Abstract

ABSTRACTThe objective of the present research is to explore miRNAs expression profiles in lung tissue of rat treated by nanosized SiO2 in the light of normal at diverse dosages, time, predict their target genes, and probe the biological function and regulation of miRNA in the lung damage process caused by nanosized SiO2. Up-regulation of rno-miR-208, rno-miR-212 and rno-miR-18a in lung tissue mainly characterized by inflammation of SD rats caused by nanosized SiO2 particles instilled intratracheally at 7th, 15th 30th d using Illumina HiSeq2000 sequencing technique and were further verified by quantitative reverse transcriptase polymerase chain reaction (qRT PCR) assay. Lung damage is mainly with characteristics of lung interstitial fibrosis, upregulation of rno-miR-212, rno-miR-144, rno-miR-702-3p, rno-miR-379 and rno-miR-127, down-regulation of rno-miR-541 at 60th, 90th d post-exposure. As target genes of rno-miR-208, rno-miR-212 and rno-miR-18a respectively, there was no statistical significance of programmed cell death 4 (PDCD4), LIN28B and connective tissue growth factor (CTGF) mRNA expression level (P > 0.05) compared to β-actin as internal controls detected by Real-time quantitative PCR. The differences in protein gray value ratio of PDCD4, LIN28B and CTGF detected by Western blotting test were statistically significant (P < 0.05). These results suggested that miR-208, miR-212 and miR-18a may take effects in rats' lung damage lead by nanosized SiO2. Their target genes of PDCD4, LIN28B and CTGF functioned in translation level of target genes in regulation of inflammatory signaling pathways and involved in the formation of tissue fibrosis.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.