Background
Kawasaki disease (KD) is a multisystemic vasculitis syndrome. Accumulating evidences indicated that microRNAs play a critical role in KD. However, the mechanism was still not fully understood. The study aimed to research the functions of microRNA-197-3p (miR-197-3p) in the progression of KD.
Conclusion
miR-197-3p modifies cell behaviors of proliferation, apoptosis and migration by targeting IGF1R and BCL2 in KD, providing a new perspective for the treatment of KD clinically.
Methods
Level of miR-197-3p was detected by quantitative polymerase chain reaction (qRT-PCR) in acute KD serum. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to determine cell proliferation in HCAECs. Cell apoptosis was evaluated by flow cytometry. In addition, transwell assay was used to identify the migration capacity of HCAECs in vitro. The expression of insulin-like growth factor type 1 receptor (IGF1R), B cell lymphoma 2 (BCL2), apoptosis-relative of Cleaved-caspase 3 (C-caspase 3) and Cleaved-PARP (C-PARP), as well as transition-relative of E-cadherin, N-cadherin, and Vimentin were measured by western blot assay. Lastly, dual-luciferase reporter assay was employed to verify the relationship between miR-197-3p and IGF1R or BCL2 in vitro.
Results
Level of miR-197-3p was higher in Acute KD samples than that of healthy control and convalescent KD samples. Mechanistically, the role of miR-197-3p was exerted through directly targeting IGF1R and BCL2 in KD serum-induced HCAECs. Functionally, the inhibiting effect on cell apoptosis as well as promoting effects on cell proliferation and migration of miR-197-3p deletion was abrogated by either si-IGF1R or si-BCL2.