scholarly journals Autophagy-Like Cell Death Regulates Hydrogen Peroxide and Calcium Ion Distribution in Xa3/Xa26-Mediated Resistance to Xanthomonas oryzae pv. oryzae

2019 ◽  
Vol 21 (1) ◽  
pp. 194 ◽  
Author(s):  
Jianbo Cao ◽  
Meng Zhang ◽  
Mengmeng Zhu ◽  
Limin He ◽  
Jinghua Xiao ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Calcium Ions ◽  
Calcium Ion ◽  
Durable Resistance ◽  
Xanthomonas Oryzae ◽  
Xylem Parenchyma ◽  
Autophagy Inhibitor ◽  
Parenchyma Cells ◽  
Resistance Reaction

The broad-spectrum and durable resistance gene Xa3/Xa26 against Xanthomonas oryzae pv. oryzae (Xoo) has been widely exploited in rice production in China. But the cytological features of the Xa3/Xa26-mediated resistance reaction have been rarely reported. This study reveals the cytological characteristics of the Xa3/Xa26-mediated resistance reaction against Xoo to uncover the functions of hypersensitive response programmed cell death (HR-PCD) in rice. Autophagy-like cell death, which was characterized by double-membrane bodies appearance in xylem parenchyma cell and mesophyll cell, was inhibited by autophagy inhibitor 3-methyladenin (3-MA). The autophagy-related genes were induced to reach a high level in resistance reaction. The hydrogen peroxide (H2O2) maintained a low concentration on the plasma membrane. The calcium ions localized on the apoplast were transferred into the vacuole. The autophagy inhibitor (3-MA) impaired Xa3/Xa26-mediated resistance by promoting the accumulation of H2O2, and inhibited the transfer of extracellular calcium ions into the vacuole in the xylem parenchyma cells and mesophyll cells. Therefore, the HR-PCD belongs to autophagy-like cell death in the Xa3/Xa26-mediated resistance reaction. These results suggest that the autophagy-like cell death participates in the Xa3/Xa26-mediated resistance by negatively regulating H2O2 accumulation, in order to abolish oxidative stress and possibly activate calcium ion signals in xylem parenchyma cells of the rice leaf.

Signal-regulated oxidation of proteins via MICAL

2020 ◽  
Vol 48 (2) ◽  
pp. 613-620
Author(s):  
Clara Ortegón Salas ◽  
Katharina Schneider ◽  
Christopher Horst Lillig ◽  
Manuela Gellert
Keyword(s):  
Signal Transduction ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Redox Regulation ◽  
Signal Transduction Pathways ◽  
Cellular Functions ◽  
Intracellular Signals ◽  
Amino Acid Side Chains ◽  
Specific Receptors ◽  
Sulfur Containing

Processing of and responding to various signals is an essential cellular function that influences survival, homeostasis, development, and cell death. Extra- or intracellular signals are perceived via specific receptors and transduced in a particular signalling pathway that results in a precise response. Reversible post-translational redox modifications of cysteinyl and methionyl residues have been characterised in countless signal transduction pathways. Due to the low reactivity of most sulfur-containing amino acid side chains with hydrogen peroxide, for instance, and also to ensure specificity, redox signalling requires catalysis, just like phosphorylation signalling requires kinases and phosphatases. While reducing enzymes of both cysteinyl- and methionyl-derivates have been characterised in great detail before, the discovery and characterisation of MICAL proteins evinced the first examples of specific oxidases in signal transduction. This article provides an overview of the functions of MICAL proteins in the redox regulation of cellular functions.

scholarly journals Exposure to Hydrogen Peroxide Induces Cell Death via Apoptosis in Primary Cultured Mouse Hepatocytes.

1999 ◽  
Vol 22 (12) ◽  
pp. 1296-1300 ◽  
Author(s):  
Shuuichi KANNO ◽  
Masaaki ISHIKAWA ◽  
Motoaki TAKAYANAGI ◽  
Yoshio TAKAYANAGI ◽  
Ken-ichi SASAKI
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Mouse Hepatocytes

scholarly journals Iron prochelator BSIH protects retinal pigment epithelial cells against cell death induced by hydrogen peroxide

2008 ◽  
Vol 102 (12) ◽  
pp. 2130-2135 ◽  
Author(s):  
Louise K. Charkoudian ◽  
Tzvete Dentchev ◽  
Nina Lukinova ◽  
Natalie Wolkow ◽  
Joshua L. Dunaief ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Epithelial Cells ◽  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Pigment Epithelial ◽  
Pigment Epithelial Cells

Selenium rescues orbital fibroblasts from cell death induced by hydrogen peroxide: another molecular basis for the effects of selenium in graves’ orbitopathy

Endocrine ◽  
2017 ◽  
Vol 58 (2) ◽  
pp. 386-389 ◽  
Author(s):  
Giovanna Rotondo Dottore ◽  
Riccardo Chiarini ◽  
Maria De Gregorio ◽  
Marenza Leo ◽  
Giamberto Casini ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Molecular Basis ◽  
Graves Orbitopathy ◽  
Orbital Fibroblasts

Erratum to: Selenium rescues orbital fibroblasts from cell death induced by hydrogen peroxide: another molecular basis for the effects of selenium in graves’ orbitopathy

Endocrine ◽  
2017 ◽  
Vol 58 (2) ◽  
pp. 390-390 ◽  
Author(s):  
Giovanna Rotondo Dottore ◽  
Riccardo Chiarini ◽  
Maria De Gregorio ◽  
Marenza Leo ◽  
Giamberto Casini ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Molecular Basis ◽  
Graves Orbitopathy ◽  
Orbital Fibroblasts

Overexpression of human Hsp27 inhibits serum-induced proliferation in airway smooth muscle myocytes and confers resistance to hydrogen peroxide cytotoxicity

2007 ◽  
Vol 293 (5) ◽  
pp. L1194-L1207 ◽  
Author(s):  
Sonemany Salinthone ◽  
Mariam Ba ◽  
Lisa Hanson ◽  
Jody L. Martin ◽  
Andrew J. Halayko ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Smooth Muscle ◽  
Cell Survival ◽  
Airway Smooth Muscle ◽  
Apoptotic Cell ◽  
Airway Remodeling ◽  
Small Heat Shock Protein ◽  
Nonmuscle Cells ◽  
Myocyte Proliferation

Airway smooth muscle (ASM) hypertrophy and hyperplasia are characteristics of asthma that lead to thickening of the airway wall and obstruction of airflow. Very little is known about mechanisms underlying ASM remodeling, but in vascular smooth muscle, it is known that progression of atherosclerosis depends on the balance of myocyte proliferation and cell death. Small heat shock protein 27 (Hsp27) is antiapoptotic in nonmuscle cells, but its role in ASM cell survival is unknown. Our hypothesis was that phosphorylation of Hsp27 may regulate airway remodeling by modifying proliferation, cell survival, or both. To test this hypothesis, adenoviral vectors were used to overexpress human Hsp27 in ASM cells. Cells were infected with empty vector (Ad5) or wild-type Hsp27 (AdHsp27 WT), and proliferation and death were assessed. Overexpressing Hsp27 WT caused a 50% reduction in serum-induced proliferation and increased cell survival after exposure to 100 μM hydrogen peroxide (H2O2) compared with mock-infected controls. Overexpression studies utilizing an S15A, S78A, and S82A non-phosphorylation mutant (AdHsp27 3A) and an S15D, S78D, and S82D pseudo-phosphorylation mutant (AdHsp27 3D) showed phosphorylation of Hsp27 was necessary for regulation of ASM proliferation, but not survival. Hsp27 provided protection against H2O2-induced cytotoxicity by upregulating cellular glutathione levels and preventing necrotic cell death, but not apoptotic cell death. The results support the notion that ASM cells can be stimulated to undergo proliferation and death and that Hsp27 may regulate these processes, thereby contributing to airway remodeling in asthmatics.

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