Q-j Wang1, B-f Song2, Y-h Zhang3, Y-y Ma4, Q-q Shao5, J Liu6, X Qu7. 1. Institute of Basic Medical Sciences, Qilu Hospital, Shandong University, Jinan 250012, Shandong, People's Republic of China. Electronic address: wqj_1025@163.com. 2. Institute of Basic Medical Sciences, Qilu Hospital, Shandong University, Jinan 250012, Shandong, People's Republic of China. Electronic address: bfsong1984@163.com. 3. National Key Disciplines of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan 250012, Shandong, People's Republic of China; Department of Obstetrics and Gynecology, Fourth People's Hospital of Jinan, Jinan 250031, Shandong, People's Republic of China. Electronic address: azmax@126.com. 4. National Key Disciplines of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan 250012, Shandong, People's Republic of China. Electronic address: mayuyanqilu@126.com. 5. Institute of Basic Medical Sciences, Qilu Hospital, Shandong University, Jinan 250012, Shandong, People's Republic of China. Electronic address: qianqian851230@163.com. 6. Institute of Basic Medical Sciences, Qilu Hospital, Shandong University, Jinan 250012, Shandong, People's Republic of China. Electronic address: liujia7096@163.com. 7. Institute of Basic Medical Sciences, Qilu Hospital, Shandong University, Jinan 250012, Shandong, People's Republic of China. Electronic address: quxun@sdu.edu.cn.
Abstract
INTRODUCTION: Preeclampsia (PE) is a pregnancy-specific complication and it is related to insufficient extravillous trophoblast invasion. To date, the pathophysiology of PE has not yet been fully elucidated. Response gene to complement 32 (RGC32) is a novel cellular protein, and it plays important roles in the regulation of cell differentiation, angiogenesis, migration, and invasion. This study aimed to determine the RGC32 expression and function in human placentas and to explore the underlying mechanisms. METHODS: RGC32 expression in term placentas collected after cesarean section from pregnant women with PE and normal pregnant women was determined by real-time reverse transcriptase polymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry. The effects of RGC32 expression on trophoblast invasion, migration, and the underlying mechanisms were studied in HTR8/SVneo cells. RESULTS: The messenger RNA (mRNA) and protein levels of RGC32 were significantly downregulated in preeclamptic placentas compared with normal controls (P < 0.05). RGC32 silencing significantly inhibited HTR8/SVneo cell migration and invasion (P < 0.001, respectively). These effects were associated with decreased activities and expression of matrix metalloproteinase (MMP)-2/9, and with the reduced phosphorylation level of Akt. DISCUSSION: RGC32 may play important roles in the pathophysiology of PE by directly affecting the invasion/migration of trophoblast.
INTRODUCTION: Preeclampsia (PE) is a pregnancy-specific complication and it is related to insufficient extravillous trophoblast invasion. To date, the pathophysiology of PE has not yet been fully elucidated. Response gene to complement 32 (RGC32) is a novel cellular protein, and it plays important roles in the regulation of cell differentiation, angiogenesis, migration, and invasion. This study aimed to determine the RGC32 expression and function in human placentas and to explore the underlying mechanisms. METHODS:RGC32 expression in term placentas collected after cesarean section from pregnant women with PE and normal pregnant women was determined by real-time reverse transcriptase polymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry. The effects of RGC32 expression on trophoblast invasion, migration, and the underlying mechanisms were studied in HTR8/SVneo cells. RESULTS: The messenger RNA (mRNA) and protein levels of RGC32 were significantly downregulated in preeclamptic placentas compared with normal controls (P < 0.05). RGC32 silencing significantly inhibited HTR8/SVneo cell migration and invasion (P < 0.001, respectively). These effects were associated with decreased activities and expression of matrix metalloproteinase (MMP)-2/9, and with the reduced phosphorylation level of Akt. DISCUSSION: RGC32 may play important roles in the pathophysiology of PE by directly affecting the invasion/migration of trophoblast.
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