Next Article in Journal
Causes and Mechanisms of Hematopoietic Stem Cell Aging
Next Article in Special Issue
Targeting Apolipoprotein E for Alzheimer’s Disease: An Industry Perspective
Previous Article in Journal
Role of Serotonergic System in the Antidepressant Actions of mGlu2/3 Receptor Antagonists: Similarity to Ketamine
Previous Article in Special Issue
Osmotic Demyelination: From an Oligodendrocyte to an Astrocyte Perspective
Open AccessArticle

Hypoxia Induces Astrocyte-Derived Lipocalin-2 in Ischemic Stroke

1
Institute of Neuroanatomy, RWTH Aachen University, 52074 Aachen, Germany
2
Institute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry, RWTH Aachen University Hospital, 52074 Aachen, Germany
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2019, 20(6), 1271; https://doi.org/10.3390/ijms20061271
Received: 21 January 2019 / Revised: 22 February 2019 / Accepted: 7 March 2019 / Published: 13 March 2019
Ischemic stroke causes rapid hypoxic damage to the core neural tissue which is followed by graded chronological tissue degeneration in the peri-infarct zone. The latter process is mainly triggered by neuroinflammation, activation of inflammasomes, proinflammatory cytokines, and pyroptosis. Besides microglia, astrocytes play an important role in the fine-tuning of the inflammatory network in the brain. Lipocalin-2 (LCN2) is involved in the control of innate immune responses, regulation of excess iron, and reactive oxygen production. In this study, we analyzed LCN2 expression in hypoxic rat brain tissue after ischemic stroke and in astrocyte cell cultures receiving standardized hypoxic treatment. Whereas no LCN2-positive cells were seen in sham animals, the number of LCN2-positive cells (mainly astrocytes) was significantly increased after stroke. In vitro studies with hypoxic cultured astroglia revealed that LCN2 expression is significantly increased after only 2 h, then further increased, followed by a stepwise decline. The expression pattern of several proinflammatory cytokines mainly followed that profile in wild type (WT) but not in cultured LCN2-deficient astrocytes. Our data revealed that astrocytes are an important source of LCN2 in the peri-infarct region under hypoxic conditions. However, we must also stress that brain-intrinsic LCN2 after the initial hypoxia period might come from other sources such as invaded immune cells and peripheral organs via blood circulation. In any case, secreted LCN2 might have an influence on peripheral organ functions and the innate immune system during brain hypoxia. View Full-Text
Keywords: astrocyte; hypoxia; lipocalin-2; neuroinflammation astrocyte; hypoxia; lipocalin-2; neuroinflammation
Show Figures

Figure 1

MDPI and ACS Style

Ranjbar Taklimie, F.; Gasterich, N.; Scheld, M.; Weiskirchen, R.; Beyer, C.; Clarner, T.; Zendedel, A. Hypoxia Induces Astrocyte-Derived Lipocalin-2 in Ischemic Stroke. Int. J. Mol. Sci. 2019, 20, 1271.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop