Xiaoping Li1, Rui Yang2, Ying Xu3, Yongshui Zhang4. 1. Department of Obstetrics, Jinan Maternal and Child Health Hospital, Shandong, China. 2. Department of Outpatient, Jinan Maternal and Child Health Hospital, Shandong, China. 3. Department of Prenatal Diagnosis, Jinan Maternal and Child Health Hospital, Shandong, China. 4. Department of Medicine, Jinan Maternal and Child Health Hospital, Shandong, China. Electronic address: blt5cqg@163.com.
Abstract
INTRODUCTION: Preeclampsia (PE) is a common pregnancy disorder with multisystem complications. The growing data suggest that circular RNAs (circRNAs) involve in the development of PE. This study proposed to investigate the function and potential mechanisms of circ_0001438 in PE. METHODS: The expression of circ_0001438, miR-942 and NOD-like receptor pyrin domain-containing protein 3 (NLRP3) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The expression at the protein level of NLRP3, interleukin 1 beta (IL-1β), interleukin 10 (IL-10), B-cell lymphoma 2 (Bcl-2), Cleaved-caspase-3 (Cleaved-casp-3), N-cadherin and E-cadherin was detected by Western blot. Cell proliferation was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Cell apoptosis was determined by flow cytometry assay. Cell migration and invasion were monitored by transwell assay. The target genes were obtained and verified by the online bioinformatics tool and dual-luciferase reporter assay. RESULTS: The expression of circ_0001438 and NLRP3 was enhanced in PE placenta tissues. Circ_0001438 knockdown promoted cell proliferation, migration and invasion but inhibited apoptosis and inflammatory responses in HTR-8/Svneo cells, and these effects were reversed by the inhibition of miR-942, a target of circ_0001438. Moreover, NLRP3 was bounded by miR-942. The enrichment of miR-942 accelerated cell proliferation, migration and invasion but depleted apoptosis and inflammatory responses, while these impacts were partly abolished by NLRP3 overexpression. DISCUSSION: Circ_0001438 sponged miR-942 to regulate the expression of NLRP3, and circ_0001438 aggravated the dysfunctions of human villous trophoblasts by mediating the miR-942/NLRP3 axis at least in part.
INTRODUCTION: Preeclampsia (PE) is a common pregnancy disorder with multisystem complications. The growing data suggest that circular RNAs (circRNAs) involve in the development of PE. This study proposed to investigate the function and potential mechanisms of circ_0001438 in PE. METHODS: The expression of circ_0001438, miR-942 and NOD-like receptor pyrin domain-containing protein 3 (NLRP3) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The expression at the protein level of NLRP3, interleukin 1 beta (IL-1β), interleukin 10 (IL-10), B-cell lymphoma 2 (Bcl-2), Cleaved-caspase-3 (Cleaved-casp-3), N-cadherin and E-cadherin was detected by Western blot. Cell proliferation was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Cell apoptosis was determined by flow cytometry assay. Cell migration and invasion were monitored by transwell assay. The target genes were obtained and verified by the online bioinformatics tool and dual-luciferase reporter assay. RESULTS: The expression of circ_0001438 and NLRP3 was enhanced in PE placenta tissues. Circ_0001438 knockdown promoted cell proliferation, migration and invasion but inhibited apoptosis and inflammatory responses in HTR-8/Svneo cells, and these effects were reversed by the inhibition of miR-942, a target of circ_0001438. Moreover, NLRP3 was bounded by miR-942. The enrichment of miR-942 accelerated cell proliferation, migration and invasion but depleted apoptosis and inflammatory responses, while these impacts were partly abolished by NLRP3 overexpression. DISCUSSION: Circ_0001438 sponged miR-942 to regulate the expression of NLRP3, and circ_0001438 aggravated the dysfunctions of human villous trophoblasts by mediating the miR-942/NLRP3 axis at least in part.