Formaldehyde (FA) serves as a prevailing
air pollutant, which has seriously threatened public health in recent years. Of all the known health effects,
lung injury is one of the most severe risks. However, little is known about the
circRNAs related molecular mechanism in the development of
lung injury induced by FA. This study was designed to explore the potential roles of dysregulated
circRNAs as well as its mechanism in FA-induced
lung injury. In the present study, 24 male SD rats were exposed to
formaldehyde (control, 0.5, 2.46 and 5 mg/m3) for 8 h per day for 8 weeks to induce
lung injury. We used H&E staining to evaluate the histopathological changes of
lung injury indifferent groups. The expression of
circRNAs in lung tissue was detected by real-time PCR. Meanwhile,
circRNA/
miRNA/
mRNA interaction networks were predicted by bioinformatics analysis. Our study revealed that
formaldehyde exposure resulted in abnormal histopathological changes in lung tissues. Moreover, the expression of rno_
circRNA_008646 was significantly higher in lung tissues of
formaldehyde exposure rats than in control. Bioinformatics analysis showed that one potential target
miRNA/
mRNA for rno_
circRNA_008646 was rno-miR-224/Forkhead Box I1 (FOXI1). Besides,
luciferase report gene confirmed that there was targeted binding relationship between rno_
circRNA_008646 and
rno-miR-224,
rno-miR-224 and FOXI1. Further verification experiments indicated that the expression of rno_
circRNA_008646 was negatively correlated
rno-miR-224, while it was positively correlated with FOXI1. JASPAR database showed
transcription factor FOXI1 located in promotor of CF Transmembrane Conductance Regulator (CFTR). Both FOXI1 and CFTR were up-regulated in lung tissues after
formaldehyde exposure. In conclusion, our findings suggested that
formaldehyde may induce
lung injury, and this may be caused by up-regulatedrno_
circRNA_008646, which medicated rno-miR-224/FOXI1/CFTR axis.