PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34684987-15 2021 Interestingly, Nano-GO-induced RPE cell migration and intracellular ROS production were abrogated in PLD-knockdown RPE cells, indicating that PLD activation played a crucial role in the Nano-GO-induced RPE EMT process. Reactive Oxygen Species 68-71 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 142-145 34684987-16 2021 We demonstrate for the first time that Nano-GO promotes RPE cell migration through PLD-mediated ROS production. Reactive Oxygen Species 96-99 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 83-86 23662182-8 2013 For the first time, this study demonstrated that the PLD-generated intracellular bioactive lipid signal mediator, PA, played a critical role in the ROS-induced barrier dysfunction in lung vascular ECs. Reactive Oxygen Species 148-151 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 53-56 33500617-6 2021 The mechanism was probably attributed to the accumulation of PLD in the skin tissues during the long-term circulation and further the induction of ROS to cause the oxidative damage of keratinocytes owing to the sustained release of doxorubicin from PLD. Reactive Oxygen Species 147-150 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 249-252 30286953-3 2018 Our results show that expression of A. fumigatus PLD in human cells was able to increase the production of reactive oxygen species (ROS), which play an important role in several signaling pathways as well as in lung infection. Reactive Oxygen Species 107-130 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 49-52 30286953-3 2018 Our results show that expression of A. fumigatus PLD in human cells was able to increase the production of reactive oxygen species (ROS), which play an important role in several signaling pathways as well as in lung infection. Reactive Oxygen Species 132-135 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 49-52 30286953-4 2018 Meanwhile, A. fumigatus PLD was found to interact with human endogenous histone deacetylase 6 (HDAC6), a known regulator of ROS production and inflammatory responses; PLD significantly increased the expression level of HDAC6 protein without altering its mRNA level. Reactive Oxygen Species 124-127 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 24-27 30286953-4 2018 Meanwhile, A. fumigatus PLD was found to interact with human endogenous histone deacetylase 6 (HDAC6), a known regulator of ROS production and inflammatory responses; PLD significantly increased the expression level of HDAC6 protein without altering its mRNA level. Reactive Oxygen Species 124-127 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 167-170 30286953-5 2018 These results suggest that A. fumigatus PLD may enhance the production of ROS via the accumulation of HDAC6, which may be involved in host immunomodulation during A. fumigatus infection. Reactive Oxygen Species 74-77 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 40-43 29438048-6 2018 Additionally, we observed an interplay between H2S and PLD activity in the regulation of reactive oxygen species production and stomatal movement. Reactive Oxygen Species 89-112 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 55-58 33500617-7 2021 Conclusion: The ROS generation induced by the administration of PLD has been identified to be a crucial factor in the development of HFS, which could be used as a potential therapeutic target to alleviate the HFS symptom of PLD administration. Reactive Oxygen Species 16-19 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 64-67 33500617-7 2021 Conclusion: The ROS generation induced by the administration of PLD has been identified to be a crucial factor in the development of HFS, which could be used as a potential therapeutic target to alleviate the HFS symptom of PLD administration. Reactive Oxygen Species 16-19 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 224-227 32008007-8 2020 Moreover, PLD treatment significantly decreased the levels of ROS, 4-HNE, and MDA in H2O2-treated 2BS cells. Reactive Oxygen Species 62-65 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 10-13 30945345-6 2019 PLD treatment inhibited oxidative stress induced by OGD/R, which was evidenced by the reduced level of reactive oxygen species and increased activities of catalase, superoxide dismutase, and glutathione peroxidase. Reactive Oxygen Species 103-126 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 29622768-1 2018 We have previously shown that phospholipase D (PLD) downregulation accelerates cellular senescence, which is widely believed to play an important role in aging, by stimulating reactive oxygen species (ROS) accumulation in human cells. Reactive Oxygen Species 176-199 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 30-45 29622768-1 2018 We have previously shown that phospholipase D (PLD) downregulation accelerates cellular senescence, which is widely believed to play an important role in aging, by stimulating reactive oxygen species (ROS) accumulation in human cells. Reactive Oxygen Species 176-199 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 47-50 29622768-1 2018 We have previously shown that phospholipase D (PLD) downregulation accelerates cellular senescence, which is widely believed to play an important role in aging, by stimulating reactive oxygen species (ROS) accumulation in human cells. Reactive Oxygen Species 201-204 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 30-45 29622768-1 2018 We have previously shown that phospholipase D (PLD) downregulation accelerates cellular senescence, which is widely believed to play an important role in aging, by stimulating reactive oxygen species (ROS) accumulation in human cells. Reactive Oxygen Species 201-204 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 47-50 23662182-0 2013 Phospholipase D signaling mediates reactive oxygen species-induced lung endothelial barrier dysfunction. Reactive Oxygen Species 35-58 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-15 23662182-2 2013 Earlier, we have demonstrated that ROS stimulate lung endothelial cell (EC) phospholipase D (PLD) that generates phosphatidic acid (PA), a second messenger involved in signal transduction. Reactive Oxygen Species 35-38 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 76-91 23662182-2 2013 Earlier, we have demonstrated that ROS stimulate lung endothelial cell (EC) phospholipase D (PLD) that generates phosphatidic acid (PA), a second messenger involved in signal transduction. Reactive Oxygen Species 35-38 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 93-96 23662182-3 2013 In the current study, we investigated the role of PLD signaling in the ROS-induced lung vascular EC barrier dysfunction. Reactive Oxygen Species 71-74 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 50-53 23662182-9 2013 This study also underscores the importance of PLD signaling in vascular leak and associated tissue injury in the etiology of lung diseases among critically ill patients encountering oxygen toxicity and excess ROS production during ventilator-assisted breathing. Reactive Oxygen Species 209-212 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 46-49 19366706-0 2009 Phospholipase D-mediated activation of IQGAP1 through Rac1 regulates hyperoxia-induced p47phox translocation and reactive oxygen species generation in lung endothelial cells. Reactive Oxygen Species 113-136 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-15 19519662-5 2009 Our results demonstrate that receptor-internalizing agonists (like DAMGO, beta-endorphin, methadone, piritramide, fentanyl, sufentanil, and etonitazene) strongly induce NADH/NADPH-mediated ROS synthesis via PLD-dependent signaling pathways, whereas agonists that do not induce MOPr endocytosis and PLD2 activation (like morphine, buprenorphine, hydromorphone, and oxycodone) failed to activate ROS synthesis in transfected human embryonic kidney 293 cells. Reactive Oxygen Species 189-192 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 207-210 19519662-5 2009 Our results demonstrate that receptor-internalizing agonists (like DAMGO, beta-endorphin, methadone, piritramide, fentanyl, sufentanil, and etonitazene) strongly induce NADH/NADPH-mediated ROS synthesis via PLD-dependent signaling pathways, whereas agonists that do not induce MOPr endocytosis and PLD2 activation (like morphine, buprenorphine, hydromorphone, and oxycodone) failed to activate ROS synthesis in transfected human embryonic kidney 293 cells. Reactive Oxygen Species 394-397 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 207-210 16099207-0 2005 Phospholipase D in the signaling networks of plant response to abscisic acid and reactive oxygen species. Reactive Oxygen Species 81-104 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-15 16099207-5 2005 PLD and PA play multiple roles in the signaling networks of plant response to abscisic acid and reactive oxygen species. Reactive Oxygen Species 96-119 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 9698536-3 1998 Phospholipase D (PLD) production of phosphatidic acid (PA) is thought to be pivotal in reactive oxygen species generation but its role in degranulation (i. e., protease release) remains unclear. Reactive Oxygen Species 87-110 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-15 11228747-5 1999 Pretreatment of BPAECs with N-acetyl-L-cysteine (NAC) or 2-mercaptopropionylglycine (MPG) blocked ROS-induced changes in intracellular GSH and PLD activation. Reactive Oxygen Species 98-101 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 143-146 11228747-10 1999 These results support the hypothesis that modulation of thiol-redox status (cellular nonprotein and protein thiols) may contribute to the regulation of ROS-induced protein tyrosine phosphorylation and PLD activation in vascular endothelium. Reactive Oxygen Species 152-155 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 201-204 9720761-3 1998 In this review, we will explore the molecular properties of mammalian PLD and its gene(s), the complexity of this enzyme regulation and the myriad physiological roles for PLD and PA and related metabolic products, with particular emphasis on a role in the activation of NADPH oxidase, or respiratory burst, leading to the generation of oxygen radicals. Reactive Oxygen Species 336-351 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 70-73 11446714-8 2001 PLD inhibition attenuated Ang II-induced ROS generation, with greater effects in the hypertensive group than the normotensive group (delta = 42 +/- 3.3 versus 21 +/- 2 units). Reactive Oxygen Species 41-44 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 0-3 11228747-3 1999 Previously, we have shown that ROS (hydrogen peroxide, fatty acid hydroperoxide, diperoxovanadate, and 4-hydroxynonenal) enhance protein tyrosine phosphorylation and activate phospholipase D (PLD) in bovine pulmonary artery endothelial cells (BPAECs). Reactive Oxygen Species 31-34 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 192-195 11228747-4 1999 In the present study, our aim was to investigate the role of exogenous thiol agents on ROS-induced PLD activation in conjunction with the role of cellular thiols--glutathione (GSH) and protein thiols--on PLD activation and protein tyrosine phosphorylation. Reactive Oxygen Species 87-90 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 99-102 9788899-7 1998 An immediate signaling response to increased protein tyrosine phosphorylation by ROS was activation of phospholipases such as A2, C, and D. Suramin pretreatment inhibited ROS stimulation of phospholipase D (PLD), suggesting a role for growth factor receptors in this activation. Reactive Oxygen Species 81-84 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 190-205 9788899-7 1998 An immediate signaling response to increased protein tyrosine phosphorylation by ROS was activation of phospholipases such as A2, C, and D. Suramin pretreatment inhibited ROS stimulation of phospholipase D (PLD), suggesting a role for growth factor receptors in this activation. Reactive Oxygen Species 81-84 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 207-210 9788899-7 1998 An immediate signaling response to increased protein tyrosine phosphorylation by ROS was activation of phospholipases such as A2, C, and D. Suramin pretreatment inhibited ROS stimulation of phospholipase D (PLD), suggesting a role for growth factor receptors in this activation. Reactive Oxygen Species 171-174 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 190-205 9788899-7 1998 An immediate signaling response to increased protein tyrosine phosphorylation by ROS was activation of phospholipases such as A2, C, and D. Suramin pretreatment inhibited ROS stimulation of phospholipase D (PLD), suggesting a role for growth factor receptors in this activation. Reactive Oxygen Species 171-174 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 207-210 9788899-8 1998 Further, PLD activation by ROS was attenuated by N-acetylcysteine, indicating that intracellular thiol status is critical to ROS-mediated signal transduction. Reactive Oxygen Species 27-30 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 9-12 9788899-8 1998 Further, PLD activation by ROS was attenuated by N-acetylcysteine, indicating that intracellular thiol status is critical to ROS-mediated signal transduction. Reactive Oxygen Species 125-128 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 9-12 9698536-3 1998 Phospholipase D (PLD) production of phosphatidic acid (PA) is thought to be pivotal in reactive oxygen species generation but its role in degranulation (i. e., protease release) remains unclear. Reactive Oxygen Species 87-110 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 17-20 9493913-2 1998 Cytoskeletal rearrangement by reactive oxygen species may be related to specific activation of the phospholipase D (PLD) pathway. Reactive Oxygen Species 30-53 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 99-114 9493913-2 1998 Cytoskeletal rearrangement by reactive oxygen species may be related to specific activation of the phospholipase D (PLD) pathway. Reactive Oxygen Species 30-53 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 116-119