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Upregulated long noncoding RNA Linc00261 in pre-eclampsia and its effect on trophoblast invasion and migration via regulating miR-558/TIMP4 signaling pathway.
J Cell Biochem 2019; 120(8):13243-13253JC

Abstract

Pre-eclampsia (PE) is a leading cause of maternal and perinatal morbidity and mortality but the exact underlying mechanisms of PE pathogenesis remain elusive. Accumulated data suggested that the long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of PE. The present study identified the changes of lncRNA Linc00261 in PE and its effects on trophoblasts invasion and migration. Our results showed that the expression of Linc00261 was upregulated in placental tissues of PE women compared with those of healthy pregnant women. Overexpression of Linc00261 suppressed cell invasion and migration, induced cell apoptosis, and caused cell-cycle arrest at G0 /G1 phase of HTR-8/SVneo cells; while knockdown of Linc00261 had the opposite effects on the HTR-8/SVneo cells. Mechanistic studies showed Linc00261 functioned as a competing endogenous RNA for miR-558 in HTR-8/SVneo cells, and miR-558 was negatively regulated by Linc00261. The expression level of miR-558 in the PE group was significantly lower than the control group, and the expression level of Linc00261 was negatively correlated with the expression level of miR-558 in the placental tissues of women with PE. Furthermore, miR-558 was found to negatively regulate the expression of TIMP metallopeptidase inhibitor 4 (TIMP4) via targeting the 3' untranslated region in the HTR-8/SVneo cells. Overexpression of miR-558 increased HTR-8/SVneo cell invasion and migration, which was attenuated by TIMP4 overexpression. More importantly, both overexpression of miR-558 and knockdown of TIMP4 partially reversed the suppressive effects of Linc00261 overexpression on cell invasion and migration of HTR-8/SVneo cells. Collectively, our results for the first time showed the upregulation of Linc00261 in the placental tissues of severe PE patients. The mechanistic results indicated that Linc00261 exerted the suppressive effects on the trophoblast invasion and migration via targeting miR-558/TIMP4 axis, which may involve in the pathogenesis of PE.

Authors+Show Affiliations

Center for Reproductive Medicine, Wuhan University Renmin Hospital, Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Wuhan, Hubei, China.Department of Dermatology, Wuhan University Renmin Hospital, Wuhan, Hubei, China.Center for Reproductive Medicine, Wuhan University Renmin Hospital, Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Wuhan, Hubei, China.Center for Reproductive Medicine, Wuhan University Renmin Hospital, Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Wuhan, Hubei, China.Center for Reproductive Medicine, Wuhan University Renmin Hospital, Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Wuhan, Hubei, China.Center for Reproductive Medicine, Wuhan University Renmin Hospital, Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Wuhan, Hubei, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30891826

Citation

Cheng, Dan, et al. "Upregulated Long Noncoding RNA Linc00261 in Pre-eclampsia and Its Effect On Trophoblast Invasion and Migration Via Regulating miR-558/TIMP4 Signaling Pathway." Journal of Cellular Biochemistry, vol. 120, no. 8, 2019, pp. 13243-13253.
Cheng D, Jiang S, Chen J, et al. Upregulated long noncoding RNA Linc00261 in pre-eclampsia and its effect on trophoblast invasion and migration via regulating miR-558/TIMP4 signaling pathway. J Cell Biochem. 2019;120(8):13243-13253.
Cheng, D., Jiang, S., Chen, J., Li, J., Ao, L., & Zhang, Y. (2019). Upregulated long noncoding RNA Linc00261 in pre-eclampsia and its effect on trophoblast invasion and migration via regulating miR-558/TIMP4 signaling pathway. Journal of Cellular Biochemistry, 120(8), pp. 13243-13253. doi:10.1002/jcb.28598.
Cheng D, et al. Upregulated Long Noncoding RNA Linc00261 in Pre-eclampsia and Its Effect On Trophoblast Invasion and Migration Via Regulating miR-558/TIMP4 Signaling Pathway. J Cell Biochem. 2019;120(8):13243-13253. PubMed PMID: 30891826.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Upregulated long noncoding RNA Linc00261 in pre-eclampsia and its effect on trophoblast invasion and migration via regulating miR-558/TIMP4 signaling pathway. AU - Cheng,Dan, AU - Jiang,Shan, AU - Chen,Jiao, AU - Li,Jie, AU - Ao,Liangfei, AU - Zhang,Ying, Y1 - 2019/03/19/ PY - 2018/10/03/received PY - 2018/12/03/revised PY - 2018/12/06/accepted PY - 2019/3/21/pubmed PY - 2019/3/21/medline PY - 2019/3/21/entrez KW - Linc00261 KW - TIMP metallopeptidase inhibitor 4 KW - invasion and migration KW - miR-558 KW - pre-eclampsia KW - trophoblast SP - 13243 EP - 13253 JF - Journal of cellular biochemistry JO - J. Cell. Biochem. VL - 120 IS - 8 N2 - Pre-eclampsia (PE) is a leading cause of maternal and perinatal morbidity and mortality but the exact underlying mechanisms of PE pathogenesis remain elusive. Accumulated data suggested that the long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of PE. The present study identified the changes of lncRNA Linc00261 in PE and its effects on trophoblasts invasion and migration. Our results showed that the expression of Linc00261 was upregulated in placental tissues of PE women compared with those of healthy pregnant women. Overexpression of Linc00261 suppressed cell invasion and migration, induced cell apoptosis, and caused cell-cycle arrest at G0 /G1 phase of HTR-8/SVneo cells; while knockdown of Linc00261 had the opposite effects on the HTR-8/SVneo cells. Mechanistic studies showed Linc00261 functioned as a competing endogenous RNA for miR-558 in HTR-8/SVneo cells, and miR-558 was negatively regulated by Linc00261. The expression level of miR-558 in the PE group was significantly lower than the control group, and the expression level of Linc00261 was negatively correlated with the expression level of miR-558 in the placental tissues of women with PE. Furthermore, miR-558 was found to negatively regulate the expression of TIMP metallopeptidase inhibitor 4 (TIMP4) via targeting the 3' untranslated region in the HTR-8/SVneo cells. Overexpression of miR-558 increased HTR-8/SVneo cell invasion and migration, which was attenuated by TIMP4 overexpression. More importantly, both overexpression of miR-558 and knockdown of TIMP4 partially reversed the suppressive effects of Linc00261 overexpression on cell invasion and migration of HTR-8/SVneo cells. Collectively, our results for the first time showed the upregulation of Linc00261 in the placental tissues of severe PE patients. The mechanistic results indicated that Linc00261 exerted the suppressive effects on the trophoblast invasion and migration via targeting miR-558/TIMP4 axis, which may involve in the pathogenesis of PE. SN - 1097-4644 UR - https://www.unboundmedicine.com/medline/citation/30891826/Upregulated_long_noncoding_RNA_Linc00261_in_pre_eclampsia_and_its_effect_on_trophoblast_invasion_and_migration_via_regulating_miR_558/TIMP4_signaling_pathway_ L2 - https://doi.org/10.1002/jcb.28598 DB - PRIME DP - Unbound Medicine ER -