RISS 검색 - 국내학술지논문 상세보기

부가정보

다국어 초록 (Multilingual Abstract)

Objective: Abnormal development or disruption of lymphatic vasculature has been implicated in metabolic disease or hypertensive diseases. Recent evidence suggests that offspring delivered from pregnancy complicated with preeclampsia remains increased risk for long-term, adulthood issues such as cardiovascular and metabolic diseases due to in utero fetal programming. We aim to investigate functional impairment of lymphatic endothelial progenitor cell in offspring born to preeclamptic mother.
Methods: Human umbilical cord blood lymphatic endothelial progenitor cells (LEPCs) were purified with anti-VEGFR3/Pod/CD11b microbeads using a magnetic cell sorter device in severe preeclampsia (n=10) and gestationally matched normal pregnant women (n=10) were retrospectively analyzed. Differentiation of progenitor cells to lymphatic endothelial cells (LECs) was assessed by morphology, differentiation day and the number of colonies using light microscopy in both groups. Lymph-angiogenic function of LECs differentiated was evaluated by migration, adhesion and 3D-sprouting assay.
Results: Differentiation day of LEPCs was significantly delayed (9 vs 15 days; p<0.05) and the number of LEC colonies were significantly reduced in preeclampsia compared with normal pregnancy. In addition, activity of migration, adhesion and 3D-sprouting of LECs was diminished in preeclampsia. Moreover, LEC from preeclampsia showed the increased lymphatic permeability by disorganizing VE-cadherin junctions. In vivo lymphangiogenic function of LEPC in matrigel plug of mouse was significantly decreased in preeclampsia compared with normal pregnancy.
Conclusion: In preeclampsia, differentiation potency of LEPCs to LECs was reduced and lymph-angiogenic function of LECs was significantly diminished in preeclampsia in vitro and in vivo.
Acknowledgements: This study was supported by National Research Foundation grant (NRF-2016R1D1A1B03933337, NRF-2017R1D1A1B03029081)