The Long Non-coding RNA NEAT1/miR-224-5p/IL-33 Axis Modulates Macrophage M2a Polarization and A1 Astrocyte Activation

To identify potential regulators and investigate the molecular mechanism of macrophage polarization affecting astrocyte activation from the perspective of non-coding RNA regulation, we isolated mouse bone marrow mononuclear cells (BMMNCs)–induced macrophages toward M1 or M2a polarization. Long non-c...

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Veröffentlicht in:Molecular neurobiology Jg. 58; H. 9; S. 4506 - 4519
Hauptverfasser: Liu, Dongliang, Wei, Yuehua, Liu, Yudong, Wu, Tianding, Hu, Jianzhong, Lu, Hongbin
Format: Journal Article
Sprache:Englisch
Veröffentlicht: New York Springer US 01.09.2021
Springer Nature B.V
Schlagworte:
Animals
Astrocytes
Astrocytes - cytology
Astrocytes - metabolism
Biomedical and Life Sciences
Biomedicine
Bone marrow
Cell activation
Cell Biology
Cell Polarity
Interleukin 13
Interleukin 4
Interleukin-33 - metabolism
Kinases
Leukocytes (mononuclear)
Macrophage Activation
Macrophages
Macrophages - cytology
Macrophages - metabolism
Mice
MicroRNAs - metabolism
Neurobiology
Neurology
Neurosciences
Non-coding RNA
Polarization
Proteins
RNA, Long Noncoding - metabolism
Signal Transduction - physiology
miR-224-5p
Macrophage polarization
IL-33
Long non-coding RNA NEAT1
A1 astrocyte activation
ISSN:0893-7648, 1559-1182, 1559-1182
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Zusammenfassung:To identify potential regulators and investigate the molecular mechanism of macrophage polarization affecting astrocyte activation from the perspective of non-coding RNA regulation, we isolated mouse bone marrow mononuclear cells (BMMNCs)–induced macrophages toward M1 or M2a polarization. Long non-coding RNA NEAT1 and IL-33 expression levels were significantly upregulated in M2a macrophages; NEAT1 knockdown in M2a macrophages markedly reduced the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages. NEAT1 acted as a competing endogenous RNA (ceRNA) to regulate IL-33 expression by sponging miR-224-5p in M2a macrophages; NEAT1 knockdown upregulated miR-224-5p expression, while miR-224-5p inhibition increased the protein content and concentration of IL-33. miR-224-5p inhibition exerted the opposite effects on the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages compared to NEAT1 knockdown; the effects of NEAT1 knockdown were significantly reversed by miR-224-5p inhibition. M2a macrophage conditioned medium (CM) significantly suppressed the activation of A1 astrocytes. NEAT1 knockdown M2a macrophage CM led to enhanced A1 astrocyte activation while miR-224-5p–silenced M2a macrophage CM led to a blockade of A1 astrocyte activation; the effects of NEAT1 knockdown M2a macrophage CM on A1 astrocyte activation were significantly reversed by miR-224-5p inhibition in M2a macrophages. The NEAT1/miR-224-5p/IL-33 axis modulates macrophage M2a polarization, therefore affecting A1 astrocyte activation.
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ISSN:0893-7648
1559-1182
1559-1182
DOI:10.1007/s12035-021-02405-x