Liuyan Jiang1, Meiyan Li1, Haisi Gan1, Li Yang1, Fengjuan Lin1, Min Hu2. 1. Department of Obstetrics, The Affiliated Hospital of Youjiang Medical University for Nationalities Baise, Guangxi Zhuang Autonomous Region, China. 2. Department of Obstetrics, Liuzhou Worker's Hospital, The Forth Affiliated Hospital of Guangxi Medical University Liuzhou, Guangxi Zhuang Autonomous Region, China.
Abstract
OBJECTIVE: To investigate the role of miRNA-335 on the proliferation and apoptosis of placental trophoblast cells in preeclamptic rats and its potential mechanism. METHODS: Placental trophoblast cells were isolated from preeclamptic model rats and normal ones. Trophoblast cells from the model group were divided into six groups for transfection: the blank (empty vector) group, the NC (negative control) group, the miRNA-335 mimic group, the miRNA-335 inhibitor group, the CRIM1 (overexpressed recombinant plasmid) group, and the miRNA-335 inhibitor + CRIM1 group. The miRNA-335 expressions after the transfection were determined using qRT-PCR. The mRNA and protein expressions of CRIM1, the transforming growth factor (TGF-β1), and the apoptosis-related factors (Bax and Bcl-2) in each group were determined using qRT-PCR and Western blotting. The cell proliferation and apoptosis were determined using MTT assays and flow cytometry, respectively. RESULTS: Compared with normal rats, the systolic blood pressure, diastolic blood pressure, and urinary protein levels were increased in the model rats, which had increased miRNA-335 expressions, but a decreased CRIM1 expressions (all P<0.05). The inhibition of miRNA-335 promoted the expressions of CRIM1, TGF-β1, and Bcl-2 and inhibited the expression of Bax in trophoblast cells (all P<0.05). miRNA-335 inhibition or CRIM1 over-expression promoted the proliferation and reduced the apoptosis of trophoblast cells. The combined effect of miRNA-335 inhibition or CRIM1 over-expression had an even more significant effect on the changes in the above indicators (all P<0.05). CONCLUSION: miRNA-335 inhibition can enhance the expression of CRIM1 to promote the proliferation and reduce the apoptosis of trophoblast cells in preeclamptic rats. AJTR
OBJECTIVE: To investigate the role of miRNA-335 on the proliferation and apoptosis of placental trophoblast cells in preeclamptic rats and its potential mechanism. METHODS: Placental trophoblast cells were isolated from preeclamptic model rats and normal ones. Trophoblast cells from the model group were divided into six groups for transfection: the blank (empty vector) group, the NC (negative control) group, the miRNA-335 mimic group, the miRNA-335 inhibitor group, the CRIM1 (overexpressed recombinant plasmid) group, and the miRNA-335 inhibitor + CRIM1 group. The miRNA-335 expressions after the transfection were determined using qRT-PCR. The mRNA and protein expressions of CRIM1, the transforming growth factor (TGF-β1), and the apoptosis-related factors (Bax and Bcl-2) in each group were determined using qRT-PCR and Western blotting. The cell proliferation and apoptosis were determined using MTT assays and flow cytometry, respectively. RESULTS: Compared with normal rats, the systolic blood pressure, diastolic blood pressure, and urinary protein levels were increased in the model rats, which had increased miRNA-335 expressions, but a decreased CRIM1 expressions (all P<0.05). The inhibition of miRNA-335 promoted the expressions of CRIM1, TGF-β1, and Bcl-2 and inhibited the expression of Bax in trophoblast cells (all P<0.05). miRNA-335 inhibition or CRIM1 over-expression promoted the proliferation and reduced the apoptosis of trophoblast cells. The combined effect of miRNA-335 inhibition or CRIM1 over-expression had an even more significant effect on the changes in the above indicators (all P<0.05). CONCLUSION: miRNA-335 inhibition can enhance the expression of CRIM1 to promote the proliferation and reduce the apoptosis of trophoblast cells in preeclamptic rats. AJTR
Authors: Emilie M Herzog; Alex J Eggink; Anniek Reijnierse; Martina A M Kerkhof; Ronald R de Krijger; Anton J M Roks; Irwin K M Reiss; Alex L Nigg; Paul H C Eilers; Eric A P Steegers; Régine P M Steegers-Theunissen Journal: Placenta Date: 2016-11-27 Impact factor: 3.481