Molecular mechanism of the effect of angiopoietin-like protein 8 on the proliferation, invasion and migration of placental trophoblasts in preeclampsia.
angiopoietin-like protein 8
invasion
migration
preeclampsia
proliferation
trophoblast cells
Journal
Experimental and therapeutic medicine
ISSN: 1792-0981
Titre abrégé: Exp Ther Med
Pays: Greece
ID NLM: 101531947
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
10
06
2019
accepted:
28
11
2019
entrez:
30
4
2020
pubmed:
30
4
2020
medline:
30
4
2020
Statut:
ppublish
Résumé
Preeclampsia (PE) is a pregnancy-specific systemic disorder characterized by various manifestations of organ dysfunction. Inadequate trophoblastic invasion of the uterine wall is involved in the pathogenesis of PE. Angiopoietin-like protein 8 (ANGPTL8) serves an important role in cardiovascular disease development and may have a potential effect on cell proliferation. In the present study, downregulation of ANGPTL8 promoted cell proliferation, decreased p21 expression, and increased the expression levels of cyclin-dependent kinase 2 and proliferating cell nuclear antigen in HTR8/SVneo cells. Silencing of ANGPTL8 led to significant acceleration in cell migration and invasion, and markedly enhanced the matrix metalloproteinase (MMP)-2 and MMP-9 expression levels. In addition, the protein expression levels of tissue inhibitor of matrix metalloproteinase (TIMP)-1 and TIMP-2 were decreased in the group transfected with small interfering RNA (si)-ANGPTL8-1 as compared with those in the control and si-negative control groups. Taken together, these results indicated that ANGPTL8 downregulation promoted the proliferation, migration and invasion of trophoblast cells. Thus, ANGPTL8 suppresses the viability, proliferation, migration and invasion of trophoblast cells, and may be a potential therapeutic target for the clinical treatment of PE.
Identifiants
pubmed: 32346407
doi: 10.3892/etm.2020.8647
pii: ETM-0-0-8647
pmc: PMC7185091
doi:
Types de publication
Journal Article
Langues
eng
Pagination
3461-3468Informations de copyright
Copyright: © Wang et al.
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