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Differential expression of miR-145 in children with Kawasaki disease
Chisato Shimizu1, Jihoon Kim, Petra Stepanowsky
1Department of Pediatrics, University of California San Diego, La Jolla, California, USA. c1shimizu@ucsd.edu
Background:
Kawasaki disease is an acute, self-limited vasculitis of childhood that can result in structural damage to the coronary arteries. Previous studies have implicated the TGF-β pathway in disease pathogenesis and generation of myofibroblasts in the arterial wall. microRNAs are small non-coding RNAs that modulate gene expression at the post-transcriptional level and can be transported between cells in extracellular vesicles. To understand the role that microRNAs play in modifying gene expression in Kawasaki disease, we studied microRNAs from whole blood during the acute and convalescent stages of the illness.
Methodology/Principal Findings:
RNA isolated from the matched whole blood of 12 patients with acute and convalescent Kawasaki disease were analyzed by sequencing of small RNA. This analysis revealed six microRNAs (miRs-143, -199b-5p, -618, -223, -145 and -145* (complementary strand)) whose levels were significantly elevated during the acute phase of Kawasaki disease. The result was validated using targeted qRT-PCR using an independent cohort (n = 16). miR-145, which plays a critical role in the differentiation of neutrophils and vascular smooth muscle cells, was expressed at high levels in blood samples from acute Kawasaki disease but not adenovirus-infected control patients (p = 0.005). miR-145 was also detected in small extracellular vesicles isolated from acute Kawasaki disease plasma samples. Pathway analysis of the predicted targets of the 6 differentially expressed microRNAs identified the TGF-β pathway as the top pathway regulated by microRNAs in Kawasaki disease.
Conclusion:
Sequencing of small RNA species allowed discovery of microRNAs that may participate in Kawasaki disease pathogenesis. miR-145 may participate, along with other differentially expressed microRNAs, in regulating expression of genes in the TGF-β pathway during the acute illness. If the predicted target genes are confirmed, our findings suggest a model of Kawasaki disease pathogenesis whereby miR-145 modulates TGF-β signaling in the arterial wall.
Insights
MicroRNAs, including miR-145, are elevated in acute Kawasaki disease, potentially impacting TGF-β signaling in the arterial wall. This study identifies key microRNAs involved in childhood vasculitis pathogenesis.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pediatric Immunology
Background:
- Kawasaki disease is a childhood vasculitis affecting coronary arteries.
- The TGF-β pathway is implicated in Kawasaki disease pathogenesis.
- MicroRNAs (miRNAs) are small non-coding RNAs regulating gene expression and can be intercellular mediators.
Purpose of the Study:
- To investigate the role of microRNAs in Kawasaki disease pathogenesis.
- To identify differentially expressed microRNAs in acute versus convalescent stages of Kawasaki disease.
- To explore the involvement of microRNAs in the TGF-β pathway during Kawasaki disease.
Main Methods:
- Small RNA sequencing of whole blood from patients with acute and convalescent Kawasaki disease.
- Validation of microRNA expression using quantitative reverse transcription PCR (qRT-PCR).
- Detection of microRNAs in extracellular vesicles from patient plasma.
Main Results:
- Six microRNAs (miR-143, -199b-5p, -618, -223, -145, and -145*) were significantly elevated during acute Kawasaki disease.
- miR-145 levels were high in acute Kawasaki disease but not in adenovirus-infected controls, and were found in extracellular vesicles.
- Pathway analysis indicated the TGF-β pathway as a primary target regulated by these microRNAs.
Conclusions:
- MicroRNA sequencing identified potential players in Kawasaki disease pathogenesis.
- miR-145 and other differentially expressed microRNAs may regulate TGF-β pathway genes during acute illness.
- Findings suggest a model where miR-145 modulates TGF-β signaling in the arterial wall in Kawasaki disease.