American journal of translational research · 2022
Long noncoding RNA urothelial carcinoma associated 1 protects human placental vascular endothelial cells from hypoxia-induced damage by regulating the miR-197-3p/histone deacetylase-2 axis in patients with pregnancy-induced hypertension.
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Li Jie, Lu Yiling, Wang Ying, Wang Xiaoyu, Kang Xinyi, Tang Weichun, Chen Liping
Аннотация
PURPOSE: Pregnancy-induced hypertension (PIH) is a major cause of mortality among pregnant women, fetuses, and newborns. This study assessed the role of long noncoding RNA (lncRNA) urothelial carcinoma associated 1 (UCA1) in PIH development.
METHODS: Serum samples were collected from 30 pregnant women with PIH and 30 healthy pregnant women. Serum UCA1, miR-197-3p, and histone deacetylase-2 (HDAC2) mRNA level was evaluated using quantitative polymerase chain reaction. The expression of UCA1, miR-197-3p and HDAC2 in human placental vascular endothelial cells (HPVECs) was regulated by transfection. HPVECs were treated with hypoxia reoxygenation (H/R) to establish the PIH cell model. Methyl thiazolyl tetrazolium (MTT) assay, the terminal transferase uridyl nick end labelling (Tunel) assay and tubule formation assay were performed to assess the viability, apoptosis and angiogenesis of HPVECs. Dual-luciferase reporter gene assay, RNA pull-down assay, and RNA immunoprecipitation assay were performed to identify the binding between two genes. Western blot analysis was used for protein expression detection.
RESULTS: In pregnant women with PIH, serum UCA1 and HDAC2 expression was downregulated and serum miR-197-3p expression was upregulated. H/R induction decreased the viability and angiogenesis of HPVECs, and increased the apoptosis of HPVECs. In H/R-induced HPVECs, UCA1 upregulation increased the viability and angiogenesis, and decreased the apoptosis. Downregulation of UCA1 had a contrasting result. UCA1 competitively binds to miR-197-3p to upregulate the expression of HDAC2. HDAC2 knockdown counteracted the effect of UCA1 upregulation on the viability, apoptosis and angiogenesis of HPVECs.
CONCLUSIONS: LncRNA UCA1 protected HPVECs from hypoxia-induced damage by regulating the miR-197-3p/HDAC2 axis in PIH.
METHODS: Serum samples were collected from 30 pregnant women with PIH and 30 healthy pregnant women. Serum UCA1, miR-197-3p, and histone deacetylase-2 (HDAC2) mRNA level was evaluated using quantitative polymerase chain reaction. The expression of UCA1, miR-197-3p and HDAC2 in human placental vascular endothelial cells (HPVECs) was regulated by transfection. HPVECs were treated with hypoxia reoxygenation (H/R) to establish the PIH cell model. Methyl thiazolyl tetrazolium (MTT) assay, the terminal transferase uridyl nick end labelling (Tunel) assay and tubule formation assay were performed to assess the viability, apoptosis and angiogenesis of HPVECs. Dual-luciferase reporter gene assay, RNA pull-down assay, and RNA immunoprecipitation assay were performed to identify the binding between two genes. Western blot analysis was used for protein expression detection.
RESULTS: In pregnant women with PIH, serum UCA1 and HDAC2 expression was downregulated and serum miR-197-3p expression was upregulated. H/R induction decreased the viability and angiogenesis of HPVECs, and increased the apoptosis of HPVECs. In H/R-induced HPVECs, UCA1 upregulation increased the viability and angiogenesis, and decreased the apoptosis. Downregulation of UCA1 had a contrasting result. UCA1 competitively binds to miR-197-3p to upregulate the expression of HDAC2. HDAC2 knockdown counteracted the effect of UCA1 upregulation on the viability, apoptosis and angiogenesis of HPVECs.
CONCLUSIONS: LncRNA UCA1 protected HPVECs from hypoxia-induced damage by regulating the miR-197-3p/HDAC2 axis in PIH.