http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Quan Limei (검색결과 1 건)
- 무료
- 기관 내 무료
- 유료
-
Quan Limei,Jin Yan,Wang Jianfang,Dai Xiwang,Zhu Shuli,Sheng Zengwei 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.2
Background PE is a common pregnancy disease that can cause various pathologies in pregnant women. GEO microarray data revealed low expression of FGD5-AS1 in placenta tissues from patients with severe PE. As predicted by ENCORI, FGD5-AS1 sponges miR-16-5p, and IGF2, and promotes cell proliferation, differentiation, and metabolism. Objectives This study aimed to interrogate the interaction of FGD5-AS1/miR-16-5p/IGF2 axis and the mechanism of FGD5-AS1 in hypoxia-induced trophoblast cell injury. Results Our findings revealed that FGD5-AS1 and IGF2 were substantially decreased in PE patients than that in normal pregnant females, whereas miR-16-5p was increased in PE patients than that in normal pregnant females. In vitro studies showed that FGD5-AS1 were reduced in trophoblast cells after hypoxia treatment, accompanied by decreased viability and increased apoptosis, also reduced invasion, migration and angiogenesis. However, FGD5-AS1 overexpression substantially reversed these effects. Further mechanistic analysis showed that FGD5-AS1 could target miR-16-5p to regulate IGF2. FGD5-AS1 promoted the expression of IGF2 by sponging miR-16-5p, thereby increasing the viability of trophoblast cells after hypoxia treatment and promoting invasion and migration. Conclusion Overall, our findings demonstrated that FGD5-AS1 promoted growth and mobility of trophoblast cells by regulating miR-16-5p/IGF2 axis in PE.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
