ROS Signaling Under Oxidative Stress in Plants

2020 ◽  
pp. 269-286
Author(s):  
Deepesh Bhatt ◽  
Saurabh C. Saxena ◽  
Sandeep Arora
Keyword(s):  
Oxidative Stress ◽  
Ros Signaling

scholarly journals MicroRNA and Oxidative Stress Interplay in the Context of Breast Cancer Pathogenesis

2019 ◽  
Vol 20 (20) ◽  
pp. 5143 ◽  
Author(s):  
Giulia Cosentino ◽  
Ilaria Plantamura ◽  
Alessandra Cataldo ◽  
Marilena V. Iorio
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Progression ◽  
Genome Instability ◽  
Pathological Condition ◽  
Cell Metabolism ◽  
Comprehensive Overview ◽  
Ros Signaling ◽  
Cancer Pathogenesis ◽  
Regulatory Functions

Oxidative stress is a pathological condition determined by a disturbance in reactive oxygen species (ROS) homeostasis. Depending on the entity of the perturbation, normal cells can either restore equilibrium or activate pathways of cell death. On the contrary, cancer cells exploit this phenomenon to sustain a proliferative and aggressive phenotype. In fact, ROS overproduction or their reduced disposal influence all hallmarks of cancer, from genome instability to cell metabolism, angiogenesis, invasion and metastasis. A persistent state of oxidative stress can even initiate tumorigenesis. MicroRNAs (miRNAs) are small non coding RNAs with regulatory functions, which expression has been extensively proven to be dysregulated in cancer. Intuitively, miRNA transcription and biogenesis are affected by the oxidative status of the cell and, in some instances, they participate in defining it. Indeed, it is widely reported the role of miRNAs in regulating numerous factors involved in the ROS signaling pathways. Given that miRNA function and modulation relies on cell type or tumor, in order to delineate a clearer and more exhaustive picture, in this review we present a comprehensive overview of the literature concerning how miRNAs and ROS signaling interplay affects breast cancer progression.

scholarly journals ROS signaling, oxidative stress and Nrf2 in pancreatic beta-cell function

2010 ◽  
Vol 244 (1) ◽  
pp. 77-83 ◽  
Author(s):  
Jingbo Pi ◽  
Qiang Zhang ◽  
Jingqi Fu ◽  
Courtney G. Woods ◽  
Yongyong Hou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Ros Signaling ◽  
Pancreatic Beta Cell Function

scholarly journals Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-α/NOX2/ROS Signaling Pathway in Monocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Yunfei Chai ◽  
Zhongming Cao ◽  
Runying Yu ◽  
Yong Liu ◽  
Dongdong Yuan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Cx43 Expression ◽  
Ros Signaling ◽  
Pathway Activation ◽  
Carboxyl Terminal ◽  
Umbilical Vein Endothelial Cells ◽  
Inflammation Reaction

Dexmedetomidine is widely used for sedating patients in operation rooms or intensive care units. Its protective functions against oxidative stress, inflammation reaction, and apoptosis have been widely reported. In present study, we explored the effects of dexmedetomidine on monocyte-endothelial adherence. We built lipopolysaccharide- (LPS-) induced monocyte-endothelial adherence models with U937 monocytes and human umbilical vein endothelial cells (HUVECs) and observed the effects of dexmedetomidine on U937-HUVEC adhesion. Specific siRNA was designed to knock-down Connexin43 (Cx43) expression in U937 monocytes. Gö6976, GSK2795039, and NAC were used to inhibit PKC-α, NOX2, and ROS, respectively. Then, we detected whether dexmedetomidine could downregulate Cx43 expression and its downstream PKC-α/NOX2/ROS signaling pathway activation and ultimately result in the decrease of U937-HUVEC adhesion. The results showed that dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), could inhibit adhesion of molecule expression (VLA-4 and LFA-1) and U937-HUVEC adhesion. Simultaneously, it also attenuated Cx43 expression in U937 monocytes. With the downregulation of Cx43 expression, the activity of PKC-α and its related NOX2/ROS signaling pathway were reduced. Inhibiting PKC-α/NOX2/ROS signaling pathway with Gö6976, GSK2795039, and NAC, respectively, VLA-4, LFA-1 expression, and U937-HUVEC adhesion were all decreased. In summary, we concluded that dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), decreased Cx43 expression in U937 monocytes and PKC-α associated with carboxyl-terminal domain of Cx43 protein. With the downregulation of PKC-α, the NOX2/ROS signaling pathway was inhibited, resulting in the decrease of VLA-4 and LFA-1 expression. Ultimately, U937-HUVEC adhesion was reduced.

scholarly journals The Role of Serine-Threonine Protein Phosphatase PP2A in Plant Oxidative Stress Signaling—Facts and Hypotheses

2019 ◽  
Vol 20 (12) ◽  
pp. 3028 ◽  
Author(s):  
Csaba Máthé ◽  
Tamás Garda ◽  
Csongor Freytag ◽  
Márta M-Hamvas
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Protein Phosphatase ◽  
Protein Phosphatases ◽  
Crop Improvement ◽  
Regulatory Function ◽  
Future Research ◽  
Stress Signaling ◽  
Ros Signaling ◽  
External Signals

Abiotic and biotic factors induce oxidative stress involving the production and scavenging of reactive oxygen species (ROS). This review is a survey of well-known and possible roles of serine-threonine protein phosphatases in plant oxidative stress signaling, with special emphasis on PP2A. ROS mediated signaling involves three interrelated pathways: (i) perception of extracellular ROS triggers signal transduction pathways, leading to DNA damage and/or the production of antioxidants; (ii) external signals induce intracellular ROS generation that triggers the relevant signaling pathways and (iii) external signals mediate protein phosphorylation dependent signaling pathway(s), leading to the expression of ROS producing enzymes like NADPH oxidases. All pathways involve inactivation of serine-threonine protein phosphatases. The metal dependent phosphatase PP2C has a negative regulatory function during ABA mediated ROS signaling. PP2A is the most abundant protein phosphatase in eukaryotic cells. Inhibitors of PP2A exert a ROS inducing activity as well and we suggest that there is a direct relationship between these two effects of drugs. We present current findings and hypotheses regarding PP2A-ROS signaling connections related to all three ROS signaling pathways and anticipate future research directions for this field. These mechanisms have implications in the understanding of stress tolerance of vascular plants, having applications regarding crop improvement.

Targeting dysregulation of redox homeostasis in noise-induced hearing loss: Oxidative stress and ROS signaling

2019 ◽  
Vol 135 ◽  
pp. 46-59 ◽  
Author(s):  
Anna Rita Fetoni ◽  
Fabiola Paciello ◽  
Rolando Rolesi ◽  
Gaetano Paludetti ◽  
Diana Troiani
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Redox Homeostasis ◽  
Noise Induced Hearing Loss ◽  
Ros Signaling

Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp (Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Secondary Metabolites ◽  
Human Health ◽  
Grass Carp ◽  
Aquatic Environment ◽  
Ctenopharyngodon Idellus

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.

Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov
Keyword(s):  
Oxidative Stress ◽  
Head And Neck ◽  
Transcriptional Activation ◽  
Platinum Resistance ◽  
Mrna Levels ◽  
Strong Positive Correlation ◽  
Platinum Compounds ◽  
Copper Chelation ◽  
Novel Approach ◽  
Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

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