Background: Long noncoding RNAs (lncRNAs) are important regulatory molecules in various biological and pathological processes. We herein aimed to explore whether maternally expressed gene 8 (MEG8) promotes M1 macrophage polarization in Henoch-Schonlein purpura (HSP) rats and to investigate the underlying mechanism.
Methods: Relative MEG8 and miR-181a-5p expression and suppressor of SH2 domain-containing tyrosine phosphatase 2 (SHP2) RNA level were examined using quantitative reverse transcription polymerase chain reaction. Expression of SHP2 and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway-related proteins was detected using western blot. Luciferase activity assay was performed to test whether miR-181a-5p could bind to MEG8 or SHP2. The macrophage phenotype was determined using flow cytometry analysis and enzyme-linked immunosorbent assay.
Results: The macrophage polarization toward the M2 phenotype was observed in
peripheral blood from HSP rats. Furthermore, MEG8 and SHP2 expression were down-regulated but miR-181a-5p was up-regulated in monocyte-derived macrophages from HSP rats compared with the control group. Furthermore, MEG8 acted as a sponge for miR-181a-5p to facilitate SHP2 expression. Moreover, miR-181a-5p mimic and SHP2 knockdown significantly reversed the MEG8 overexpression-mediated suppression of the JAK2/STAT3 signaling and promotion of M1 polarization.
Conclusion: IncRNA MEG8 sponging miR-181a-5p contributes to M1 macrophage polarization by regulating SHP2 expression in Henoch Schonlein purpura rats.
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Posted 03 Mar, 2021
Posted 03 Mar, 2021
Background: Long noncoding RNAs (lncRNAs) are important regulatory molecules in various biological and pathological processes. We herein aimed to explore whether maternally expressed gene 8 (MEG8) promotes M1 macrophage polarization in Henoch-Schonlein purpura (HSP) rats and to investigate the underlying mechanism.
Methods: Relative MEG8 and miR-181a-5p expression and suppressor of SH2 domain-containing tyrosine phosphatase 2 (SHP2) RNA level were examined using quantitative reverse transcription polymerase chain reaction. Expression of SHP2 and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway-related proteins was detected using western blot. Luciferase activity assay was performed to test whether miR-181a-5p could bind to MEG8 or SHP2. The macrophage phenotype was determined using flow cytometry analysis and enzyme-linked immunosorbent assay.
Results: The macrophage polarization toward the M2 phenotype was observed in
peripheral blood from HSP rats. Furthermore, MEG8 and SHP2 expression were down-regulated but miR-181a-5p was up-regulated in monocyte-derived macrophages from HSP rats compared with the control group. Furthermore, MEG8 acted as a sponge for miR-181a-5p to facilitate SHP2 expression. Moreover, miR-181a-5p mimic and SHP2 knockdown significantly reversed the MEG8 overexpression-mediated suppression of the JAK2/STAT3 signaling and promotion of M1 polarization.
Conclusion: IncRNA MEG8 sponging miR-181a-5p contributes to M1 macrophage polarization by regulating SHP2 expression in Henoch Schonlein purpura rats.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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