The molecular basis of cellular defense mechanisms

Biochimie ◽  
1997 ◽  
Vol 79 (8) ◽  
pp. 534
Author(s):  
G. Milon
Keyword(s):  
Molecular Basis ◽  
Defense Mechanisms ◽  
Cellular Defense

scholarly journals Molecular Basis of Citrus sunki Susceptibility and Poncirus trifoliata Resistance Upon Phytophthora parasitica Attack

2018 ◽  
Vol 31 (3) ◽  
pp. 386-398 ◽  
Author(s):  
Ronaldo José Durigan Dalio ◽  
Heros José Máximo ◽  
Tiago Silva Oliveira ◽  
Thamara de Medeiros Azevedo ◽  
Henrique Leme Felizatti ◽  
...  
Keyword(s):  
Molecular Basis ◽  
Defense Mechanisms ◽  
Time Course ◽  
Poncirus Trifoliata ◽  
Disease Development ◽  
Phytophthora Parasitica ◽  
Defense Strategies ◽  
Molecular Core ◽  
Pathogen Effector ◽  
Plant Pathogen Interactions

Coevolution has shaped the molecular basis of an extensive number of defense mechanisms in plant-pathogen interactions. Phytophthora parasitica, a hemibiothrophic oomycete pathogen and the causal agent of citrus root rot and gummosis, interacts differently with Citrus sunki and Poncirus trifoliata, two commonly favored citrus rootstocks that are recognized as susceptible and resistant, respectively, to P. parasitica. The molecular core of these interactions remains elusive. Here, we provide evidence on the defense strategies employed by both susceptible and resistant citrus rootstocks, in parallel with P. parasitica deployment of effectors. Time course expression analysis (quantitative real-time polymerase chain reaction) of several defense-related genes were evaluated during i) plant disease development, ii) necrosis, and iii) pathogen effector gene expression. In C. sunki, P. parasitica deploys effectors, including elicitins, NPP1 (necrosis-inducing Phytophthora protein 1), CBEL (cellulose-binding elicitor and lectin activity), RxLR, and CRN (crinkler), and, consequently, this susceptible plant activates its main defense signaling pathways that result in the hypersensitive response and necrosis. Despite the strong plant-defense response, it fails to withstand P. parasitica invasion, confirming its hemibiothrophic lifestyle. In Poncirus trifoliata, the effectors were strongly expressed, nevertheless failing to induce any immunity manipulation and disease development, suggesting a nonhost resistance type, in which the plant relies on preformed biochemical and anatomical barriers.

The role of corneal crystallins in the cellular defense mechanisms against oxidative stress

2008 ◽  
Vol 19 (2) ◽  
pp. 100-112 ◽  
Author(s):  
Natalie Lassen ◽  
William J. Black ◽  
Tia Estey ◽  
Vasilis Vasiliou
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Cellular Defense

scholarly journals Oxidative damage and cellular defense mechanisms in sea urchin models of aging

2013 ◽  
Vol 63 ◽  
pp. 254-263 ◽  
Author(s):  
Colin Du ◽  
Arielle Anderson ◽  
Mae Lortie ◽  
Rachel Parsons ◽  
Andrea Bodnar
Keyword(s):  
Oxidative Damage ◽  
Sea Urchin ◽  
Defense Mechanisms ◽  
Cellular Defense

Aging and Cellular Defense Mechanisms

1992 ◽  
Vol 663 (1 Aging and Cel) ◽  
pp. 1-3 ◽  
Author(s):  
PAOLO U. GIACOMONI
Keyword(s):  
Defense Mechanisms ◽  
Cellular Defense

scholarly journals Hemolysis Derived Products Toxicity and Endothelium: Model of the Second Hit

Toxins ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 660 ◽  
Author(s):  
Marie Frimat ◽  
Idris Boudhabhay ◽  
Lubka T. Roumenina
Keyword(s):  
Defense Mechanisms ◽  
Cell Injury ◽  
Vascular Diseases ◽  
Heme Oxygenase 1 ◽  
Cellular Defense ◽  
Molecular Pattern ◽  
Free Heme ◽  
Multiple Challenges ◽  
Inflammatory Phenotypes ◽  
Multiple Hit

Vascular diseases are multifactorial, often requiring multiple challenges, or ‘hits’, for their initiation. Intra-vascular hemolysis illustrates well the multiple-hit theory where a first event lyses red blood cells, releasing hemolysis-derived products, in particular cell-free heme which is highly toxic for the endothelium. Physiologically, hemolysis derived-products are rapidly neutralized by numerous defense systems, including haptoglobin and hemopexin which scavenge hemoglobin and heme, respectively. Likewise, cellular defense mechanisms are involved, including heme-oxygenase 1 upregulation which metabolizes heme. However, in cases of intra-vascular hemolysis, those systems are overwhelmed. Heme exerts toxic effects by acting as a damage-associated molecular pattern and promoting, together with hemoglobin, nitric oxide scavenging and ROS production. In addition, it activates the complement and the coagulation systems. Together, these processes lead to endothelial cell injury which triggers pro-thrombotic and pro-inflammatory phenotypes. Moreover, among endothelial cells, glomerular ones display a particular susceptibility explained by a weaker capacity to counteract hemolysis injury. In this review, we illustrate the ‘multiple-hit’ theory through the example of intra-vascular hemolysis, with a particular focus on cell-free heme, and we advance hypotheses explaining the glomerular susceptibility observed in hemolytic diseases. Finally, we describe therapeutic options for reducing endothelial injury in hemolytic diseases.

scholarly journals Cellular Defense Mechanisms in Bivalve Molluscs

2008 ◽  
Vol 43 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Keisuke G. Takahashi ◽  
Kiyokuni Muroga
Keyword(s):  
Defense Mechanisms ◽  
Bivalve Molluscs ◽  
Cellular Defense
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