Olive compounds attenuate oxidative damage induced in HEK-293 cells via MAPK signaling pathway

2017 ◽  
Vol 39 ◽  
pp. 18-27 ◽  
Author(s):  
Amina Maalej ◽  
Maurizio Forte ◽  
Zouhaier Bouallagui ◽  
Stella Donato ◽  
Luigi Mita ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells

Betulinic acid attenuates dexamethasone-induced oxidative damage through the JNK-P38 MAPK signaling pathway in mice

2018 ◽  
Vol 103 ◽  
pp. 499-508 ◽  
Author(s):  
Lijuan Zhu ◽  
Xianglian Yi ◽  
Jing Zhao ◽  
Zhihang Yuan ◽  
Lixin Wen ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Betulinic Acid ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway

scholarly journals β-Arrestin mediates oxytocin receptor signaling, which regulates uterine contractility and cellular migration

2011 ◽  
Vol 300 (3) ◽  
pp. E468-E477 ◽  
Author(s):  
Chad A. Grotegut ◽  
Liping Feng ◽  
Lan Mao ◽  
R. Phillips Heine ◽  
Amy P. Murtha ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Mapk Signaling ◽  
Oxytocin Receptor ◽  
Cellular Migration ◽  
Wild Type ◽  
Uterine Contractility ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
Uterine Muscle ◽  
293 Cells

Desensitization of the oxytocin receptor (OXTR) in the setting of prolonged oxytocin exposure may lead to dysfunctional labor, which increases the risk for cesarean delivery, and uterine atony, which may result in postpartum hemorrhage. The molecular mechanism for OXTR desensitization is through the agonist-mediated recruitment of the multifunctional protein β-arrestin. In addition to its desensitizing function, β-arrestins have recently been shown to simultaneously activate downstream signaling. We tested whether oxytocin stimulation promotes β-arrestin-mediated OXTR desensitization in vivo and activates β-arrestin-mediated mitogen-activated protein kinase (MAPK) growth signaling. Uterine muscle strips isolated from wild-type mice exhibited diminished uterine contractility following repeated exposure to oxytocin, whereas uterine muscle strips from β-arrestin-1 and β-arrestin-2 knockout mice showed no desensitization. Utilizing siRNA knockdown of β-arrestin-1 and β-arrestin-2 in HEK-293 cells expressing the OXTR, we demonstrated oxytocin-mediated MAPK signaling that was dependent on β-arrestin-1 and β-arrestin-2. Wild-type and β-arrestin-1 and β-arrestin-2 knockout mice receiving intravenous oxytocin also demonstrated oxytocin-mediated MAPK signaling that was dependent on β-arrestin-1 and β-arrestin-2. Finally, to test the significance of β-arrestin-mediated signaling from the OXTR, HEK-293 cells expressing the OXTR showed β-arrestin-dependent proliferation in a cell migration assay following oxytocin treatment. In conclusion, β-arrestin is a multifunctional scaffold protein that mediates both desensitization of the OXTR, leading to decreases in uterine contractility, and MAPK growth signaling following stimulation by oxytocin. The development of unique OXTR ligands that prevent receptor desensitization may be a novel approach in the treatment of adverse clinical events secondary to prolonged oxytocin therapy.

scholarly journals Interaction between bradykinin and natriuretic peptides via RGS protein activation in HEK-293 cells

2012 ◽  
Vol 303 (12) ◽  
pp. C1260-C1268 ◽  
Author(s):  
Marina Dobrivojević ◽  
Aleksandra Sinđić ◽  
Bayram Edemir ◽  
Stefanie Kalweit ◽  
Wolf-Georg Forssmann ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Specific Inhibitor ◽  
Rgs Proteins ◽  
Patch Clamp Technique ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Intracellular Ca

In this study, the interaction of natriuretic peptides (NP) and bradykinin (BK) signaling pathways was identified by measuring membrane potential ( Vm) and intracellular Ca2+ using the patch-clamp technique and flow cytometry in HEK-293 cells. BK and NP receptor mRNA was identified using RT-PCR. BK (100 nM) depolarized cells activating bradykinin receptor type 2 (B2R) and Ca2+-dependent Cl− channels inhibitable by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 10 μM). The BK-induced Ca2+ signal was blocked by the B2R inhibitor HOE 140. [Des-Arg9]-bradykinin, an activator of B1R, had no effect on intracellular Ca2+. NP [atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and urodilatin] depolarized HEK-293 cells inhibiting K+ channels. ANP, urodilatin, BNP [binding to natriuretic peptide receptor (NPR)-A] and 8-bromo-(8-Br)-cGMP inhibited the BK-induced depolarization while CNP (binding to NPR-Bi) failed to do so. The inhibitory effect on BK-triggered depolarization could be reversed by blocking PKG using the specific inhibitor KT 5823. BK-stimulated depolarization as well as Ca2+ signaling was completely blocked by the phospholipase C (PLC) inhibitor U-73122 (10 nM). The inositol 1,4,5-trisphosphate receptor blocker 2-aminoethoxydiphenyl borate (2-APB; 50 μM) completely inhibited the BK-induced Ca2+ signaling. UTP, another activator of the PLC-mediated Ca2+ signaling pathway, was blocked by U-73122 as well but not by 8-Br-cGMP, indicating an intermediate regulatory step for NP via PKG in BK signaling such as regulators of G-protein signaling (RGS) proteins. When RGS proteins were inhibited by CCG-63802 in the presence of BK and 8-Br-cGMP, cells started to depolarize again. In conclusion, as natural antagonists of the B2R signaling pathway, NP may also positively interact in pathological conditions caused by BK.

scholarly journals Protective effects of lipid extract from brains of silver carp against oxidative damage in HEK-293 cells

RSC Advances ◽  
2017 ◽  
Vol 7 (49) ◽  
pp. 30855-30861
Author(s):  
Caixia Wang ◽  
Wenshui Xia ◽  
Qixing Jiang ◽  
Yanshun Xu ◽  
Peipei Yu
Keyword(s):  
Oxidative Damage ◽  
Silver Carp ◽  
Oxidative Injury ◽  
Lipid Extract ◽  
Protective Effects ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells

Lipids extracted form silver carp brain effectively resisted H2O2-induced oxidative injury in HEK-293 cells.

Over-expressed human BON cell P2Y11Rs in HEK-293 cells are coupled predominantly to a cAMP-dependent signaling pathway

2003 ◽  
Vol 124 (4) ◽  
pp. A341
Author(s):  
Jianjing Xue ◽  
Jacqueline E. Wunderlich ◽  
Fievos L. Christofi ◽  
Yu-Zhong Wang ◽  
Yongcheol Jeon ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Dependent Signaling Pathway

MAPK: A Key Player in the Development and Progression of Stroke

2020 ◽  
Vol 19 (4) ◽  
pp. 248-256
Author(s):  
Yangmin Zheng ◽  
Ziping Han ◽  
Haiping Zhao ◽  
Yumin Luo
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Complex Disease ◽  
Therapeutic Targets ◽  
Cell Types ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Effective Prevention ◽  
Prevention And Treatment ◽  
Different Cell Types

Conclusion: Stroke is a complex disease caused by genetic and environmental factors, and its etiological mechanism has not been fully clarified yet, which brings great challenges to its effective prevention and treatment. MAPK signaling pathway regulates gene expression of eukaryotic cells and basic cellular processes such as cell proliferation, differentiation, migration, metabolism and apoptosis, which are considered as therapeutic targets for many diseases. Up to now, mounting evidence has shown that MAPK signaling pathway is involved in the pathogenesis and development of ischemic stroke. However, the upstream kinase and downstream kinase of MAPK signaling pathway are complex and the influencing factors are numerous, the exact role of MAPK signaling pathway in the pathogenesis of ischemic stroke has not been fully elucidated. MAPK signaling molecules in different cell types in the brain respond variously after stroke injury, therefore, the present review article is committed to summarizing the pathological process of different cell types participating in stroke, discussed the mechanism of MAPK participating in stroke. We further elucidated that MAPK signaling pathway molecules can be used as therapeutic targets for stroke, thus promoting the prevention and treatment of stroke.

scholarly journals STAMBP promotes lung adenocarcinoma metastasis by regulating the EGFR/MAPK signaling pathway

Neoplasia ◽  
2021 ◽  
Vol 23 (6) ◽  
pp. 607-623
Author(s):  
Hui Xu ◽  
Xiaomei Yang ◽  
Xiaofeng Xuan ◽  
Di Wu ◽  
Jieru Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway
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