J Jiang1, Z-M Zhao. 1. Department of Obstetric, The Second People's Hospital of Liaocheng, Linqing, China. ywjm6u98651026@163.com.
Abstract
OBJECTIVE: To investigate the role of HOXD-AS1 in preeclampsia and its underlying mechanism. PATIENTS AND METHODS: A total of 50 preeclampsia primiparas and 34 normal pregnancies admitted in our hospital from July 2015 to July 2017 were selected as the study group and control group, respectively. Age, body weight, blood pressure, 24-h urinary protein and neonatal weight were compared between the two groups. HOXD-AS1 expression in the placenta tissues was detected by quantitative Real-time PCR (qRT-PCR). Preeclampsia patients were further assigned into high and low expression group according to their HOXD-AS1 expressions. The relationship between HOXD-AS1 expression and blood pressure, 24-h urinary protein and neonatal weight in preeclampsia patients were analyzed. For in vitro experiments, transfection efficacy of pcDNA-HOXD-AS1 and si-HOXD-AS1 were detected by qRT-PCR. Proliferative and colony formation abilities in BeWo and Wish cells were detected by CCK-8 and colony formation assay, respectively. Moreover, protein expressions of p-p38, p-JNK, and p-ERK were detected by Western blot. RESULTS: The systolic blood pressure, diastolic blood pressure and urinary protein in preeclampsia patients were higher than those of normal pregnancies. However, neonatal weight in preeclampsia patients was lower than that of normal pregnancies. HOXD-AS1 expressions were gradually increased in normal pregnancies, patients with late onset preeclampsia and patients with early onset preeclampsia sequentially. Additionally, higher levels of systolic pressure, diastolic pressure and 24-h urinary protein, as well as lower neonatal weight, were observed in preeclampsia patients with high expression of HOXD-AS1 than those with low expression. In vitro results demonstrated that proliferative and colony formation abilities in trophoblasts were elevated after HOXD-AS1 knockdown. Western blot data illustrated that protein expressions of p-p38 and p-JNK were decreased, while p-ERK expression was increased after overexpression of HOXD-AS1 in trophoblasts. CONCLUSIONS: HOXD-AS1 participates in the development and progression of preeclampsia by regulating trophoblast proliferation via the MAPK pathway.
OBJECTIVE: To investigate the role of HOXD-AS1 in preeclampsia and its underlying mechanism. PATIENTS AND METHODS: A total of 50 preeclampsia primiparas and 34 normal pregnancies admitted in our hospital from July 2015 to July 2017 were selected as the study group and control group, respectively. Age, body weight, blood pressure, 24-h urinary protein and neonatal weight were compared between the two groups. HOXD-AS1 expression in the placenta tissues was detected by quantitative Real-time PCR (qRT-PCR). Preeclampsiapatients were further assigned into high and low expression group according to their HOXD-AS1 expressions. The relationship between HOXD-AS1 expression and blood pressure, 24-h urinary protein and neonatal weight in preeclampsiapatients were analyzed. For in vitro experiments, transfection efficacy of pcDNA-HOXD-AS1 and si-HOXD-AS1 were detected by qRT-PCR. Proliferative and colony formation abilities in BeWo and Wish cells were detected by CCK-8 and colony formation assay, respectively. Moreover, protein expressions of p-p38, p-JNK, and p-ERK were detected by Western blot. RESULTS: The systolic blood pressure, diastolic blood pressure and urinary protein in preeclampsiapatients were higher than those of normal pregnancies. However, neonatal weight in preeclampsiapatients was lower than that of normal pregnancies. HOXD-AS1 expressions were gradually increased in normal pregnancies, patients with late onset preeclampsia and patients with early onset preeclampsia sequentially. Additionally, higher levels of systolic pressure, diastolic pressure and 24-h urinary protein, as well as lower neonatal weight, were observed in preeclampsiapatients with high expression of HOXD-AS1 than those with low expression. In vitro results demonstrated that proliferative and colony formation abilities in trophoblasts were elevated after HOXD-AS1 knockdown. Western blot data illustrated that protein expressions of p-p38 and p-JNK were decreased, while p-ERK expression was increased after overexpression of HOXD-AS1 in trophoblasts. CONCLUSIONS:HOXD-AS1 participates in the development and progression of preeclampsia by regulating trophoblast proliferation via the MAPK pathway.