Activation of Nuclear Factor Erythroid 2–Related Factor 2 Coordinates Dimethylarginine Dimethylaminohydrolase/PPAR-γ/Endothelial Nitric Oxide Synthase Pathways That Enhance Nitric Oxide Generation in Human Glomerular Endothelial Cells

Luo, Zhiwei; Aslam, Shakil; Welch, William J.; Wilcox, Christopher S.

doi:10.1161/hypertensionaha.114.04760

Cited by 41 publications

(35 citation statements)

References 33 publications

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“…There were significant correlations between Nrf2 and PPAR-γ, as well as the individual NOS isoforms, despite the unchanged gene transcriptions, which suggests the regulatory role of Nrf2 in NOS expressions in the heart and aorta; this mechanism remained unaltered by Epi. The coordinating role of Nrf2 in PPAR-γ expressions and endothelial NO generation was previously found by Luo et al [66]. Regarding Epi effects, relatively few in vivo and in vitro studies have investigated the genomic and proteomic effects of purified Epi, especially the expressions of the genes that were investigated in this study.…”

Section: Discussionsupporting

confidence: 59%

(–)-Epicatechin Reduces the Blood Pressure of Young Borderline Hypertensive Rats During the Post-Treatment Period

et al. 2020

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This study investigated the effects of (–)-epicatechin (Epi) in young male borderline hypertensive rats (BHR) during two weeks of treatment (Epi group, 100 mg/kg/day p.o.) and two weeks post treatment (PE group). Epi reduced blood pressure (BP), which persisted for two weeks post treatment. This was associated with delayed reduction of anxiety-like behaviour. Epi significantly increased nitric oxide synthase (NOS) activities in the aorta and left heart ventricle (LHV) vs. the age-matched controls without affecting the brainstem and frontal neocortex. Furthermore, Epi significantly reduced the superoxide production in the aorta and relative content of iron-containing compounds in blood. Two weeks post treatment, the NOS activities and superoxide productions in the heart and aorta did not differ from the age-matched controls. The gene expressions of the NOSs (nNOS, iNOS, eNOS), nuclear factor erythroid 2-related factor 2 (Nrf2), and peroxisome proliferator-activated receptor-γ (PPAR-γ) remained unaltered in the aorta and LHV of the Epi and PE groups. In conclusion, while Epi-induced a decrease of the rats’ BP persisted for two weeks post treatment, continuous Epi treatments seem to be necessary for maintaining elevated NO production as well as redox balance in the heart and aorta without changes in the NOSs, Nrf2, and PPAR-γ gene expressions.

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Section: Discussionsupporting

confidence: 59%

(–)-Epicatechin Reduces the Blood Pressure of Young Borderline Hypertensive Rats During the Post-Treatment Period

et al. 2020

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“…PPARc agonists up-regulate Nrf2, and knockdown of PPAR-c reduced the mRNA expression for Nrf2 [46]. This indicates a tight, positive, twoway reinforcing transcriptional interaction between PPAR-c and Nrf2 that may improve endothelial function [46]. The interaction of PPARc with Nrf2 following ICH was illustrated in Figure 3.…”

Section: Peroxisome Proliferator-activated Receptor-c (Ppar-c)mentioning

confidence: 96%

“…Expression of Nrf2 was reduced by knockdown of PPAR-c, whereas PPAR-c was reduced by knockdown of Nrf2, thereby demonstrating two-way positive interactions. PPARc agonists up-regulate Nrf2, and knockdown of PPAR-c reduced the mRNA expression for Nrf2 [46]. This indicates a tight, positive, twoway reinforcing transcriptional interaction between PPAR-c and Nrf2 that may improve endothelial function [46].…”

Section: Peroxisome Proliferator-activated Receptor-c (Ppar-c)mentioning

confidence: 97%

Haematoma scavenging in intracerebral haemorrhage: from mechanisms to the clinic

Wang

Sun

et al. 2017

J Cellular Molecular Medi

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The products of erythrocyte lyses, haemoglobin (Hb) and haem, are recognized as neurotoxins and the main contributors to delayed cerebral oedema and tissue damage after intracerebral haemorrhage (ICH). Finding a means to efficiently promote absorption of the haemolytic products (Hb and haem) around the bleeding area in the brain through stimulating the function of the body's own garbage cleaning system is a novel clinical challenge and critical for functional recovery after ICH. In this review, available information of the brain injury mechanisms underlying ICH and endogenous haematoma scavenging system is provided. Meanwhile, potential intervention strategies are discussed. Intracerebral blood itself has ‘toxic’ effects beyond its volume effect after ICH. Haptoglobin–Hb–CD163 as well as haemopexin–haem–LRP1 is believed to be the most important endogenous scavenging pathway which participates in blood components resolution following ICH. PPARγ–Nrf2 activates the aforementioned clearance pathway and then accelerates haematoma clearance. Meanwhile, the scavenger receptors as novel targets for therapeutic interventions to treat ICH are also highlighted.

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“…The cysteine disulfide bridges in oxidized proteins were reduced by Trx system 32 . It was found that PPARγ could up-regulate Nrf2 33 34 . Our previous study had found that Tau protected against As 2 O 3 -induced autophagy in pancreas of rat offsprings through Nrf2/Trx pathway 35 .…”

mentioning

confidence: 99%

Taurine protects against As2O3-induced autophagy in livers of rat offsprings through PPARγ pathway

Bai

Yao

Jiang

et al. 2016

Sci Rep

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Chronic exposures to arsenic had been associated with metabolism diseases. Peroxisome proliferator-activated receptor gamma (PPARγ) was found in the liver, regulated metabolism. Here, we found that the expression of PPARγ was decreased, the generation of reactive oxygen species (ROS) and autophagy were increased after treatment with As2O3 in offsprings’ livers. Taurine (Tau), a sulfur-containing β–amino acid could reverse As2O3-inhibited PPARγ. Tau also inhibit the generation of ROS and autophagy. We also found that As2O3 caused autophagic cell death and ROS accelerated in HepG2 cells. Before incubation with As2O3, the cells were pretreated with PPARγ activator Rosiglitazone (RGS), we found that autophagy and ROS was inhibited in HepG2 cells, suggesting that inhibition of PPARγ contributed to As2O3-induced autophagy and the generation of ROS. After pretreatment with Tau, the level of PPARγ was improved and the autophagy and ROS was inhibited in As2O3-treated cells, suggesting that Tau could protect hepatocytes against As2O3 through modulating PPARγ pathway.

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Activation of Nuclear Factor Erythroid 2–Related Factor 2 Coordinates Dimethylarginine Dimethylaminohydrolase/PPAR-γ/Endothelial Nitric Oxide Synthase Pathways That Enhance Nitric Oxide Generation in Human Glomerular Endothelial Cells

Cited by 41 publications

References 33 publications

(–)-Epicatechin Reduces the Blood Pressure of Young Borderline Hypertensive Rats During the Post-Treatment Period

(–)-Epicatechin Reduces the Blood Pressure of Young Borderline Hypertensive Rats During the Post-Treatment Period

Haematoma scavenging in intracerebral haemorrhage: from mechanisms to the clinic

Taurine protects against As2O3-induced autophagy in livers of rat offsprings through PPARγ pathway

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