Our results also show that A20 expression was significantly reduced in blood leukocytes and ASM obtained from patients with asthma compared to cells obtained from healthy subjects which was restored after incubation with IRL201104 in vitro, when added alone, or in combination with LPS or TNF-α in ASM.
Together, our study provides the first in vitro evidence highlighting the antiproliferative and antimigratory roles of miR-638 in human ASMC remodeling and suggests that targeted overexpression of miR-638 in ASMCs may provide a novel therapeutic strategy for preventing ASM hyperplasia associated with asthma.