Link between PI3K/AKT/PTEN Pathway and NOX Proteinin Diseases

Nakanishi, Atsuko; Wada, Yoko; Kitagishi, Yasuko; Matsuda, Satoru

doi:10.14336/ad.2014.0500203

Cited by 73 publications

(69 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inactivation of GSK-3β with phosphorylation at Ser9 is implicated in TGFβl-induced cell senescence, which might be association of disruption of complex IV activity [43]. GSK-3β inactivation by LiCl can be a result of activation of PI3K-Akt signaling, which is recently reported to be linked to activation of enzymes in NADPH oxidase family, leading to enhancement of ROS production [44]. GSK-3β has been known to inhibit the activity of glycogen synthase.…”

Section: Gsk-3β Regulates Mitochondrial Bioenergeticsmentioning

confidence: 99%

The Key Roles of GSK-3β in Regulating Mitochondrial Activity

Yang

Chen

Gao

et al. 2017

Cell Physiol Biochem

184

119

View full text Add to dashboard Cite

Glycogen synthase kinase-3β (GSK-3β), a serine/threonine protein kinase, has been reported to show essential roles in molecular pathophysiology of many diseases. Mitochondrion is a dynamic organelle for producing cellular energy and determining cell fates. Stress-induced translocated GSK-3β may interact with mitochondrial proteins, including PI3K-Akt, PGC-1α, HK II, PKCε, components of respiratory chain, and subunits of mPTP. Mitochondrial pool of GSK-3β has been implicated in mediation of mitochondrial functions. GSK-3β exhibits the regulatory effects on mitochondrial biogenesis, mitochondrial bioenergetics, mitochondrial permeability, mitochondrial motility, and mitochondrial apoptosis. The versatile functions of GSK-3β might be associated with its wide range of substrates. Accumulative evidence demonstrates that GSK-3β inactivation may be potentially developed as the promising strategy in management of many diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Intensive efforts have been made for exploring GSK-3β inhibitors. Natural products provide us a great source for screening new lead compounds in inactivation of GSK-3β. The key roles of GSK-3β in mediation of mitochondrial functions are discussed in this review.

show abstract

Section: Gsk-3β Regulates Mitochondrial Bioenergeticsmentioning

confidence: 99%

The Key Roles of GSK-3β in Regulating Mitochondrial Activity

Yang

Chen

Gao

et al. 2017

Cell Physiol Biochem

184

119

View full text Add to dashboard Cite

show abstract

“…AKT signaling PI3K/AKT signaling plays an important role in cell growth and cellular oxidative stress [20]. Therefore, in this study we investigated the role of PI3K/AKT signaling in PRDX6 protection against oxidative damage.…”

Section: Prdx6 Protection Against H2o2-induced Cellular Injury Partiamentioning

confidence: 99%

PRDX6 Protects ARPE-19 Cells from Oxidative Damage via PI3K/AKT Signaling

Zhao

et al. 2015

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Oxidative stress that damages cells of the retinal pigment epithelium (RPE) can cause the development of hereditary retinal disease (HRD). PRDX6, which is a member of the PRDX family, is essential for removing metabolic free radicals from the body. However, the effect of PRDX6 on oxidative stress in HRD remains unknown. In this study, we sought to investigate the role of PRDX6 in oxidative stress-induced HRD in ARPE-19 cells and the molecular mechanism involved. Methods: ARPE-19 cells were used in the current study. Intracellular ROS levels were determined by flow cytometry. Lipid peroxidation was measured using a commercial MDA assay kit. Cellular variability was determined by MTT assay. Apoptosis was determined using an Annexin V-FITC Apoptosis Detection Kit. mRNA and protein expression levels were detected by real-time PCR and western blot analysis, respectively. Results: We found that H₂O₂ and blue light could induce significant oxidative stress damage and cell death in ARPE-19 cells. Furthermore, we found that PRDX6 levels significantly decreased after H₂O₂ treatment. PRDX6 overexpression protected ARPE-19 cells from H₂O₂- and blue light-induced oxidative damage, while PRDX6 knockdown enhanced oxidative damage in these cells. Mechanistically, we found that PRDX6 prevented oxidative damage and promoted ARPE-19 cell survival through the PI3K/AKT signaling pathway. Conclusions: Collectively, these results suggest that PRDX6 protects ARPE-19 cells from H₂O₂-induced oxidative stress and apoptosis and that this protection is mediated at least partially through the PI3K/AKT pathway.

show abstract

“…The PI3K/Akt pathway is a cascade of events, whose dysregulation in OS plays a critical role in a large number of pathological processes, such as tumorigenesis [7], cell proliferation [8], cell cycle progression [9], inhibition of apoptosis [10], cell invasion [11], metastasis [12], angiogenesis [13] and chemoresistance [14]. After activation, the PI3K/Akt pathway can modulate many downstream targets to regulate various cellular functions.…”

Section: Introductionmentioning

confidence: 99%

PI3K/Akt signaling mediated Hexokinase-2 expression inhibits cell apoptosis and promotes tumor growth in pediatric osteosarcoma

Zhuo

et al. 2015

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

Link between PI3K/AKT/PTEN Pathway and NOX Proteinin Diseases

Cited by 73 publications

References 55 publications

The Key Roles of GSK-3β in Regulating Mitochondrial Activity

The Key Roles of GSK-3β in Regulating Mitochondrial Activity

PRDX6 Protects ARPE-19 Cells from Oxidative Damage via PI3K/AKT Signaling

PI3K/Akt signaling mediated Hexokinase-2 expression inhibits cell apoptosis and promotes tumor growth in pediatric osteosarcoma

Contact Info

Product

Resources

About