scholarly journals Cerium-Promoted Ginsenosides Accumulation by Regulating Endogenous Methyl Jasmonate Biosynthesis in Hairy Roots of Panax ginseng

Molecules ◽  
2021 ◽  
Vol 26 (18) ◽  
pp. 5623
Author(s):  
Ru Zhang ◽  
Shiquan Tan ◽  
Bianling Zhang ◽  
Pengcheng Hu ◽  
Ling Li
Keyword(s):  
Methyl Jasmonate ◽  
Hairy Roots ◽  
Signal Pathways ◽  
Ros Production ◽  
Oxygen Species ◽  
Direct Stimulation ◽  
Key Enzyme ◽  
Mda Content ◽  
Ginsenoside Content ◽  
Stimulation Of

Among rare earth elements, cerium has the unique ability of regulating the growth of plant cells and the biosynthesis of metabolites at different stages of plant development. The signal pathways of Ce3+-mediated ginsenosides biosynthesis in ginseng hairy roots were investigated. At a low concentration, Ce3+ improved the elongation and biomass of hairy roots. The Ce3+-induced accumulation of ginsenosides showed a high correlation with the reactive oxygen species (ROS), as well as the biosynthesis of endogenous methyl jasmonate (MeJA) and ginsenoside key enzyme genes (PgSS, PgSE and PgDDS). At a Ce3+ concentration of 20 mg L−1, the total ginsenoside content was 1.7-fold, and the total ginsenosides yield was 2.7-fold that of the control. Malondialdehyde (MDA) content and the ROS production rate were significantly higher than those of the control. The activity of superoxide dismutase (SOD) was significantly activated within the Ce3+ concentration range of 10 to 30 mg L−1. The activity of catalase (CAT) and peroxidase (POD) strengthened with the increasing concentration of Ce3+ in the range of 20–40 mg L−1. The Ce3+ exposure induced transient production of superoxide anion (O2•−) and hydrogen peroxide (H2O2). Together with the increase in the intracellular MeJA level and enzyme activity for lipoxygenase (LOX), there was an increase in the gene expression level of MeJA biosynthesis including PgLOX, PgAOS and PgJMT. Our results also revealed that Ce3+ did not directly influence PgSS, PgSE and PgDDS activity. We speculated that Ce3+-induced ROS production could enhance the accumulation of ginsenosides in ginseng hairy roots via the direct stimulation of enzyme genes for MeJA biosynthesis. This study demonstrates a potential approach for understanding and improving ginsenoside biosynthesis that is regulated by Ce3+-mediated signal transduction.

Stimulation of Rg3 ginsenoside biosynthesis in ginseng hairy roots elicited by methyl jasmonate

2012 ◽  
Vol 112 (1) ◽  
pp. 87-93 ◽  
Author(s):  
Ok Tae Kim ◽  
Nam Hee Yoo ◽  
Gum Soog Kim ◽  
Young Chang Kim ◽  
Kyong Hwan Bang ◽  
...  
Keyword(s):  
Methyl Jasmonate ◽  
Hairy Roots ◽  
Ginsenoside Biosynthesis ◽  
Stimulation Of

Stimulation of Na,K-ATPase by low potassium requires reactive oxygen species

2003 ◽  
Vol 285 (2) ◽  
pp. C319-C326 ◽  
Author(s):  
Xiaoming Zhou ◽  
Wu Yin ◽  
Sonia Q. Doi ◽  
Shawn W. Robinson ◽  
Kunio Takeyasu ◽  
...  
Keyword(s):  
Binding Sites ◽  
Regulatory Element ◽  
Protein Abundance ◽  
Oxygen Species ◽  
Ouabain Binding ◽  
Direct Stimulation ◽  
Negative Regulatory Element ◽  
Low K ◽  
Cat Expression ◽  
Stimulation Of

The signaling pathway that transduces the stimulatory effect of low K+ on the biosynthesis of Na,K-ATPase remains largely unknown. The present study was undertaken to examine whether reactive oxygen species (ROS) mediated the effect of low K+ in Madin-Darby canine kidney (MDCK) cells. Low K+ increased ROS activity in a time- and dose-dependent manner, and this effect was abrogated by catalase and N-acetylcysteine (NAC). To determine the role of ROS in low-K+-induced gene expression, the cells were first stably transfected with expression constructs in which the reporter gene chloramphenicol acetyl transferase (CAT) was under the control of the avian Na,K-ATPase α-subunit 1.9 kb and 900-bp 5′-flanking regions that have a negative regulatory element. Low K+ increased the CAT expression in both constructs. Catalase or NAC inhibited the effect of low K+. To determine whether the increased CAT activity was mediated through releasing the repressive effect or a direct stimulation of the promoter, the cells were transfected with a CAT expression construct directed by a 96-bp promoter fragment that has no negative regulatory element. Low K+ also augmented the CAT activity expressed by this construct. More importantly, both catalase and NAC abolished the effect of low K+. Moreover, catalase and NAC also inhibited low-K+-induced increases in the Na,K-ATPase α1- and β1-subunit protein abundance and ouabain binding sites. The antioxidants had no significant effect on the basal levels of CAT activity, protein abundance, or ouabain binding sites. In conclusion, low K+ enhances the Na,K-ATPase gene expression by a direct stimulation of the promoter activity, and ROS mediate this stimulation and also low-K+-induced increases in the Na,K-ATPase protein contents and cell surface molecules.

scholarly journals Reactive oxygen species production via NADPH oxidase mediates TGF-β-induced cytoskeletal alterations in endothelial cells

2005 ◽  
Vol 289 (4) ◽  
pp. F816-F825 ◽  
Author(s):  
Taishan Hu ◽  
Satish P. RamachandraRao ◽  
Senthuran Siva ◽  
Cathryn Valancius ◽  
Yanqing Zhu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Kinase Inhibitor ◽  
Reactive Oxygen ◽  
Dominant Negative ◽  
Type I ◽  
Ros Production ◽  
Oxygen Species ◽  
Stimulation Of

Cytoskeletal alterations in endothelial cells have been linked to nitric oxide generation and cell-cell interactions. Transforming growth factor (TGF)-β has been described to affect cytoskeletal rearrangement in numerous cell types; however, the underlying pathway is unclear. In the present study, we found that human umbilical vein endothelial cells (HUVEC) have marked cytoskeletal alterations with short-term TGF-β treatment resulting in filipodia formation and F-actin assembly. The cytoskeletal alterations were blocked by the novel TGF-β type I receptor/ALK5 kinase inhibitor (SB-505124) but not by the p38 kinase inhibitor (SB-203580). TGF-β also induced marked stimulation of reactive oxygen species (ROS) within 5 min of TGF-β exposure. TGF-β stimulation of ROS was mediated by the NAPDH oxidase homolog Nox4 as DPI, an inhibitor of NADPH oxidase, and dominant-negative Nox4 adenovirus blocked ROS production. Finally, inhibition of ROS with ROS scavengers or dominant-negative Nox4 blocked the TGF-β effect on cytoskeleton changes in endothelial cells. In conclusion, our studies show for the first time that TGF-β-induced ROS production in human endothelial cells is via Nox4 and that TGF-β alteration of cytoskeleton in HUVEC is mediated via a Nox4-dependent pathway.

Roles of reactive oxygen species in methyl jasmonate and nitric oxide-induced tanshinone production in Salvia miltiorrhiza hairy roots

2011 ◽  
Vol 31 (5) ◽  
pp. 873-883 ◽  
Author(s):  
Zong-Suo Liang ◽  
Dong-Feng Yang ◽  
Xiao Liang ◽  
Yue-Jin Zhang ◽  
Yan Liu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Methyl Jasmonate ◽  
Hairy Roots ◽  
Salvia Miltiorrhiza ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Rho-Family Small GTPases: From Highly Polarized Sensory Neurons to Cancer Cells

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 92 ◽  
Author(s):  
Takehiko Ueyama
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Small Gtpases ◽  
In Vivo Studies ◽  
Signal Pathways ◽  
Ros Production ◽  
Oxygen Species ◽  
Rho Family Gtpases ◽  
Rho Family

The small GTPases of the Rho-family (Rho-family GTPases) have various physiological functions, including cytoskeletal regulation, cell polarity establishment, cell proliferation and motility, transcription, reactive oxygen species (ROS) production, and tumorigenesis. A relatively large number of downstream targets of Rho-family GTPases have been reported for in vitro studies. However, only a small number of signal pathways have been established at the in vivo level. Cumulative evidence for the functions of Rho-family GTPases has been reported for in vivo studies using genetically engineered mouse models. It was based on different cell- and tissue-specific conditional genes targeting mice. In this review, we introduce recent advances in in vivo studies, including human patient trials on Rho-family GTPases, focusing on highly polarized sensory organs, such as the cochlea, which is the primary hearing organ, host defenses involving reactive oxygen species (ROS) production, and tumorigenesis (especially associated with RAC, novel RAC1-GSPT1 signaling, RHOA, and RHOBTB2).

Angiotensin II stimulation of VEGF mRNA translation requires production of reactive oxygen species

2006 ◽  
Vol 290 (4) ◽  
pp. F927-F936 ◽  
Author(s):  
Denis Feliers ◽  
Yves Gorin ◽  
Goutam Ghosh-Choudhury ◽  
Hanna E. Abboud ◽  
Balakuntalam S. Kasinath
Keyword(s):  
Reactive Oxygen Species ◽  
Respiratory Chain ◽  
Mrna Translation ◽  
Mitochondrial Respiratory Chain ◽  
Ros Production ◽  
Oxygen Species ◽  
Ang Ii ◽  
Vegf Expression ◽  
Vegf Mrna ◽  
Stimulation Of

ANG II, a mediator of renal injury in diabetic renal disease, promotes vascular endothelial growth factor (VEGF) mRNA translation in proximal tubular epithelial (MCT) cells (Feliers D, Duraisamy S, Barnes JL, Ghosh-Choudhury G, and Kasimath BS. Am J Physiol Renal Physiol 288: F521–F529, 2005). The mechanism by which ANG II elicits this effect is not known. ANG II is known to induce oxidative stress and the rapidity of the effect suggested a role for reactive oxygen species (ROS). The aim of this study is to test the hypothesis that ANG II regulates VEGF mRNA translation in MCT cells through ROS production. In MCT cells exposed to 1 nM ANG II, ROS production was increased in a time-dependent manner. Inhibition of ROS production by N-acetylcysteine (NAC), a precursor of glutathione, and diphenyleneiodonium (DPI), an inhibitor of flavoproteins that include NAD(P)H oxidase, prevented ANG II-stimulated VEGF protein expression. NAC and DPI also inhibited phosphorylation of 4E-BP1 on Thr46 and association of eIF4E with eIF4G, steps that are important in the initiation phase of mRNA translation. NAC and DPI also blocked Akt activation which is required for 4E-BP1 phosphorylation. LY-294002, a selective phosphatidylinositol (PI 3-kinase) inhibitor, did not prevent ROS accumulation in response to ANG II, whereas DPI blocked ANG II activation of PI 3-kinase, demonstrating that ROS production is upstream of the PI 3-kinase signaling pathway. Preincubation with catalase abolished ANG II stimulation of VEGF expression and mRNA translation, suggesting involvement of hydrogen peroxide (H2O2). H2O2 reproduced the effects of ANG II on VEGF expression and aforementioned parameters of mRNA translation. Finally, neither preincubation of MCT cells with specific inhibitors of the mitochondrial respiratory chain nor inactivation of the mitochondrial respiratory chain in MCT cells prevented ANG II stimulation of VEGF expression. Inhibition of nitric oxide synthase by l-NAME had no effect on ANG II stimulation of VEGF expression. These data show that ROS, generated probably through activation of an NAD(P)H oxidase, mediate ANG II stimulation of VEGF mRNA translation.

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