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bp(HM:"macrophage M1 polarization")

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Entity

Name
macrophage M1 polarization
Namespace
HM
Namespace Version
None
Pattern
.*

Appears in Networks 1

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 11

a(CHEBI:"N-acetyl-L-cysteine") negativeCorrelation bp(HM:"macrophage M1 polarization") View Subject | View Object

Likewise, NAC was able to prevent iron-induced M1 polarization in M0, M1, and M2 BMDMs (supplemental Figure 13), indicating that the alteration of macrophage plasticity in response to iron is mostly explained by its pro-oxidant properties. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Spleen
MeSH
Anemia, Sickle Cell
Text Location
Results

a(CHEBI:"desferrioxamine B") negativeCorrelation bp(HM:"macrophage M1 polarization") View Subject | View Object

Treatment with Hx or DFO diminished the increase of some M1 polarization markers in BMDMs following treatment with hemolytic RBCs (supplemental Figure 14). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

a(CHEBI:"iron(2+)") positiveCorrelation bp(HM:"macrophage M1 polarization") View Subject | View Object

Likewise, NAC was able to prevent iron-induced M1 polarization in M0, M1, and M2 BMDMs (supplemental Figure 13), indicating that the alteration of macrophage plasticity in response to iron is mostly explained by its pro-oxidant properties. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Spleen
MeSH
Anemia, Sickle Cell
Text Location
Results

a(CHEBI:heme) increases bp(HM:"macrophage M1 polarization") View Subject | View Object

This is the case in a mouse model of SCD, which is hallmarked by hemolysis, increased circulating Hb/heme, and low levels of Hp and Hx and shows elevated hepatic macrophage iron levels and M1 polarization. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

a(CHEBI:heme) increases bp(HM:"macrophage M1 polarization") View Subject | View Object

Importantly, by scavenging free heme, Hx prevents heme-induced M1 macrophage polarization and thus avoids both TLR4 activation and ROS formation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

a(CHEBI:heme) increases bp(HM:"macrophage M1 polarization") View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

bp(GO:"inflammatory response") positiveCorrelation bp(HM:"macrophage M1 polarization") View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

p(HGNC:HBB) increases bp(HM:"macrophage M1 polarization") View Subject | View Object

This is the case in a mouse model of SCD, which is hallmarked by hemolysis, increased circulating Hb/heme, and low levels of Hp and Hx and shows elevated hepatic macrophage iron levels and M1 polarization. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

p(HGNC:HPX) negativeCorrelation bp(HM:"macrophage M1 polarization") View Subject | View Object

Treatment with Hx or DFO diminished the increase of some M1 polarization markers in BMDMs following treatment with hemolytic RBCs (supplemental Figure 14). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

p(MGI:Hpx) negativeCorrelation bp(HM:"macrophage M1 polarization") View Subject | View Object

Importantly, by scavenging free heme, Hx prevents heme-induced M1 macrophage polarization and thus avoids both TLR4 activation and ROS formation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

p(MGI:Hpx) negativeCorrelation bp(HM:"macrophage M1 polarization") View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

Out-Edges 7

bp(HM:"macrophage M1 polarization") positiveCorrelation a(CHEBI:"iron(2+)") View Subject | View Object

Likewise, NAC was able to prevent iron-induced M1 polarization in M0, M1, and M2 BMDMs (supplemental Figure 13), indicating that the alteration of macrophage plasticity in response to iron is mostly explained by its pro-oxidant properties. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Spleen
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(HM:"macrophage M1 polarization") negativeCorrelation a(CHEBI:"N-acetyl-L-cysteine") View Subject | View Object

Likewise, NAC was able to prevent iron-induced M1 polarization in M0, M1, and M2 BMDMs (supplemental Figure 13), indicating that the alteration of macrophage plasticity in response to iron is mostly explained by its pro-oxidant properties. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Spleen
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(HM:"macrophage M1 polarization") negativeCorrelation p(HGNC:HPX) View Subject | View Object

Treatment with Hx or DFO diminished the increase of some M1 polarization markers in BMDMs following treatment with hemolytic RBCs (supplemental Figure 14). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(HM:"macrophage M1 polarization") negativeCorrelation a(CHEBI:"desferrioxamine B") View Subject | View Object

Treatment with Hx or DFO diminished the increase of some M1 polarization markers in BMDMs following treatment with hemolytic RBCs (supplemental Figure 14). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(HM:"macrophage M1 polarization") negativeCorrelation p(MGI:Hpx) View Subject | View Object

Importantly, by scavenging free heme, Hx prevents heme-induced M1 macrophage polarization and thus avoids both TLR4 activation and ROS formation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

bp(HM:"macrophage M1 polarization") negativeCorrelation p(MGI:Hpx) View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

bp(HM:"macrophage M1 polarization") positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

Our data support the idea that heme-induced phenotypic switching of macrophages toward a proinflammatory phenotype can contribute to the exacerbation of inflammation and chronic tissue injury in hemolytic disorders and that Hx therapy could alleviate these pathophysiologic consequences by preventing macrophage inflammatory activation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

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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.