽  
Broad Spectrum ◽  
Mode Of Action ◽  
Bacterial Pathogens ◽  
Model Membranes ◽  
Membrane Disruption ◽  
Attractive Alternative ◽  
Bacterial Cells

Antimicrobial peptides are an attractive alternative to traditional antibiotics, due to their physicochemical properties, activity toward a broad spectrum of bacteria, and mode-of-actions distinct from those used by current antibiotics. In general, antimicrobial peptides kill bacteria by either disrupting their membrane, or by entering inside bacterial cells to interact with intracellular components. Characterization of their mode-of-action is essential to improve their activity, avoid resistance in bacterial pathogens, and accelerate their use as therapeutics. Here we review experimental biophysical tools that can be employed with model membranes and bacterial cells to characterize the mode-of-action of antimicrobial peptides.

scholarly journals Nanomechanical Characterization of the Synergism of Antimicrobial Peptides PGLa and Mag2 for Lipid Membrane Disruption

2021 ◽  
Vol 120 (3) ◽  
pp. 191a
Author(s):  
Fabio Perissinotto ◽  
Sebastien Janel ◽  
Javier Lopez-Alonso ◽  
Vincent Dupres ◽  
Burkhard Bechinger ◽  
...  
Keyword(s):  
Antimicrobial Peptides ◽  
Lipid Membrane ◽  
Membrane Disruption

scholarly journals Discovery and molecular characterization of a Bcl-2-regulated cell death pathway in schistosomes

2011 ◽  
Vol 108 (17) ◽  
pp. 6999-7003 ◽  
Author(s):  
E. F. Lee ◽  
O. B. Clarke ◽  
M. Evangelista ◽  
Z. Feng ◽  
T. P. Speed ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Characterization ◽  
Cell Death Pathway ◽  
Regulated Cell Death

Mechanisms of Regulated Cell Death: Current Perspectives

2021 ◽  
pp. 030098582110055
Author(s):  
Sara Francesca Santagostino ◽  
Charles-Antoine Assenmacher ◽  
James C. Tarrant ◽  
Adeyemi O. Adedeji ◽  
Enrico Radaelli
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Regulated Cell Death ◽  
Morphologic Characteristics ◽  
Adaptive Processes ◽  
Molecular Machinery ◽  
Extracellular Microenvironment ◽  
Apoptosis And Necrosis ◽  
Microscopic Findings

Balancing cell survival and cell death is fundamental to development and homeostasis. Cell death is regulated by multiple interconnected signaling pathways and molecular mechanisms. Regulated cell death (RCD) is implicated in fundamental processes such as organogenesis and tissue remodeling, removal of unnecessary structures or cells, and regulation of cell numbers. RCD can also be triggered by exogenous perturbations of the intracellular or extracellular microenvironment when the adaptive processes that respond to stress fail. During the past few years, many novel forms of non-apoptotic RCD have been identified, and the characterization of RCD mechanisms at a molecular level has deepened our understanding of diseases encountered in human and veterinary medicine. Given the complexity of these processes, it has become clear that the identification of RCD cannot be based simply on morphologic characteristics and that descriptive and diagnostic terms presently used by pathologists—such as individual cell apoptosis or necrosis—appear inadequate and possibly misleading. In this review, the current understanding of the molecular machinery of each type of non-apoptotic RCD mechanisms is outlined. Due to the continuous discovery of new mechanisms or nuances of previously described processes, the limitations of the terms apoptosis and necrosis to indicate microscopic findings are also reported. In addition, the need for a standard panel of biomarkers and functional tests to adequately characterize the underlying RCD and its role as a mechanism of disease is considered.

scholarly journals Cryo-EM structural analysis of FADD:Caspase-8 complexes defines the catalytic dimer architecture for co-ordinated control of cell fate

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Joanna L. Fox ◽  
Michelle A. Hughes ◽  
Xin Meng ◽  
Nikola A. Sarnowska ◽  
Ian R. Powley ◽  
...  
Keyword(s):  
Cell Death ◽  
Structural Analysis ◽  
Cell Fate ◽  
Catalytic Domain ◽  
Caspase 8 ◽  
Type I ◽  
Signaling Complex ◽  
Catalytic Domains ◽  
Regulated Cell Death ◽  
Death Effector

AbstractRegulated cell death is essential in development and cellular homeostasis. Multi-protein platforms, including the Death-Inducing Signaling Complex (DISC), co-ordinate cell fate via a core FADD:Caspase-8 complex and its regulatory partners, such as the cell death inhibitor c-FLIP. Here, using electron microscopy, we visualize full-length procaspase-8 in complex with FADD. Our structural analysis now reveals how the FADD-nucleated tandem death effector domain (tDED) helical filament is required to orientate the procaspase-8 catalytic domains, enabling their activation via anti-parallel dimerization. Strikingly, recruitment of c-FLIPS into this complex inhibits Caspase-8 activity by altering tDED triple helix architecture, resulting in steric hindrance of the canonical tDED Type I binding site. This prevents both Caspase-8 catalytic domain assembly and tDED helical filament elongation. Our findings reveal how the plasticity, composition and architecture of the core FADD:Caspase-8 complex critically defines life/death decisions not only via the DISC, but across multiple key signaling platforms including TNF complex II, the ripoptosome, and RIPK1/RIPK3 necrosome.

Lytic regulated cell death in aquaculture fish

2021 ◽  
Author(s):  
Xiaojing Xia ◽  
Bin He ◽  
Xiulin Zhang ◽  
Zhe Cheng ◽  
Mingcheng Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Regulated Cell Death ◽  
Aquaculture Fish

Galectin-3 is modulated in pancreatic cancer cells under hypoxia and nutrient deprivation

2020 ◽  
Vol 401 (10) ◽  
pp. 1153-1165 ◽  
Author(s):  
Antônio F. da Silva Filho ◽  
Lucas B. Tavares ◽  
Maira G. R. Pitta ◽  
Eduardo I. C. Beltrão ◽  
Moacyr J. B. M. Rêgo
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Ductal Adenocarcinoma ◽  
Reverse Transcription Pcr ◽  
Pancreatic Cancer Cells ◽  
Through Flow ◽  
Galectin 3

AbstractPancreatic ductal adenocarcinoma is one of the most aggressive tumors with a microenvironment marked by hypoxia and starvation. Galectin-3 has been evaluated in solid tumors and seems to present both pro/anti-tumor effects. So, this study aims to characterize the expression of Galectin-3 from pancreatic tumor cells and analyze its influence for cell survive and motility in mimetic microenvironment. For this, cell cycle and cell death were accessed through flow cytometry. Characterization of inside and outside Galectin-3 was performed through Real-Time Quantitative Reverse Transcription PCR (qRT-PCR), immunofluorescence, Western blot, and ELISA. Consequences of Galectin-3 extracellular inhibition were investigated using cell death and scratch assays. PANC-1 showed increased Galectin-3 mRNA expression when cultivated in hypoxia for 24 and 48 h. After 24 h in simultaneously hypoxic/deprived incubation, PANC-1 shows increased Galectin-3 protein and secreted levels. For Mia PaCa-2, cultivation in deprivation was determinant for the increasing in Galectin-3 mRNA expression. When cultivated in simultaneously hypoxic/deprived condition, Mia PaCa-2 also presented increasing for the Galectin-3 secreted levels. Treatment of PANC-1 cells with lactose increased the death rate when cells were incubated simultaneously hypoxic/deprived condition. Therefore, it is possible to conclude that the microenvironmental conditions modulate the Galectin-3 expression on the transcriptional and translational levels for pancreatic cancer cells.

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