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Complement 5a-mediated trophoblasts dysfunction is involved in the development of pre-eclampsia

文献类型：期刊论文

作者Ma, Yu2,3; Kong, Ling-Ran2,3; Ge, Qian2,3; Lu, Yuan-Yuan2,3; Hong, Mo-Na2,3; Ruan, Cheng-Chao2,3; Gao, Ping-Jin1,2,3,5,6; Zhang, Yu4; Ruan, Cheng-Chao1,5,6; ,
刊名JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
出版日期2018
卷号22期号:2页码:1034-1046
ISSN号1582-4934
关键词pre-eclampsia complement 5a C5a receptor placenta trophoblasts angiogenesis arterial stiffness
DOI10.1111/jcmm.13466
文献子类Article
英文摘要Pre-eclampsia (PE) is a life-threatening multisystem disorder leading to maternal and neonatal mortality and morbidity. Emerging evidence showed that activation of the complement system is implicated in the pathological processes of PE. However, little is known about the detailed cellular and molecular mechanism of complement activation in the development of PE. In this study, we reported that complement 5a (C5a) plays a pivotal role in aberrant placentation, which is essential for the onset of PE. We detected an elevated C5a deposition in macrophages and C5a receptor (C5aR) expression in trophoblasts of pre-eclamptic placentas. Further study showed that C5a stimulated trophoblasts towards an anti-angiogenic phenotype by mediating the imbalance of angiogenic factors such as soluble fms-like tyrosine kinase 1 (sFlt1) and placental growth factor (PIGF). Additionally, C5a inhibited the migration and tube formation of trophoblasts, while, C5aR knockdown with siRNA rescued migration and tube formation abilities. We also found that maternal C5a serum level was increased in women with PE and was positively correlated with maternal blood pressure and arterial stiffness. These results demonstrated that the placental C5a/C5aR pathway contributed to the development of PE by regulating placental trophoblasts dysfunctions, suggesting that C5a may be a novel therapeutic possibility for the disease.
学科主题Cell Biology ; Research & Experimental Medicine
WOS关键词PULSE-WAVE VELOCITY ; ARTERIAL STIFFNESS ; NORMAL-PREGNANCY ; INDUCED HYPERTENSION ; MEDIATED INHIBITION ; PLACENTAL ISCHEMIA ; URINARY-EXCRETION ; VASCULAR INJURY ; ACTIVATION ; C5A
语种英语
出版者WILEY
WOS记录号WOS:000423361500031
版本出版稿
源URL[http://202.127.25.144/handle/331004/649]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Shanghai Jiao Tong Univ, Sch Med, Shanghai, Peoples R China,
2.Shanghai Jiao Tong Univ, Sch Med, State Key Lab Med Genom, Shanghai Key Lab Hypertens,Dept Hypertens,Ruijin, Shanghai, Peoples R China;
3.Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Hypertens, Shanghai, Peoples R China;
4.Shanghai Jiao Tong Univ, Ren Ji Hosp, Dept Obstet & Gynecol, Sch Med, Shanghai, Peoples R China;
5.Chinese Acad Sci, Shanghai Inst Biol Sci, Lab Vasc Biol, Inst Hlth Sci, Shanghai, Peoples R China;
6.Chinese Acad Sci, Shanghai Inst Biol Sci, Key Lab Stem Cell Biol, Inst Hlth Sci, Shanghai, Peoples R China;
推荐引用方式
GB/T 7714		 Ma, Yu,Kong, Ling-Ran,Ge, Qian,et al. Complement 5a-mediated trophoblasts dysfunction is involved in the development of pre-eclampsia[J]. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,2018,22(2):1034-1046.
APA Ma, Yu.,Kong, Ling-Ran.,Ge, Qian.,Lu, Yuan-Yuan.,Hong, Mo-Na.,...&,.(2018).Complement 5a-mediated trophoblasts dysfunction is involved in the development of pre-eclampsia.JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,22(2),1034-1046.
MLA Ma, Yu,et al."Complement 5a-mediated trophoblasts dysfunction is involved in the development of pre-eclampsia".JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 22.2(2018):1034-1046.

入库方式： OAI收割

来源：上海营养与健康研究所

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