Identification of long non-coding RNA in formaldehyde-induced cardiac dysplasia in rats

Formaldehyde exposure during pregnancy can cause fetal congenital heart disease (CHD). However, the regu-latory mechanism remains unclear. Studies on the biology of long non-coding RNAs (lncRNAs) show that lncRNAs can influence cardiac development and disease. However, expression patterns and regulatory mecha-nisms of action of lncRNAs in formaldehyde-induced CHD remain unclear. We used high-throughput sequencing strategies as a means of identifying lncRNA expression profiles in heart tissues of normal and formaldehyde-exposed newborn rats. Overall, 763 differentially expressed lncRNAs were identified, including 325 and 438 that were respectively up-regulated and down-regulated. GO and KEGG analyses indicated that the Ras and hedgehog signaling pathways may be important regulatory pathways in CHD caused by exposure to formalde-hyde. A lncRNA-miRNA-mRNA co-expression network was constructed and a key miRNA, rno-miR-665, was identified. Furthermore, qRT-PCR analysis verified that the novel lncRNAs: MSTRG.27313.2, MSTRG.30629.2, MSTRG.36520.33, MSTRG.91234.1, and MSTRG.91233.9, were upregulated in the formaldehyde-exposed group. These differentially expressed lncRNAs identified during formaldehyde-induced CHD in newborn rats help explain CHD pathogenesis and provide an effective reference for diagnosing and treating CHD.

Automated summary

Formaldehyde exposure during pregnancy can cause fetal congenital heart disease (CHD). High-throughput sequencing was used to identify the expression profiles of long non-coding RNAs (lncRNAs) in heart tissues of normal and formaldehyde-exposed newborn rats. A total of 763 differentially expressed lncRNAs were identified, and the Ras and hedgehog signaling pathways were identified as important regulatory pathways in CHD caused by formaldehyde exposure. Several upregulated lncRNAs were validated and may provide a reference for diagnosing and treating CHD.