Curcumin protects neurons against oxygen-glucose deprivation/reoxygenation-induced injury through activation of peroxisome proliferator-activated receptor-γ function

2014 ◽  
Vol 92 (11) ◽  
pp. 1549-1559 ◽  
Author(s):  
Zun-Jing Liu ◽  
Hong-Qiang Liu ◽  
Cheng Xiao ◽  
Hui-Zhen Fan ◽  
Qing Huang ◽  
...  
Keyword(s):  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Oxygen-glucose deprivation and reoxygenation on human cerebral organoids alters expression related to lipid metabolism

2020 ◽  
Author(s):  
Naoki Iwasa ◽  
Takeshi K. Matsui ◽  
Naritaka Morikawa ◽  
Yoshihiko M. Sakaguchi ◽  
Tomo Shiota ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Peroxisome Proliferator ◽  
Cerebral Tissue ◽  
Peroxisome Proliferator Activated Receptor ◽  
Induced Pluripotent ◽  
Effect Of Oxygen ◽  
Relationship Of ◽  
The Impact

AbstractIschemic stroke is one of the most common neurological disease. However, the impact of ischemic stroke on human cerebral tissue remains largely unknown; due to a lack of ischemic human brain samples. In this study, we used cerebral organoids derived from human induced pluripotent stem cells to evaluate the effect of oxygen-glucose deprivation/reoxygenation (OGD/R). We identified 15 differentially expressed genes (DEGs); and found that all the DEGs were downregulated. Pathway analysis showed the relationship of vitamin digestion and absorption, fat digestion and absorption, peroxisome proliferator-activated receptor signaling pathway, and complement and coagulation cascades. These findings indicate the mechanisms underlying ischemic injury in human cerebral tissue.

scholarly journals Gene Expression Profiles of Human Cerebral Organoids Identify PPAR Pathway and PKM2 as Key Markers for Oxygen-Glucose Deprivation and Reoxygenation

2021 ◽  
Vol 15 ◽  
Author(s):  
Naoki Iwasa ◽  
Takeshi K. Matsui ◽  
Naohiko Iguchi ◽  
Kaoru Kinugawa ◽  
Naritaka Morikawa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Expression Profiles ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Signaling ◽  
The Impact

Ischemic stroke is one of the most common neurological diseases. However, the impact of ischemic stroke on human cerebral tissue remains largely unknown due to a lack of ischemic human brain samples. In this study, we applied cerebral organoids derived from human induced pluripotent stem cells to evaluate the effect of oxygen-glucose deprivation/reoxygenation (OGD/R). Pathway analysis showed the relationships between vitamin digestion and absorption, fat digestion and absorption, peroxisome proliferator-activated receptor (PPAR) signaling pathway, and complement and coagulation cascades. Combinational verification with transcriptome and gene expression analysis of different cell types revealed fatty acids-related PPAR signaling pathway and pyruvate kinase isoform M2 (PKM2) as key markers of neuronal cells in response to OGD/R. These findings suggest that, although there remain some limitations to be improved, our ischemic stroke model using human cerebral organoids would be a potentially useful tool when combined with other conventional two-dimensional (2D) mono-culture systems.

scholarly journals Glucose deprivation, oxidative stress and peroxisome proliferator-activated receptor-α (PPARA) cause peroxisome proliferation in preimplantation mouse embryos

Reproduction ◽  
2009 ◽  
Vol 138 (3) ◽  
pp. 493-505 ◽  
Author(s):  
Sarah Jansen ◽  
Kara Cashman ◽  
Jeremy G Thompson ◽  
Marie Pantaleon ◽  
Peter L Kaye
Keyword(s):  
Oxidative Stress ◽  
Ex Vivo ◽  
Glucose Deprivation ◽  
Mouse Embryos ◽  
Peroxisome Proliferator ◽  
Ros Production ◽  
Peroxisome Proliferator Activated Receptor ◽  
Preimplantation Mouse ◽  
Proliferation Response

Ex vivotwo-cell mouse embryos deprived of glucosein vitrocan develop to blastocysts by increasing their pyruvate consumption; however, zygotes when glucose-deprived cannot adapt this metabolic profile and degenerate as morulae. Prior to their death, these glucose-deprived morulae exhibit upregulation of the H+-monocarboxylate co-transporter SLC16A7 and catalase, which partly co-localize in peroxisomes. SLC16A7 has been linked to redox shuttling for peroxisomal β-oxidation. Peroxisomal function is unclear during preimplantation development, but as a peroxisomal transporter in embryos, SLC16A7 may be involved and influenced by peroxisome proliferators such as peroxisome proliferator-activated receptor-α (PPARA). PCR confirmedPparamRNA expression in mouse embryos. Zygotes were cultured with or without glucose and with the PPARA-selective agonist WY14643 and the developing embryos assessed for expression of PPARA and phospho-PPARA in relation to the upregulation of SLC16A7 and catalase driven by glucose deprivation, indicative of peroxisomal proliferation. Reactive oxygen species (ROS) production and relationship to PPARA expression were also analysed. In glucose-deprived zygotes, ROS was elevated within 2 h, as were PPARA expression within 8 h and catalase and SLC16A7 after 12–24 h compared with glucose-supplied embryos. Inhibition of ROS production prevented this induction of PPARA and SLC16A7. Selective PPARA agonism with WY14643 also induced SLC16A7 and catalase expression in the presence of glucose. These data suggest that glucose-deprived cleavage stage embryos, although supplied with sufficient monocarboxylate-derived energy, undergo oxidative stress and exhibit elevated ROS, which in turn upregulates PPARA, catalase and SLC16A7 in a classical peroxisomal proliferation response.

scholarly journals Neuronal Pentraxin 1 Promotes Hypoxic-Ischemic Neuronal Injury by Impairing Mitochondrial Biogenesis via Interactions With Active Bax[6A7] and Mitochondrial Hexokinase II

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142110128
Author(s):  
Md Al Rahim ◽  
Shabarish Thatipamula ◽  
Giulio M. Pasinetti ◽  
Mir Ahamed Hossain
Keyword(s):  
Brain Injury ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Biogenesis ◽  
Nuclear Dna ◽  
Glucose Deprivation ◽  
Neuronal Cultures ◽  
Peroxisome Proliferator ◽  
Hexokinase Ii ◽  
Peroxisome Proliferator Activated Receptor ◽  
Neuronal Pentraxin

Mitochondrial dysfunction is a key mechanism of cell death in hypoxic-ischemic brain injury. Neuronal pentraxin 1 (NP1) has been shown to play crucial roles in mitochondria-mediated neuronal death. However, the underlying mechanism(s) of NP1-induced mitochondrial dysfunction in hypoxia-ischemia (HI) remains obscure. Here, we report that NP1 induction following HI and its subsequent localization to mitochondria, leads to disruption of key regulatory proteins for mitochondrial biogenesis. Brain mitochondrial DNA (mtDNA) content and mtDNA-encoded subunit I of complex IV (mtCOX-1) expression was increased post-HI, but not the nuclear DNA-encoded subunit of complex II (nSDH-A). Up-regulation of mitochondrial proteins COXIV and HSP60 further supported enhanced mtDNA function. NP1 interaction with active Bax (Bax6A7) was increased in the brain after HI and in oxygen-glucose deprivation (OGD)-induced neuronal cultures. Importantly, NP1 colocalized with mitochondrial hexokinase II (mtHKII) following OGD leading to HKII dissociation from mitochondria. Knockdown of NP1 or SB216763, a GSK-3 inhibitor, prevented OGD-induced mtHKII dissociation and cellular ATP decrease. NP1 also modulated the expression of mitochondrial transcription factor A ( Tfam) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), regulators of mitochondrial biogenesis, following HI. Together, we reveal crucial roles of NP1 in mitochondrial biogenesis involving interactions with Bax[6A7] and mtHKII in HI brain injury.

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