Fig. 3: EV-derived XIST suppressed the activation of NLRP3 inflammasome and pyroptosis of HL-1 cells. | Laboratory Investigation

Fig. 3: EV-derived XIST suppressed the activation of NLRP3 inflammasome and pyroptosis of HL-1 cells.

From: LncRNA XIST shuttled by adipose tissue-derived mesenchymal stem cell-derived extracellular vesicles suppresses myocardial pyroptosis in atrial fibrillation by disrupting miR-214-3p-mediated Arl2 inhibition

Fig. 3: EV-derived XIST suppressed the activation of NLRP3 inflammasome and pyroptosis of HL-1 cells.

A NLRP3, ASC, caspase-1, and GSDMD mRNA expression in HL-1 cells treated with CM and GW4869 + CM detected by qRT-PCR. B Protein expression of H, NLRP3, ASC, cleaved-caspase-1/caspase-1, and cleaved-GSDMD/GSDMD in HL-1 cells treated with CM and GW4869 + CM detected by Western blot analysis. C Detection of pro-inflammatory factors IL-1β and IL-18 in the supernatant of HL-1 cells treated with CM and GW4869 + CM by ELISA. D Flow cytometric analysis of EV uptake by HL-1 cells with the duration of the culture. E Detection of XIST expression in HL-1 cells treated with EVs, NC EVs, XIST EVs, or controls by qRT-PCR. F qRT-PCR analysis of NLRP3, ASC, caspase-1, and GSDMD mRNA expression in HL-1 cells treated with EVs, NC EVs, XIST EVs, or controls. G Western blot analysis of NLRP3, ASC, cleaved-caspase-1/caspase-1, and cleaved-GSDMD/GSDMD protein expression in HL-1 cells treated with EVs, NC EVs, XIST EVs, or controls. H Detection of pro-inflammatory factors IL-1β and IL-18 by ELISA in the supernatant of HL-1 cells treated with EVs, NC EVs, XIST EVs, or controls. *p < 0.05 versus normal HL-1 cells (normal or CM); #p < 0.05 versus HL-1 cells receiving AF induction and PBS; &p < 0.05 versus HL-1 cells receiving AF induction and NC EVs. Comparison between two groups was analyzed by unpaired t-test and among multiple groups was by one-way ANOVA with Tukey’s post hoc test. All experiments were repeated three times with similar results.

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