Characterization of neural cell types expressing peroxiredoxins in mouse brain

Jin, Meihua; Lee, Young-Ho; Kim, Jin Man; Sun, Haiyan; Moon, Eun‐Yi; Shong, Minho; Kim, Sun-Uk; Lee, Sang Ho; Lee, Tae‐Hoon; Yu, Dae‐Yeul; Lee, Dong‐Seok

doi:10.1016/j.neulet.2005.02.048

Cited by 102 publications

(116 citation statements)

References 24 publications

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“…Addition of this protein to human myeloid cells results in the activation of NF-B and a subsequent increase in the expression of its known target genes, Icam-1 and iNOS (36). Expression of Prdx4 has been previously reported to be localized to OLs in the brain (46). Blocking secreted Prdx4 with a neutralizing antibody suppressed the protective effects of HUCB cells on OLs exposed to OGD.…”

Section: Discussionmentioning

confidence: 94%

Human Umbilical Cord Blood Cells Protect Oligodendrocytes from Brain Ischemia through Akt Signal Transduction

Rowe

Leonardo

Recio

et al. 2012

Journal of Biological Chemistry

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Background: Human umbilical cord blood cells are an effective experimental treatment for stroke. Results: These cells activate Akt to increase peroxiredoxin 4 and are essential for oligodendrocyte survival during ischemia. Conclusion: Akt and peroxiredoxin 4 are key molecules in transducing the cellular protection elicited by cord blood cells. Significance: Identifying this signaling pathway provides new pharmaceutical targets for stroke treatment.

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Section: Discussionmentioning

confidence: 94%

Human Umbilical Cord Blood Cells Protect Oligodendrocytes from Brain Ischemia through Akt Signal Transduction

Rowe

Leonardo

Recio

et al. 2012

Journal of Biological Chemistry

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“…9) In our previous study, the mapping of the distributions of all six Prx subtypes in the mouse brain by immunohistochemistry indicated specific roles for these proteins in preferential neural cell types. 10) In particular, Prx I distribution was not consistent in studies from human and murine species. In human brain, Prx I was dominantly expressed in astrocytes, 11) but oligodendrocytes and schwann cells were main reservoir for Prx I in rat central and pheripheral nervous systems, respectively.…”

mentioning

confidence: 94%

“…In human brain, Prx I was dominantly expressed in astrocytes, 11) but oligodendrocytes and schwann cells were main reservoir for Prx I in rat central and pheripheral nervous systems, respectively. 10,12) The differential results between both species indicate that the cells expressing Prx I in the brain was not determined clearly yet or controversial. Recent reports in the human pathogenic brains showed that altered expression patterns of Prxs frequently found in the brains of patients suffering from degenerative diseases, such as sporadic Creutzfeldt Jacob disease, Alzheimer's disease, Down's syndrome, and Pick's disease.…”

mentioning

confidence: 99%

Peroxiredoxin I Is an Indicator of Microglia Activation and Protects against Hydrogen Peroxide-Mediated Microglial Death

Kim

Hwang

Sun

et al. 2008

Biological & Pharmaceutical Bulletin

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Reactive oxygen species (ROS) are constantly generated during aerobic metabolism, as well as in response to oxidative stimuli. Although ROS are indispensable for some normal biological processes, including cell proliferation and differentiation, excess ROS or cumulative oxidative stresses result in several disease pathologies. 1) ROS may be key molecules in neuropathologic conditions, such as ischemia/reperfusion injury 2) and neurodegeneration, 3) including Parkinson's disease (PD) and Alzheimer's disease (AD). 4,5) Recently, the differential expression patterns of antioxidant enzymes that eliminate ROS, such as superoxide dismutases (SODs), catalase, glutathione peroxidases (GPXs), and peroxiredoxins (Prxs), have been detected in the brains of patients with diseases in which ROS and antioxidants appear to be associated with neurodegeneration. [6][7][8] The Prx family of antioxidant proteins, which has recently been characterized, is induced by several oxidative stress conditions and associated primarily with the removal of H 2 O 2 for the protection of cells from oxidative damages.9) In our previous study, the mapping of the distributions of all six Prx subtypes in the mouse brain by immunohistochemistry indicated specific roles for these proteins in preferential neural cell types.10) In particular, Prx I distribution was not consistent in studies from human and murine species. In human brain, Prx I was dominantly expressed in astrocytes, 11) but oligodendrocytes and schwann cells were main reservoir for Prx I in rat central and pheripheral nervous systems, respectively. 10,12) The differential results between both species indicate that the cells expressing Prx I in the brain was not determined clearly yet or controversial. Recent reports in the human pathogenic brains showed that altered expression patterns of Prxs frequently found in the brains of patients suffering from degenerative diseases, such as sporadic Creutzfeldt Jacob disease, Alzheimer's disease, Down's syndrome, and Pick's disease. 7,8) These findings suggest the involvement of Prxs in maintaining the physiological integrity of the brain against oxidative damages. Therefore, it is important to determine the intercellular distribution and roles of Prx I for the instructive clues in oxidative stress-related brain pathogenesis.Bacterial lipopolysaccharide (LPS) is present on the outer membranes of all Gram-negative bacteria. LPS activates macrophages and microglia, leading to the generation of inflammatory mediators, and it causes cell damage and death. LPS is cytotoxic for a variety of cell types via the induction of apoptosis, 13,14) which is closely related to increased levels of ROS.15,16) Although microglial death is thought to be an important parameter in neuroinflammatory processes, the effects of LPS on ROS-mediated microglial death and related signaling pathways or mechanisms are largely unknown. It has been shown that microglial death pathways are regulated by the representative ROS-dependent mitogen-activated protein kinases (MAPKs), p38 ...

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“…FA also imparts regulatory action on the PI3K/Akt and MAPK/ ERK signaling pathways [93,190]. The apoptotic activity of FA was completely inhibited in the presence of a PI3K inhibitor indicating that the anti-apoptotic effects of FA depend on the PI3K/Akt pathway.…”

Section: Regulatory Action Of Ferulic Acid In Pi3k/akt Signalingmentioning

confidence: 99%

The Gut Microflora and its Metabolites Regulate the Molecular Crosstalk between Diabetes and Neurodegeneration

Lomis¹

2015

J Diabetes Metab

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The gut microflora is a community of trillions of bacterial cells synergistically inhabiting the human gastrointestinal tract. These microbes contact everything that is consumed and release regulatory factors that affect host energy homeostasis, lipid and carbohydrate metabolism, activation of immune cells, oxidative state, epithelial cell wall integrity and even neurological signals. The gut microflora is essentially an independent organ supporting human health where imbalances in the gut community populations (dysbiosis) manifest in disease. Diabetes and neurodegenerative disorders such as Alzheimer's and Parkinson's disease share a similar molecular pathology rooted in gut microflora activity. Both of these conditions are associated with a dysbiosis characterized by low species diversity, a higher proportion of pathobionts at the expense of symbionts, an abundance of proinflammatory microbes and fewer butyrate-producing strains. Many of these factors can be ameliorated with Lactobacillus spp. and Bifidobacterium spp. probiotic treatment aimed to reestablish healthy gut microflora diversity. Indeed, certain commensal and pathogenic strains promote chronic low-grade inflammation that stresses cellular infrastructure eventually leading to apoptosis in both the pancreas and the brain. Also, lack of some beneficial fermentation products such as butyrate and ferulic acid initiates a cascade of events disrupting metabolic homeostasis. Finally, signaling initiated by the microflora and its metabolites has been shown to disrupt the delicate intracellular balance of PI3K/Akt/mTOR signaling, which fundamentally regulates events leading up to diabetes and neurodegenerative disease pathogenesis. The following review investigates the relationship between the manifestation and molecular signaling of diabetes and neurodegenerative disorders and how the balance of gut microflora populations is critical to both prevent and possibly treat these diseases.

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Characterization of neural cell types expressing peroxiredoxins in mouse brain

Cited by 102 publications

References 24 publications

Human Umbilical Cord Blood Cells Protect Oligodendrocytes from Brain Ischemia through Akt Signal Transduction

Human Umbilical Cord Blood Cells Protect Oligodendrocytes from Brain Ischemia through Akt Signal Transduction

Peroxiredoxin I Is an Indicator of Microglia Activation and Protects against Hydrogen Peroxide-Mediated Microglial Death

The Gut Microflora and its Metabolites Regulate the Molecular Crosstalk between Diabetes and Neurodegeneration

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