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. 2022 Aug 10;78(6):617–630. doi: 10.1136/thoraxjnl-2021-218194

Figure 5.

Figure 5

miRNA-181a transfer through MSC EVs negates the pro-inflammatory response in human MDMs when stimulated with LPS or hyper-inflammatory ARDS plasma. (A) Immunoblot of PTEN, pSTAT5, STAT5 and β-actin in human MDM lysates after stimulation with LPS for 24 hours. Immunoblots were quantified by densitometry and normalised using total STAT5 expression for pSTAT5 or β-actin expression for PTEN/SOCS1 (n=4). (B) Levels of TNF-α secretion by MDMs after stimulation with LPS for 24 hours (n=3–4). (C) Levels of TNF-α secretion by MDMs after stimulation with healthy or pooled hypo-inflammatory or hyper-inflammatory ARDS plasma for 24 hours (n=3–6). (D) Immunoblot of PTEN, pSTAT5, STAT5, SOCS1 and β-actin in human MDMs lysates after stimulation with healthy or hypo-inflammatory or hyper-inflammatory ARDS plasma for 24 hours. Immunoblots were quantified by densitometry and normalised using total STAT5 expression for pSTAT5 or β-actin expression for PTEN/SOCS1 (bottom panel, n=2). Data are represented as mean±SD. Kruskal-Wallis test with post-hoc Dunn’s test (A, B, C). ARDS, acute respiratory distress syndrome; EVs, extracellular vesicles; LNA, locked nucleic acid; LPS, lipopolysaccharide; MDM, monocyte-derived macrophages; miRNA, micro RNA; MSCs, mesenchymal stromal cells; pSTAT, phosphorylated STAT; PTEN, phosphatase and tensin homolog; SOCS1, suppressor of cytokine signalling 1; STAT, signal transducers and activators of transcription ;TNF, tumour necrosis factor.