scholarly journals Timing the multiple cell death pathways initiated by Rose Bengal acetate photodynamic therapy

2011 ◽  
Vol 2 (6) ◽  
pp. e169-e169 ◽  
Author(s):  
E Panzarini ◽  
V Inguscio ◽  
L Dini
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Rose Bengal ◽  
Cell Death Pathways ◽  
Rose Bengal Acetate ◽  
Multiple Cell

scholarly journals Overview of Cell Death Mechanisms Induced by Rose Bengal Acetate-Photodynamic Therapy

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Elisa Panzarini ◽  
Valentina Inguscio ◽  
Luciana Dini
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Rose Bengal ◽  
Intracellular Localization ◽  
Photochemical Reactions ◽  
Ros Generation ◽  
Invasive Treatment ◽  
Rose Bengal Acetate ◽  
Efficient Induction ◽  
Apoptotic Pathways

Photodynamic Therapy (PDT) is a non-invasive treatment for different pathologies, cancer included, using three key components: non-toxic light-activated drug (Photosensitizer, PS), visible light, and oxygen. Their interaction triggers photochemical reactions leading to Reactive Oxygen Species (ROS) generation, that mediate cytotoxicity and cell death. In the present paper, the most important findings about the synthetic dye Rose Bengal Acetate (RBAc), an emerging photosensitizer for its efficient induction of cell death, will be reported with the aim to integrate RBAc phototoxicity to novel therapeutic PDT strategies against tumour cells. After its perinuclear intracellular localization, RBAc causes multiple subcellular organelles damage, that is, mitochondria, Endoplasmic Reticulum (ER), lysosomes, and Golgi complex. Indeed, RBAc exerts long-term phototoxicity through activation of both caspase-independent and- dependent apoptotic pathways and autophagic cell death. In particular, this latter cell death type may promote cell demise when apoptotic machinery is defective. The deep knowledge of RBAc photocytotoxicity will allow to better understand its potential photomedicine application in cancer.

Targeting multiple cell death pathways extends the shelf life and preserves the function of human and mouse neutrophils for transfusion

2021 ◽  
Vol 13 (604) ◽  
pp. eabb1069
Author(s):  
Yuping Fan ◽  
Yan Teng ◽  
Fabien Loison ◽  
Aiming Pang ◽  
Anongnard Kasorn ◽  
...  
Keyword(s):  
Cell Death ◽  
Shelf Life ◽  
Ex Vivo ◽  
Combined Treatment ◽  
Bacterial Killing ◽  
Immunodeficient Mice ◽  
Cell Death Pathways ◽  
Multiple Cell ◽  
Human And Mouse

Clinical outcomes from granulocyte transfusion (GTX) are disadvantaged by the short shelf life and compromised function of donor neutrophils. Spontaneous neutrophil death is heterogeneous and mediated by multiple pathways. Leveraging mechanistic knowledge and pharmacological screening, we identified a combined treatment, caspases–lysosomal membrane permeabilization–oxidant–necroptosis inhibition plus granulocyte colony-stimulating factor (CLON-G), which altered neutrophil fate by simultaneously targeting multiple cell death pathways. CLON-G prolonged human and mouse neutrophil half-life in vitro from less than 1 day to greater than 5 days. CLON-G–treated aged neutrophils had equivalent morphology and function to fresh neutrophils, with no impairment to critical effector functions including phagocytosis, bacterial killing, chemotaxis, and reactive oxygen species production. Transfusion with stored CLON-G–treated 3-day-old neutrophils enhanced host defenses, alleviated infection-induced tissue damage, and prolonged survival as effectively as transfusion with fresh neutrophils in a clinically relevant murine GTX model of neutropenia-related bacterial pneumonia and systemic candidiasis. Last, CLON-G treatment prolonged the shelf life and preserved the function of apheresis-collected human GTX products both ex vivo and in vivo in immunodeficient mice. Thus, CLON-G treatment represents an effective and applicable clinical procedure for the storage and application of neutrophils in transfusion medicine, providing a therapeutic strategy for improving GTX efficacy.

Genetic Regulation of RIPK1 and Necroptosis

2021 ◽  
Vol 55 (1) ◽  
pp. 235-263
Author(s):  
Daichao Xu ◽  
Chengyu Zou ◽  
Junying Yuan
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Genetic Regulation ◽  
Caspase 8 ◽  
Inflammatory Signaling ◽  
Interacting Protein ◽  
Multiple Factors ◽  
Cell Death Pathways ◽  
Upstream Regulator ◽  
Multiple Cell

The receptor-interacting protein kinase 1 (RIPK1) is recognized as a master upstream regulator that controls cell survival and inflammatory signaling as well as multiple cell death pathways, including apoptosis and necroptosis. The activation of RIPK1 kinase is extensively modulated by ubiquitination and phosphorylation, which are mediated by multiple factors that also control the activation of the NF-κB pathway. We discuss current findings regarding the genetic modulation of RIPK1 that controls its activation and interaction with downstream mediators, such as caspase-8 and RIPK3, to promote apoptosis and necroptosis. We also address genetic autoinflammatory human conditions that involve abnormal activation of RIPK1. Leveraging these new genetic and mechanistic insights, we postulate how an improved understanding of RIPK1 biology may support the development of therapeutics that target RIPK1 for the treatment of human inflammatory and neurodegenerative diseases.

scholarly journals Protective effects of GPR37 via regulation of inflammation and multiple cell death pathways after ischemic stroke in mice

2019 ◽  
Vol 33 (10) ◽  
pp. 10680-10691 ◽  
Author(s):  
Myles R. McCrary ◽  
Michael Q. Jiang ◽  
Michelle M. Giddens ◽  
James Y. Zhang ◽  
Sharon Owino ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Protective Effects ◽  
Cell Death Pathways ◽  
Multiple Cell

scholarly journals Cell Death Pathways in Photodynamic Therapy of Cancer

Cancers ◽  
2011 ◽  
Vol 3 (2) ◽  
pp. 2516-2539 ◽  
Author(s):  
Pawel Mroz ◽  
Anastasia Yaroslavsky ◽  
Gitika B Kharkwal ◽  
Michael R. Hamblin
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Death Pathways ◽  
Photodynamic Therapy Of Cancer

scholarly journals TNF provokes cardiomyocyte apoptosis and cardiac remodeling through activation of multiple cell death pathways

2007 ◽  
Vol 117 (9) ◽  
pp. 2692-2701 ◽  
Author(s):  
Sandra B. Haudek ◽  
George E. Taffet ◽  
Michael D. Schneider ◽  
Douglas L. Mann
Keyword(s):  
Cell Death ◽  
Cardiac Remodeling ◽  
Cardiomyocyte Apoptosis ◽  
Cell Death Pathways ◽  
Multiple Cell

Abstract 1853: The Chk1 inhibitor, SRA737, synergizes with niraparib to kill cancer cells via multiple cell death pathways

2018 ◽  
Author(s):  
Laurence Booth ◽  
Jane Roberts ◽  
Andrew Poklepovic ◽  
Ryan J. Hansen ◽  
Bryan Strouse ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Cell Death Pathways ◽  
Multiple Cell ◽  
Chk1 Inhibitor
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