Nitric Oxide as a Pro-apoptotic as well as Anti-apoptotic Modulator

Choi, Byung Min; Pae, Hyun Ock; Jang, Seon Il; Kim, Young Myeong; Chung, Hun Taeg

doi:10.5483/bmbrep.2002.35.1.116

Cited by 205 publications

(159 citation statements)

References 100 publications

(113 reference statements)

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“…35 In contrast, in the same knockout strain the absence of clusterin reduces cell death in neonatal hypoxia-ischaemia via a caspase-3-independent brain injury pathway, 36 suggesting it functions to exacerbate neuronal damage under these circumstances. Interestingly, there are a number of other molecules such as nitric oxide (for review see Choi et al 37 ) and HIF1a (for review see Piret et al 38 ) that serve to promote or inhibit cell death depending on the cellular context and clusterin may fit into this same category.…”

Section: Discussionmentioning

confidence: 99%

Clusterin secreted by astrocytes enhances neuronal differentiation from human neural precursor cells

Cordero-Llana

Scott²,

Maslen

et al. 2011

Cell Death Differ

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Neuronal differentiation from expanded human ventral mesencephalic neural precursor cells (NPCs) is very limited. Astrocytes are known to secrete neurotrophic factors, and so in order to enhance neuronal survival from NPCs, we tested the effect of regional astrocyte-conditioned medium (ACM) from the rat cortex, hippocampus and midbrain on this process. Human NPC's were expanded in FGF-2 before differentiation for 1 or 4 weeks in ACM. The results show that ACM from the hippocampus and midbrain increase the number of neurons from expanded human NPCs, an effect that was not observed with cortical ACM. In addition, both hippocampal and midbrain ACM increased the number and length of phosphorylated neurofilaments. MALDI-TOF analysis used to determine differences in media revealed that although all three regional ACMs had cystatin C, a-2 macroglobulin, extracellular matrix glycoprotein and vimentin, only hippocampal and midbrain ACM also contained clusterin, which when immunodepleted from midbrain ACM eliminated the observed effects on neuronal differentiation. Furthermore, clusterin is a highly glycosylated protein that has no effect on cell proliferation but decreases apoptotic nuclei and causes a sustained increase in phosphorylated extracellular signalregulated kinase, implicating its role in cell survival and differentiation. These findings further reveal differential effects of regional astrocytes on NPC behavior and identify clusterin as an important mediator of NPC-derived neuronal survival and differentiation. Cell Death and Differentiation (2011) 18, 907-913; doi:10.1038/cdd.2010.169; published online 7 January 2011Astrocytes are essential regulators of neuronal function, and produce diffusible and non-diffusible neuron supporting signals, including neurotrophic factors and membrane-bound molecules (for review see Barres 1 ). Interestingly, emerging evidence highlights that there are many regional differences in astrocytes in respect to structure and function and soluble factor production, for example, astrocytes from the hippocampus and their conditioned media can support the survival of neurons from regions other than the hippocampus. 2 In contrast, astrocytes from the mesencephalon release factors, which are more effective at promoting dopamine neuron survival than cortical or striatal astrocytes. 3 These studies show that the astrocytes from neurogenic regions 4 release more neurogenic factors than astrocytes from the non-neurogenic regions.It is well established that stem cells can be isolated from the developing and adult rodent CNS, and expanded in vitro using EGF and FGF2 (for review see Gage 5 ) More recently the same has been shown to be true for the developing human fetal CNS. 6 These cells are capable of long-term expansion in vitro to achieve B50 population doublings. 6 However, as they progress in culture with time, their differentiation pattern changes with the number of neurons declining and the number of astrocytes predominating. 7 Previous studies have shown that astrocyte-conditioned medi...

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Section: Discussionmentioning

confidence: 99%

Clusterin secreted by astrocytes enhances neuronal differentiation from human neural precursor cells

Cordero-Llana

Scott²,

Maslen

et al. 2011

Cell Death Differ

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“…5,7 The long-lasting overproduction of NO acts as a modulator of apoptosis, activating the caspase family through the release of cytochrome c into the cytosol. 20,21 Once in the cytosol, cytochrome c interacts with Apaf-1 (apoptotic protease-activating factor 1), leading to the activation of caspase-9 and subsequent caspases, thereby leading to apoptosis. The activated caspases lead to cleavage of the nuclear lamin and breakdown of the nucleus through caspase-3.…”

Section: Results and Analysismentioning

confidence: 99%

Meconium-induced release of nitric oxide in rabbit alveolar cells

2008

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Previous studies have shown meconium-induced lung injury occurs throughout release of inflammatory cytokines. The exact mechanism of cytokine-induced apoptosis is not known. In this study we hypothesized that meconium-induced apoptosis in the lungs is mediated through the production of inducible nitric oxide (NO). We studied two groups of newborn rabbit pups: one group was instilled with meconium and other with normal saline. We measured precursors of NO in lung lavage from both groups of rabbits and NO levels were calculated accordingly. The levels of NO and NO-derivatives increased significantly in both groups. However NO expression in meconium group 2 h after meconium instillation was significantly higher than in saline-instilled group suggesting NO production plays a role in meconium-induced inflammation.

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“…However, although the antiapoptotic role of these proteins has been thoroughly documented, little is known about the precise mechanism through which Bcl-2 and the other members of this family can act in this process 4 .…”

Section: Inhibitors Of Caspase Activation In Apoptosismentioning

confidence: 99%

“…Some authors show an anti-apoptotic action of melatonin in different organs, such as thymus, kidney, brain and liver, attributing this mainly to its antioxidating properties [7][8][9][10][11][12]33,34 when eliminating radicals hydroxyl (OH -), peroxyl (ROO -) 26, superoxides 4 and cardiolipin oxidation from mitochondrias 35 . In the lacrimal glands of hamsters, this hormone prevents cell damage caused by the buildup of porphyrins, due to its capacity of decreasing the RNAm synthesis of aminolevulinate synthetase, enzyme involved in the production of porphyrins, and also due to increasing the levels of RNAm of antioxidating enzymes such as manganese superoxide dismutase (Mn-SOD) and copper-zinc superoxide dismutase (Cu-Zn-SOD) 36 .…”

Section: Melatonin Action In Apoptosismentioning

confidence: 99%

“…On the other hand, this process could be inhibited by the activation of anti-apoptotic molecules (Bcl-2, FLIP) that block the appearance and evolution of these cell alterations. Thus, homeostasis (essential structural and functional balance for the survival of a cell population) depends on the balance between the activation of pro-and anti-apoptotic molecules 4,5 .…”

Section: Introductionmentioning

confidence: 99%

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Melatonina: modulador de morte celular

Ferreira

Maganhin

Simões

et al. 2010

Rev. Assoc. Med. Bras.

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Apoptosis or planned cell death is a biological phenomenon that is essential for the development and maintenance of a cell population. In this process, senescent or damaged cells are eliminated after activation of a cell death program involving participation of pro-apoptotic molecules (Fas, Bax, caspases 2,3,6,7, 8 and 9). Molecule activation causes typical morphological changes, such as cell shrinkage, loss of adhesion to the extracellular matrix and neighboring cells, chromatin condensation, DNA fragmentation and formation of apoptotic bodies. Anti-apoptotic molecules (Bcl-2, FLIP) block the emergence and evolution of these cell changes and prevent cell death. The balance between pro-and anti-apoptotic molecules ensures tissue homeostasis. When apoptosis is out of control, it contributes to the emergence of several neoplastic, autoimmune and neurodegenerative diseases. Several inducing and inhibiting agents of apoptosis are recognized as potential weapons in the fight against disorders related to cell proliferation and death among, among which stand hormones out. Melatonin has been reported as an important anti-apoptotic agent in various tissues by reducing cell calcium uptake, mitigating the production of oxygen reactive species and decreasing pro-apoptotic proteins, such as Bax. The knowledge of new agents capable of acting on the course of apoptosis is important and valuable for developing further therapies against various diseases. Thus, the objective of this review was to clarify the main aspects of cell death by apoptosis and the role of melatonin in this process

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Nitric Oxide as a Pro-apoptotic as well as Anti-apoptotic Modulator

Cited by 205 publications

References 100 publications

Clusterin secreted by astrocytes enhances neuronal differentiation from human neural precursor cells

Clusterin secreted by astrocytes enhances neuronal differentiation from human neural precursor cells

Meconium-induced release of nitric oxide in rabbit alveolar cells

Melatonina: modulador de morte celular

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