scholarly journals Modulation of Host Programmed Cell Death Pathways by the Intracellular Protozoan Parasite, Toxoplasma gondii — Implications for Maintenance of Chronic Infection and Potential Therapeutic Applications

10.5772/61529 ◽  
2015 ◽  
Author(s):  
Sandra K. Halonen
Keyword(s):  
Cell Death ◽  
Toxoplasma Gondii ◽  
Programmed Cell Death ◽  
Chronic Infection ◽  
Protozoan Parasite ◽  
Therapeutic Applications ◽  
Cell Death Pathways ◽  
Intracellular Protozoan Parasite

Metronidazole induces programmed cell death in the protozoan parasite Blastocystis hominis

Microbiology ◽  
2004 ◽  
Vol 150 (1) ◽  
pp. 33-43 ◽  
Author(s):  
A. M. A. Nasirudeen ◽  
Yap Eu Hian ◽  
Mulkit Singh ◽  
Kevin S. W. Tan
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Protozoan Parasite ◽  
Blastocystis Hominis

Mitochondrial DNA–Related Mitochondrial Dysfunction in Neurodegenerative Diseases

2002 ◽  
Vol 126 (3) ◽  
pp. 271-280
Author(s):  
Russell H. Swerdlow
Keyword(s):  
Cell Death ◽  
Mitochondrial Dna ◽  
Programmed Cell Death ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Cell Lines ◽  
Late Onset ◽  
Cell Death Pathways ◽  
Mitochondrial Genotype ◽  
Cybrid Cell

Abstract Mitochondrial dysfunction occurs in several late-onset neurodegenerative diseases. Determining its origin and significance may provide insight into the pathogeneses of these disorders. Regarding origin, one hypothesis proposes mitochondrial dysfunction is driven by mitochondrial DNA (mtDNA) aberration. This hypothesis is primarily supported by data from studies of cytoplasmic hybrid (cybrid) cell lines, which facilitate the study of mitochondrial genotype-phenotype relationships. In cybrid cell lines in which mtDNA from persons with certain neurodegenerative diseases is assessed, mitochondrial physiology is altered in ways that are potentially relevant to programmed cell death pathways. Connecting mtDNA-related mitochondrial dysfunction with programmed cell death underscores the crucial if not central role for these organelles in neurodegenerative pathophysiology. This review discusses the cybrid technique and summarizes cybrid data implicating mtDNA-related mitochondrial dysfunction in certain neurodegenerative diseases.

MicroRNA Regulation of Programmed Cell Death Pathways in Cancer

2012 ◽  
Vol 6 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Miao Ming ◽  
Xu Zhao ◽  
Zi-yi Zhao ◽  
Bo Liu ◽  
Jin-ku Bao
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Microrna Regulation ◽  
Cell Death Pathways

Mitochondrial dynamics in yeast cell death and aging

2011 ◽  
Vol 39 (5) ◽  
pp. 1520-1526 ◽  
Author(s):  
Ralf J. Braun ◽  
Benedikt Westermann
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mitochondrial Dynamics ◽  
Progressive Increase ◽  
Mitochondrial Morphology ◽  
Aging Research ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cell Death Pathways ◽  
Dependent Cell ◽  
Mitochondrial Networks

Mitochondria play crucial roles in programmed cell death and aging. Different stimuli activate distinct mitochondrion-dependent cell death pathways, and aging is associated with a progressive increase in mitochondrial damage, culminating in oxidative stress and cellular dysfunction. Mitochondria are highly dynamic organelles that constantly fuse and divide, forming either interconnected mitochondrial networks or separated fragmented mitochondria. These processes are believed to provide a mitochondrial quality control system and enable an effective adaptation of the mitochondrial compartment to the metabolic needs of the cell. The baker's yeast, Saccharomyces cerevisiae, is an established model for programmed cell death and aging research. The present review summarizes how mitochondrial morphology is altered on induction of cell death or on aging and how this correlates with the induction of different cell death pathways in yeast. We highlight the roles of the components of the mitochondrial fusion and fission machinery that affect and regulate cell death and aging.

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