NDLI: Acute hypoxia induces HIF-independent monocyte adhesion to endothelial cells through increased intercellular adhesion molecule-1 expression: the role of hypoxic inhibition of prolyl hydroxylase activity for the induction of NF-kappa B.

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Acute hypoxia induces HIF-independent monocyte adhesion to endothelial cells through increased intercellular adhesion molecule-1 expression: the role of hypoxic inhibition of prolyl hydroxylase activity for the induction of NF-kappa B.

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Acute hypoxia induces HIF-independent monocyte adhesion to endothelial cells through increased intercellular adhesion molecule-1 expression: the role of hypoxic inhibition of prolyl hydroxylase activity for the induction of NF-kappa B.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Winning, Sandra Frede, Stilla Splettstoesser, Frank Fandrey, Joachim
Description	Country affiliation: Germany Author Affiliation: Winning S ( Institut für Physiologie, Universität Duisburg-Essen, Essen, Germany.)
Abstract	Myeloid cells recruited to sites of bacterial inflammation are exposed to low oxygen tension, hypoxia, and high concentrations of inflammatory cytokines that significantly affect myeloid cell function. Therefore, we analyzed the direct consequences of acute and severe hypoxia on monocytic adhesion to the endothelium in coculture experiments. Marked upregulation of monocytic ICAM-1, but no other monocytic adhesion molecule, was responsible for an approximately 50-fold increase in adhesion of the monocytic cells THP-1 to human and rat endothelial cells. ICAM-1 expression was rapidly induced after the onset of severe hypoxia, but it decreased after 4 h. Knockdown of ICAM-1 by siRNA in endothelial and monocytic cells abolished the adhesion, indicating that ICAM-1 expression on both cell types was indispensable for hypoxia-induced adhesion of monocytes to the endothelium. siRNA-mediated knockdown of hypoxia inducible factor (HIF)-1alpha, HIF-2alpha, and the NF-kappaB family member p65 revealed that hypoxic upregulation of ICAM-1 resulted from hypoxic NF-kappaB induction but not from activation of HIFs. Within the leukocyte-adhesion cascade, our results provide evidence for prolyl hydroxylase-dependent but HIF-independent activation of hypoxia-induced monocyte-endothelial adhesion and assign a new function to monocytic ICAM-1 under acute hypoxic conditions.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	3
Volume Number	185
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2010-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Hypoxia Immunology Endothelium, Vascular Cytology Hypoxia-inducible Factor 1, Alpha Subunit Physiology Intercellular Adhesion Molecule-1 Biosynthesis Monocytes Nf-kappa B Procollagen-proline Dioxygenase Antagonists & Inhibitors Acute Disease Amino Acids, Dicarboxylic Pharmacology Animals Basic Helix-loop-helix Transcription Factors Cell Adhesion Cell Line Cell Line, Tumor Coculture Techniques Enzymology Enzyme Activation Drug Effects Genetics Metabolism Rna, Messenger Up-regulation Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Prolyl hydroxylase-1 negatively regulates IkappaB kinase-beta, giving insight into hypoxia-induced NFkappaB activity.

Interdependence of hypoxic and innate immune responses.

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Role of reactive oxygen species in the regulation of HIF-1 by prolyl hydroxylase 2 under mild hypoxia.

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Endogenous 2-oxoglutarate levels impact potencies of competitive HIF prolyl hydroxylase inhibitors.

Hypoxia-inducible factor 1 (HIF-1) promotes extracellular matrix remodeling under hypoxic conditions by inducing P4HA1, P4HA2, and PLOD2 expression in fibroblasts.

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Acute hypoxia induces HIF-independent monocyte adhesion to endothelial cells through increased intercellular adhesion molecule-1 expression: the role of hypoxic inhibition of prolyl hydroxylase activity for the induction of NF-kappa B.

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Acute hypoxia induces HIF-independent monocyte adhesion to endothelial cells through increased intercellular adhesion molecule-1 expression: the role of hypoxic inhibition of prolyl hydroxylase activity for the induction of NF-kappa B.