microRNA-140-5p from human umbilical cord mesenchymal stem cells-released exosomes suppresses preeclampsia
Yan Jiang1, Ting Luo1, Qiang Xia2
1Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, No.238 Jiefang Road, Wuchang, Wuhan, 430000, Hubei, China.
This work unraveled the action of human umbilical cord mesenchymal stem cells-released exosomes (huc-MSCs-EXO) transfer of miR-140-5p in preeclampsia (PE). miR-140-5p and follistatin-like 3 (FSTL3) expression in placental tissues of PE patients was tested. EXO were isolated from huc-MSCs. Hypoxic trophoblast cells were co-cultured with huc-MSCs-EXO. Cell biological functions, angiogenesis, and inflammation were evaluated. Suppressed miR-140-5p and induced FSTL3 levels were measured in PE. Huc-MSCs-EXO drove biological functions and angiogenesis while hindering inflammation in hypoxic trophoblast cells. Increasing miR-140-5p further improved the positive role of huc-MSCs-EXO for hypoxic trophoblast cells, but the miR-140-5p-mediated effect in hypoxic trophoblast cells was abrogated by overexpressing FSTL3. miR-140-5p from huc-MSCs-EXO suppresses PE through repressing FSTL3.
This work unraveled the action of human umbilical cord mesenchymal stem cells-released exosomes (huc-MSCs-EXO) transfer of miR-140-5p in preeclampsia (PE). miR-140-5p and follistatin-like 3 (FSTL3) expression in placental tissues of PE patients was tested. EXO were isolated from huc-MSCs. Hypoxic trophoblast cells were co-cultured with huc-MSCs-EXO. Cell biological functions, angiogenesis, and inflammation were evaluated. Suppressed miR-140-5p and induced FSTL3 levels were measured in PE. Huc-MSCs-EXO drove biological functions and angiogenesis while hindering inflammation in hypoxic trophoblast cells. Increasing miR-140-5p further improved the positive role of huc-MSCs-EXO for hypoxic trophoblast cells, but the miR-140-5p-mediated effect in hypoxic trophoblast cells was abrogated by overexpressing FSTL3. miR-140-5p from huc-MSCs-EXO suppresses PE through repressing FSTL3.
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