Protecting P-type plasma membrane H+-ATPases from ROS

2021 ◽  
Vol 478 (8) ◽  
pp. 1511-1513
Author(s):  
Sarah C. Stainbrook ◽  
Joseph M. Jez
Keyword(s):  
Reactive Oxygen Species ◽  
Plasma Membrane ◽  
Reactive Oxygen ◽  
Transport Proteins ◽  
Common Mechanism ◽  
Oxygen Species ◽  
Cellular Membranes ◽  
Biochemical Journal ◽  
P Type

P-type ATPase are ubiquitous transport proteins across all kingdoms of life. These proteins share a common mechanism involving phosphorylation of an invariant aspartate to facilitate movement of substrates from protons to phospholipids across cellular membranes. In this issue of the Biochemical Journal, Welle et al. identify a conserved cysteine near the functionally critical aspartate of P-type plasma membrane H+-ATPases that protects the protein from reactive oxygen species.

Reactive oxygen species produced via plasma membrane NADPH oxidase regulate anthocyanin synthesis in apple peel

Planta ◽  
2014 ◽  
Vol 240 (5) ◽  
pp. 1023-1035 ◽  
Author(s):  
Jiangli Zhang ◽  
Changsheng Chen ◽  
Di Zhang ◽  
Houhua Li ◽  
Pengmin Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Plasma Membrane ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Anthocyanin Synthesis ◽  
Oxygen Species ◽  
Apple Peel

Abstract 44: Reactive Oxygen Species Mediate TLR4 MyD88 Independent Signaling in Human Hemoglobin-Associated Macrophages Through TLR4 Lipid Raft Interactions

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Aloke Finn ◽  
Masataka Nakano ◽  
Rohini Polavarapu ◽  
Vinit Karmali ◽  
Omar Saeed ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Plasma Membrane ◽  
Lipid Raft ◽  
Foam Cell ◽  
Large Fraction ◽  
Reactive Oxygen ◽  
Intraplaque Hemorrhage ◽  
Oxygen Species ◽  
Intracellular Iron ◽  
Lps Treatment

Objectives: Experimental data indicate an important role for Toll-like Receptor 4 (TLR4) MyD88 independent signaling in upregulating Interferon β (IFN-β) production and driving atherosclerosis. We recently identified a distinct non-foam cell macrophage (M(Hb) or Hb-associated macrophage) in areas of intraplaque hemorrhage characterized by reduced reactive oxygen species (ROS) and pro-inflammatory cytokines. In this study, we investigated the role of iron and ROS in mediating TLR4 MyD88 independent signaling in these cells. Methods and Results: Areas rich in M(Hb) in atherosclerotic plaques demonstrated significantly reduced IFN-β expression compared to foam cell areas by immunostaining and quantitative PCR. M(Hb) did not upregulate IFN-β when exposed to ox LDL in contrast to control macrophages, a response which was inhibited in the presence of a TLR4 blocking antibody. To further investigate TLR4 responses in M(Hb), we used the TLR4 activator LPS. LPS produced significant increases in IFN-β in control macrophages but had no effect in M(Hb). This defect could be corrected by raising intracellular iron by pretreating M(Hb) with hepcidin prior to LPS treatment, suggesting redox state mediates this effect. The interaction of TLR4 with TRIF was examined by immunoprecipitation of lysates from control or M(Hb) cells treated with LPS using a TLR4 antibody and immunoblotting for TRIF. LPS treatment of control but not M(Hb) cells resulted in an increase in TRIF. Hepcidin pretreatment of M(Hb) corrected this interaction in response to LPS while differentiating monocytes in superoxide dismutase prevented it. Lastly, the interaction between lipid rafts and TLR4 was examined using FITC-cholera toxin (CTx) and a TLR4 antibody. In control cells the distribution of CTx on the plasma membrane was homogeneous and TLR4 localized to both the membrane and intracellular compartment. After LPS, a large fraction of TLR4 translocated to the plasma membrane, and colocalization of TLR4 and CTx was observed. In M(Hb) the LPS- induced translocation of TLR4 to the membrane rafts was inhibited. Conclusion: M(Hb) cells modulate TLR4 MyD88 independent signaling through reducing ROS which inhibits TLR4 lipid raft interactions.

scholarly journals NADPH Oxidase-Mediated Reactive Oxygen Species Production: Subcellular Localization and Reassessment of Its Role in Plant Defense

2009 ◽  
Vol 22 (7) ◽  
pp. 868-881 ◽  
Author(s):  
Jeannine Lherminier ◽  
Taline Elmayan ◽  
Jérôme Fromentin ◽  
Khadija Tantaoui Elaraqui ◽  
Simona Vesa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Plasma Membrane ◽  
Nadph Oxidase ◽  
Subcellular Localization ◽  
Acquired Resistance ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Wild Type ◽  
Hydrogen Peroxide Production

Chemiluminescence detection of reactive oxygen species (ROS) triggered in tobacco BY-2 cells by the fungal elicitor cryptogein was previously demonstrated to be abolished in cells transformed with an antisense construct of the plasma membrane NADPH oxidase, NtrbohD. Here, using electron microscopy, it has been confirmed that the first hydrogen peroxide production occurring a few minutes after challenge of tobacco cells with cryptogein is plasma membrane located and NtrbohD mediated. Furthermore, the presence of NtrbohD in detergent-resistant membrane fractions could be associated with the presence of NtrbohD-mediated hydrogen peroxide patches along the plasma membrane. Comparison of the subcellular localization of ROS in wild-type tobacco and in plants transformed with antisense constructs of NtrbohD revealed that this enzyme is also responsible for the hydrogen peroxide production occurring at the plasma membrane after infiltration of tobacco leaves with cryptogein. Finally, the reactivity of wild-type and transformed plants to the elicitor and their resistance against the pathogenic oomycete Phytophthora parasitica were examined. NtrbohD-mediated hydrogen peroxide production does not seem determinant for either hypersensitive response development or the establishment of acquired resistance but it is most likely involved in the signaling pathways associated with the protection of the plant cell.

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