Integrative Analysis of MicroRNAs and mRNAs in LPS-Induced Macrophage Inflammation Based on Adipose Tissue Stem Cell Therapy.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Severe inflammation can lead to multiple organ dysfunction syndrome, which has high mortality. Adipose-derived stem cells have been shown to affect the inflammatory response of macrophages. However, the molecular mechanism of the anti-inflammatory capacity of adipose-derived stem cells (ADSCs) remains to be understood. In the present study, a macrophage inflammation model was established by LPS, and treated with different volumes of ADSC supernatant. Then, we investigated the key genes in the LPS group and treatment group by RT-PCR, RNA sequencing technology, and bioinformatics analysis. A total of 26 miRNAs and 11,882 mRNAs were differentially expressed between them. The expression of 15 of the miRNAs (9 upregulated and 6 downregulated) was confirmed by RT-PCR. GO and KEGG pathway analyses of the targets of the 9 significantly upregulated miRNAs showed that they were related to immune system process, inflammatory response, lipopolysaccharide, and TNF-α, NF-κB, Toll-like receptor, and MAPK signaling pathways. Moreover, a miRNA-mRNA network also revealed 8 important genes (Mapkapk2, Sepp1, Cers6, Snn, ZfP568, Ccdc93, Pofut1, Pik3cd). We finally confirmed the expression of these 8 targeted genes by performing the RT-PCR analysis. This study may provide a new understanding of the molecular mechanism of ADSCs in the inflammatory response related to multiple miRNAs and mRNAs.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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