Xanthine Oxidase‐Derived ROS Display a Biphasic Effect on Endothelial Cells Adhesion and FAK Phosphorylation

Ben-Mahdi, Meriem Hind; Dang, Pham My-Chan; Gougerot‐Pocidalo, Marie‐Anne; O’Dowd, Yvonne; El-Benna, Jamel; Pasquier, Claude

doi:10.1155/2016/9346242

Cited by 18 publications

(11 citation statements)

References 44 publications

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“…68,69 In glioma and ischemia, the hypoxic condition and low pH allow XO to form a large amount of H 2 O 2 , O 2 − , and OH• via the Haber-Weiss-Fenton reaction. [70][71][72] Cytochrome P450 (CYP) CYPis a monooxygenase with a heme (FeIII) prosthetic group, 73,74 and its isoforms in different regions of the body regulate the biotransformation pathway of several endogenous and exogenous toxins, chemicals, xenobiotics, and organic molecules. This system can generate different ROS species (…”

Section: Peroxisomesmentioning

confidence: 99%

The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports

Ghosh

Chakraborty

Sarkar

et al. 2019

Sig Transduct Target Ther

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Glioma and cerebral ischemic stroke are two major events that lead to patient death worldwide. Although these conditions have different physiological incidences,~10% of ischemic stroke patients develop cerebral cancer, especially glioma, in the postischemic stages. Additionally, the high proliferation, venous thrombosis and hypercoagulability of the glioma mass increase the significant risk of thromboembolism, including ischemic stroke. Surprisingly, these events share several common pathways, viz. hypoxia, cerebral inflammation, angiogenesis, etc., but the proper mechanism behind this co-occurrence has yet to be discovered. The hypercoagulability and presence of the D-dimer level in stroke are different in cancer patients than in the noncancerous population. Other factors such as atherosclerosis and coagulopathy involved in the pathogenesis of stroke are partially responsible for cancer, and the reverse is also partially true. Based on clinical and neurosurgical experience, the neuronal structures and functions in the brain and spine are observed to change after a progressive attack of ischemia that leads to hypoxia and atrophy. The major population of cancer cells cannot survive in an adverse ischemic environment that excludes cancer stem cells (CSCs). Cancer cells in stroke patients have already metastasized, but early-stage cancer patients also suffer stroke for multiple reasons. Therefore, stroke is an early manifestation of cancer. Stroke and cancer share many factors that result in an increased risk of stroke in cancer patients, and vice-versa. The intricate mechanisms for stroke with and without cancer are different. This review summarizes the current clinical reports, pathophysiology, probable causes of co-occurrence, prognoses, and treatment possibilities.

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Section: Peroxisomesmentioning

confidence: 99%

The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports

Ghosh

Chakraborty

Sarkar

et al. 2019

Sig Transduct Target Ther

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“…When renal tissues or cells exposed to I/R damage, the content of ROS altered with the change of GJ function, but the underlying mechanism responsible to I/R-induced injuries was still not clear. Many researches had already showed that ROS played an essential role in decision of cell destiny: death or survival in some pathological process, including I/R injury [ 40 , 41 ]. ROS could initiate the cascade of cell damage, apoptosis/necrosis, and pro-inflammatory responses, also could trigger cell apoptosis through various signaling pathways, such as inflammation, oxidative stress or ERS response [ 42 , 43 ].…”

Section: Discussionmentioning

confidence: 99%

Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury

Huang

Wang

et al. 2018

J Transl Med

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BackgroundIschemia–reperfusion (I/R)-induced acute kidney injury (AKI) not only prolongs the length of hospital stay, but also seriously affects the patient’s survival rate. Although our previous investigation has verified that reactive oxygen species (ROS) transferred through gap junction composed of connexin32 (Cx32) contributed to AKI, its underlying mechanisms were not fully understood and viable preventive or therapeutic regimens were still lacking. Among various mechanisms involved in organs I/R-induced injuries, endoplasmic reticulum stress (ERS)-related apoptosis is currently considered to be an important participant. Thus, in present study, we focused on the underlying mechanisms of I/R-induced AKI, and postulated that Cx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI.MethodsWe established renal I/R models with Cx32+/+ and Cx32−/− mice, which underwent double kidneys clamping and recanalization. ROS scavenger (N-acetylcysteine, NAC) and ERS inhibitors (4-phenyl butyric acid, 4-PBA, and tauroursodeoxycholic acid, TUDCA) were used to decrease the content of ROS and attenuate ERS activation, respectively.ResultsRenal damage was progressively exacerbated in a time-dependent manner at the reperfusion stage, that was consistent with the alternation of ERS activation, including glucose regulated protein 78 (BiP/GRP78), X box-binding protein1, and C/EBP homologous protein expression. TUDCA or 4-PBA application attenuated I/R-induced ERS activation and protected against renal tubular epithelial cells apoptosis and renal damage. Cx32 deficiency decreased ROS generation and distribution between the neighboring cells, which attenuated I/R-induced ERS activation, and improved cell apoptosis and renal damage.ConclusionCx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI. Cx32 deficiency, ROS elimination, and ERS inhibition all could protect against I/R-induced AKI.Electronic supplementary materialThe online version of this article (10.1186/s12967-018-1493-8) contains supplementary material, which is available to authorized users.

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“…The capability of measuring ROS in culture media allowed us to then use the cells for immunoblotting of downstream signaling molecules. Several PTKs, such as focal adhesion kinase (FAK), proline-rich tyrosine kinase 2 (Pyk2), and Src, have been shown to be activated by ROS [17–21, 28]. We investigated whether PMA-induced ROS generation could increase FAK activity in HT-29 cells.…”

Section: Resultsmentioning

confidence: 99%

A Quantitative Method to Measure Low Levels of ROS in Nonphagocytic Cells by Using a Chemiluminescent Imaging System

Kim

Jeong

Murphy

et al. 2019

Oxidative Medicine and Cellular Longevity

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Chemiluminescence (CL) is one of the most useful methods for detecting reactive oxygen species (ROS). Although fluorescence dyes or genetically encoded biosensors have been developed, CL is still used due to its high sensitivity, ease of use, and low cost. While initially established and used to measure high levels of ROS in phagocytic cells, CL assays are not ideal for measuring low levels of ROS. Here, we developed a newly modified CL assay using a chemiluminescent imaging system for measuring low concentrations of ROS in nonphagocytic cells. We found that dissolving luminol in NaOH, rather than DMSO, increased the H2O2-induced CL signal and that the addition of 4-iodophenylboronic acid (4IPBA) further increased CL intensity. Our new system also increased the rate and intensity of the CL signal in phorbol 12-myristate 13-acetate- (PMA-) treated HT-29 colon cancer cells compared to those in luminol only. We were able to quantify ROS levels from both cells and media in parallel using an H2O2 standard. A significant benefit to our system is that we can easily measure stimulus-induced ROS formation in a real-time manner and also investigate intracellular signaling pathways from a single sample simultaneously. We found that PMA induced tyrosine phosphorylation of protein tyrosine kinases (PTKs), such as focal adhesion kinase (FAK), protein tyrosine kinase 2 (Pyk2), and Src, and increased actin stress fiber formation in a ROS-dependent manner. Interestingly, treatment with either N-acetyl-L-cysteine (NAC) or diphenyleneiodonium (DPI) reduced the PMA-stimulated phosphorylation of these PTKs, implicating a potential role in cellular ROS signaling. Thus, our newly optimized CL assay using 4IPBA and a chemiluminescent imaging method provides a simple, real-time, and low-cost method for the quantification of low levels of ROS.

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Xanthine Oxidase‐Derived ROS Display a Biphasic Effect on Endothelial Cells Adhesion and FAK Phosphorylation

Cited by 18 publications

References 44 publications

The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports

The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports

Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury

A Quantitative Method to Measure Low Levels of ROS in Nonphagocytic Cells by Using a Chemiluminescent Imaging System

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