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a(CHEBI:"calcium cation") decreases bp(MESH:Apoptosis) View Subject | View Object

The cytoplasmic in- crease in calcium triggers the secretion of mitogenic factors and activates the signalling cascades involved in cell prolif- eration, migration and angiogenesis and the inhibition of apoptosis PubMed:28901280

a(MESH:Acetylcholine) association bp(MESH:Apoptosis) View Subject | View Object

but ACh is also released by non-neuronal tissues where it is involved in cell-to-cell communication, and con- trols essential functions such as cell proliferation, adhesion, migration, secretion, survival and apoptosis, in an autocrine, paracrine or juxtacrine manner PubMed:28901280

a(CHEBI:heme) increases bp(MESH:Apoptosis) View Subject | View Object

Moreover, heme induces apoptosis in human brain vascular endothelial cells (HBVEC) by STAT3 (signal transducer and activator of transcription 3)-dependent activation of matrix metallopeptidase 3 (MMP3; Liu et al., 2013). PubMed:24904418

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Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Cerebral Hemorrhage
Text Location
Review

a(MESH:"Reactive Nitrogen Species") positiveCorrelation bp(MESH:Apoptosis) View Subject | View Object

Apoptosis has been found to be a major rout for the elimination of cells after a variety of stresses including ROS and RNS [30]. PubMed:30324533

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Hematoma
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a(MESH:"Reactive Oxygen Species") positiveCorrelation bp(MESH:Apoptosis) View Subject | View Object

Apoptosis has been found to be a major rout for the elimination of cells after a variety of stresses including ROS and RNS [30]. PubMed:30324533

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Hematoma
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complex(a(CHEBI:"hydrogen peroxide"), a(CHEBI:heme), a(CHEBI:nitrite)) positiveCorrelation bp(MESH:Apoptosis) View Subject | View Object

Figure 3a depicts the morphology of SHSY5Y cells after treated with various conditions. Compared with heme/H2O2 treatment, cells exposing to heme/ H2O2/NO2 − exacerbated cell apoptotic and reduced cell yield. PubMed:30324533

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Hematoma
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complex(a(CHEBI:"hydrogen peroxide"), a(CHEBI:heme), a(CHEBI:nitrite)) positiveCorrelation bp(MESH:Apoptosis) View Subject | View Object

As quantified in Fig. 3c, although heme/H2O2/NO2 − increased the apoptotic rate to 32 ± 6.4%, BSA or BSA-T pretreatment caused a statistically significant reduced apoptotic rate (10 ± 5.0% and 15 ± 6.1%, respectively). PubMed:30324533

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Hematoma
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p(HGNC:ALB) negativeCorrelation bp(MESH:Apoptosis) View Subject | View Object

However, pretreatment with 2 μM BSA or BSA-T, we found that both BSA and BSA-T efficiently inhibited heme/H2O2/NO2 −- induced cell apoptotic and increased cell yields. PubMed:30324533

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Hematoma
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p(HGNC:ALB) negativeCorrelation bp(MESH:Apoptosis) View Subject | View Object

As quantified in Fig. 3c, although heme/H2O2/NO2 − increased the apoptotic rate to 32 ± 6.4%, BSA or BSA-T pretreatment caused a statistically significant reduced apoptotic rate (10 ± 5.0% and 15 ± 6.1%, respectively). PubMed:30324533

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Hematoma
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p(MGI:Hpx) negativeCorrelation bp(MESH:Apoptosis) View Subject | View Object

In conclusion, an Hx-based therapy shows beneficial effects, in that it counteracts heme-induced proinflammatory activation of macrophages and attenuates some of its pathophysiologic consequences, such as chronic inflammation, hepatic fibrosis, and apoptosis (Figure 7E). PubMed:26675351

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Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
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Results

p(HGNC:ALB, pmod(Ph, Tyr)) negativeCorrelation bp(MESH:Apoptosis) View Subject | View Object

However, pretreatment with 2 μM BSA or BSA-T, we found that both BSA and BSA-T efficiently inhibited heme/H2O2/NO2 −- induced cell apoptotic and increased cell yields. PubMed:30324533

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Hematoma
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p(HGNC:ALB, pmod(Ph, Tyr)) negativeCorrelation bp(MESH:Apoptosis) View Subject | View Object

As quantified in Fig. 3c, although heme/H2O2/NO2 − increased the apoptotic rate to 32 ± 6.4%, BSA or BSA-T pretreatment caused a statistically significant reduced apoptotic rate (10 ± 5.0% and 15 ± 6.1%, respectively). PubMed:30324533

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Hematoma
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Out-Edges 11

bp(MESH:Apoptosis) association a(MESH:Acetylcholine) View Subject | View Object

but ACh is also released by non-neuronal tissues where it is involved in cell-to-cell communication, and con- trols essential functions such as cell proliferation, adhesion, migration, secretion, survival and apoptosis, in an autocrine, paracrine or juxtacrine manner PubMed:28901280

bp(MESH:Apoptosis) negativeCorrelation p(MGI:Hpx) View Subject | View Object

In conclusion, an Hx-based therapy shows beneficial effects, in that it counteracts heme-induced proinflammatory activation of macrophages and attenuates some of its pathophysiologic consequences, such as chronic inflammation, hepatic fibrosis, and apoptosis (Figure 7E). PubMed:26675351

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Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(MESH:Apoptosis) increases a(MESH:"Cell-Derived Microparticles") View Subject | View Object

Activation, aging, and apoptosis of various cells, including RBCs, are accompanied by formation of microscopic extracellular membranous structures named microvesicles or microparticles (MPs). PubMed:28458720

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Cell Ontology (CL)
erythrocyte
MeSH
Veins
MeSH
beta-Thalassemia
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Review

bp(MESH:Apoptosis) positiveCorrelation a(MESH:"Reactive Oxygen Species") View Subject | View Object

Apoptosis has been found to be a major rout for the elimination of cells after a variety of stresses including ROS and RNS [30]. PubMed:30324533

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Hematoma
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bp(MESH:Apoptosis) positiveCorrelation a(MESH:"Reactive Nitrogen Species") View Subject | View Object

Apoptosis has been found to be a major rout for the elimination of cells after a variety of stresses including ROS and RNS [30]. PubMed:30324533

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Hematoma
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bp(MESH:Apoptosis) positiveCorrelation complex(a(CHEBI:"hydrogen peroxide"), a(CHEBI:heme), a(CHEBI:nitrite)) View Subject | View Object

Figure 3a depicts the morphology of SHSY5Y cells after treated with various conditions. Compared with heme/H2O2 treatment, cells exposing to heme/ H2O2/NO2 − exacerbated cell apoptotic and reduced cell yield. PubMed:30324533

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MeSH
Hematoma
Text Location
Results

bp(MESH:Apoptosis) positiveCorrelation complex(a(CHEBI:"hydrogen peroxide"), a(CHEBI:heme), a(CHEBI:nitrite)) View Subject | View Object

As quantified in Fig. 3c, although heme/H2O2/NO2 − increased the apoptotic rate to 32 ± 6.4%, BSA or BSA-T pretreatment caused a statistically significant reduced apoptotic rate (10 ± 5.0% and 15 ± 6.1%, respectively). PubMed:30324533

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MeSH
Hematoma
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Results

bp(MESH:Apoptosis) negativeCorrelation p(HGNC:ALB) View Subject | View Object

However, pretreatment with 2 μM BSA or BSA-T, we found that both BSA and BSA-T efficiently inhibited heme/H2O2/NO2 −- induced cell apoptotic and increased cell yields. PubMed:30324533

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MeSH
Hematoma
Text Location
Results

bp(MESH:Apoptosis) negativeCorrelation p(HGNC:ALB) View Subject | View Object

As quantified in Fig. 3c, although heme/H2O2/NO2 − increased the apoptotic rate to 32 ± 6.4%, BSA or BSA-T pretreatment caused a statistically significant reduced apoptotic rate (10 ± 5.0% and 15 ± 6.1%, respectively). PubMed:30324533

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MeSH
Hematoma
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Results

bp(MESH:Apoptosis) negativeCorrelation p(HGNC:ALB, pmod(Ph, Tyr)) View Subject | View Object

However, pretreatment with 2 μM BSA or BSA-T, we found that both BSA and BSA-T efficiently inhibited heme/H2O2/NO2 −- induced cell apoptotic and increased cell yields. PubMed:30324533

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MeSH
Hematoma
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Results

bp(MESH:Apoptosis) negativeCorrelation p(HGNC:ALB, pmod(Ph, Tyr)) View Subject | View Object

As quantified in Fig. 3c, although heme/H2O2/NO2 − increased the apoptotic rate to 32 ± 6.4%, BSA or BSA-T pretreatment caused a statistically significant reduced apoptotic rate (10 ± 5.0% and 15 ± 6.1%, respectively). PubMed:30324533

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MeSH
Hematoma
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Results

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.