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The Role of Nanoparticles in Cancer Therapy through Apoptosis Induction
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Marveh Rahmati, Saeid Amanpour, Hadiseh Mohammadpour
There also exists a caspase-independent apoptotic pathway that is mediated by AIF (Apoptosis-Inducing Factor) [24]. AIF is phylogenetically an old flavoprotein observed in the mitochondrial intermembrane. Upon lethal stimuli, AIF translocates from mitochondria to the nucleus. It binds to DNA and mediates caspase-independent chromatin condensation and large scale DNA fragmentation [25, 26].
Cognition Enhancers
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Ramneek Kaur, Rashi Rajput, Sachin Kumar, Harleen Kaur, R. Rachana, Manisha Singh
If a neuron is stressed or injured, it might undergo apoptosis. It may be either extrinsic (which can be started by activating the receptors of cell surface) or intrinsic (involving the ER and the mitochondria). Cell death can be triggered by either of the losses of factors responsible for cell survival. Further, damage of DNA, which may thereby, cause the pro-apoptotic proteins from the mitochondria to stimulate caspase proteases and eventually, caspase activated DNase. Apoptosis can also be induced in caspase independent manner by triggering apoptosis-inducing factor (AIF) which is protein present in the intermembrane of the mitochondria. Attenuation of cell death can be triggered by stimulation of PKCγ in the hippocampus. Therefore, it is suggested that the activators of PKCγ inhibits apoptosis (Sun et al., 2009), thereby, increasing the usefulness as CE that can act on the patients specifically suffering from stroke, brain injury, and acute radiation sickness.
Mitochondrial Pathologies and Their Neuromuscular Manifestations
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Carlos Ortez, Andrés Nascimento
Cowchock syndrome (CMTX4) is a slowly progressive X-linked recessive disorder manifesting by axonal sensori-motor neuropathy, deafness, and cognitive impairment. Exome sequencing of affected individuals from a family identified a missense change c.1478A>T (p.Glu493Val) in AIFM1, the gene encoding apoptosis-inducing factor (AIF) mitochondrion-associated AIF, is a phylogenetically conserved mitochondrial flavoprotein, and one of the key caspase-independent death effectors. In this family, only males displayed the phenotype, consistent with an X-linked recessive mode of inheritance. Cranial MRI in two subjects showed multiple punctate T2 hyperintensities in the supratentorial white matter. Authors investigated the consequences of this mutation in cultured skin fibroblasts and skeletal muscle from an affected individual. They showed that the mutation alters the redox properties of AIF protein and results in increased cell death via apoptosis, without affecting the activity of the respiratory chain complexes121. MNGIE (Mitochondrial Neuro-Gastro-Intestinal Ence-phalopathy).
The ultrastructure of muscle fibers and satellite cells in experimental autoimmune encephalomyelitis after treatment with transcranial magnetic stimulation
Published in Ultrastructural Pathology, 2022
María Angeles Peña-Toledo, Evelio Luque, Manuel LaTorre, Ignacio Jimena, Fernando Leiva-Cepas, Ignacio Ruz-Caracuel, Eduardo Agüera, J. Peña-Amaro, Isaac Tunez
Skeletal muscles with a high percentage of type 1 fibers are more vulnerable to ROS-induced damage because they contain more mitochondria,23 although other components such as the sarcoplasmic reticulum, sarcolemma, and T tubes can also produce ROS.24 Furthermore, oxidative stress likely acts as a potential activator and important mediator of myonuclear apoptosis during denervation-induced muscle loss.25 All this concurs with our results because most of the myonuclei in this current study showed ultrastructural features of apoptosis in the EAE group. Although this can occur through various mechanisms, mitochondria seem to be the main organelle that release the apoptosis inducing factor that would result in the observed DNA fragmentation.26 For this reason, the severe mitochondrial involvement in our study could be responsible for the myonuclei showing apoptotic characteristics.
Dark Sweet Cherry (Prunus avium) Phenolics Enriched in Anthocyanins Induced Apoptosis in MDA-MB-453 Breast Cancer Cells through MAPK-Dependent Signaling and Reduced Invasion via Akt and PLCγ-1 Downregulation
Published in Nutrition and Cancer, 2021
Marjorie Anne A. Layosa, Nara N. Lage, Boon P. Chew, Liezl Atienza, Susanne Mertens-Talcott, Stephen Talcott, Giuliana D. Noratto
Caspases are considered as the main effectors of apoptosis, but multiple other mechanisms involving stress-inducible molecules can also induce apoptosis (7). Apoptosis can be initiated by the extrinsic death receptor pathway and/or by the intrinsic or mitochondrial pathway. The extrinsic apoptotic pathway involves the stimulation of death receptors located at the plasma membrane which in turn activates caspase-8 and the cleavage of its downstream effector caspases. The intrinsic apoptotic pathway involves the release of mitochondrial cytotoxic proteins such as cytochrome c that triggers the activation of caspase-9 and caspase-3, and apoptosis inducing factor (AIF) triggering caspase independent apoptosis (12). Crosstalk between extrinsic and intrinsic apoptotic pathways is mediated by caspase-8-mediated cleavage of BH3 interacting-domain death agonist (BID) that translocates to mitochondria, where it promotes cytochrome c release (7).
Anti-tumoral potential of a human granulysin-based, CEA-targeted cytolytic immunotoxin
Published in OncoImmunology, 2019
Raquel Ibáñez-Pérez, Patricia Guerrero-Ochoa, Sameer Al-Wasaby, Rocío Navarro, Antonio Tapia-Galisteo, Diego De Miguel, Oscar Gonzalo, Blanca Conde, Luis Martínez-Lostao, Ramón Hurtado-Guerrero, Laura Sanz, Alberto Anel
Histological studies on tissue sections obtained from resected tumors were also performed. As shown in the hematoxilin/eosin images (Figure 7a), untreated tumors from the control group or from the GRNLY-treated group presented the typical compact tissue structure of a fast-growing tumor. On the contrary, systemic injection of MFE23GRNLY caused a dramatic loss of cellularity in HeLa-CEA derived tumors (right panel of Figure 7a). Active caspase-3 immunochemistry gave some limited labeling in GRNLY-treated tumors (middle panel of Figure 7b), but this staining was much more extensive in the case of MFE23GRNLY-treated mice (right panel of Figure 7b). Upon DAPI labeling, untreated tumors or tumors treated by systemic GRNLY injection displayed nuclei with non-condensed chromatin (Figure 7c, left and middle panels, respectively). On the contrary, MFE23GRNLY-treated tumors showed less cellularity, condensed chromatin and fragmented nuclei (indicated with arrows in the right panel of Figure 7c). In addition, they also showed numerous cells with condensed chromatin concentrated in the nuclear margins (indicated with circles in the same image). This nuclear morphology is characteristic of apoptosis-inducing factor (AIF)-mediated cell death.10