Linked Life Data

18063683

Source:http://linkedlifedata.com/resource/pubmed/id/18063683

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-2-22
pubmed:abstractText
Chorionic gonadotropin (CG) is indispensable for human pregnancy because it controls implantation, decidualization, and placental development. However, its particular role in the differentiation process of invasive trophoblasts has not been fully unraveled. Here we demonstrate that the hormone promotes trophoblast invasion and migration in different trophoblast model systems. RT-PCR and Western blot analyses revealed expression of the LH/CG receptor in trophoblast cell lines and different trophoblast primary cultures. In vitro, CG increased migration and invasion of trophoblastic SGHPL-5 cells through uncoated and Matrigel-coated transwells, respectively. The hormone also increased migration of first-trimester villous explant cultures on collagen I. Proliferation of the trophoblast cell line and villous explant cultures measured by cumulative cell numbers and in situ 5-bromo-2'-deoxyuridine labeling, respectively, was unaffected by CG. Addition of the hormone activated ERK-1/2 and AKT in SGHPL-5 cells and pure, extravillous trophoblasts. Inhibition of MAPK kinase/ERK and phosphatidylinositide 3-kinase/AKT blocked phosphorylation of the kinases and attenuated CG-dependent invasion of SGHPL-5 cells. Similarly, the inhibitors decreased hormone-stimulated migration in villous explant cultures. Western blot analyses and gelatin zymography suggested that CG increased matrix metalloproteinase (MMP)-2 protein levels and activity in both culture systems. Inhibition of ERK or AKT diminished CG-induced MMP-2 expression. In summary, the data demonstrate that CG promotes trophoblast invasion and migration through activation of ERK and AKT signaling involving their downstream effector MMP-2. Because the increase of CG during the first trimester of pregnancy correlates with rising trophoblast motility, the hormone could be a critical regulator of the early invasion process.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
149
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
979-87
pubmed:dateRevised
2011-4-6
pubmed:meshHeading
pubmed-meshheading:18063683-Cell Movement, pubmed-meshheading:18063683-Cell Proliferation, pubmed-meshheading:18063683-Cells, Cultured, pubmed-meshheading:18063683-Chorionic Gonadotropin, pubmed-meshheading:18063683-Female, pubmed-meshheading:18063683-Humans, pubmed-meshheading:18063683-Luteinizing Hormone, pubmed-meshheading:18063683-Matrix Metalloproteinase 2, pubmed-meshheading:18063683-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:18063683-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:18063683-Phosphorylation, pubmed-meshheading:18063683-Pregnancy, pubmed-meshheading:18063683-Proto-Oncogene Proteins c-akt, pubmed-meshheading:18063683-Receptors, LH, pubmed-meshheading:18063683-Reproductive Control Agents, pubmed-meshheading:18063683-Signal Transduction, pubmed-meshheading:18063683-Trophoblasts
pubmed:year
2008
pubmed:articleTitle
Human chorionic gonadotropin stimulates trophoblast invasion through extracellularly regulated kinase and AKT signaling.
pubmed:affiliation
Department of Obstetrics and Fetal-Maternal Medicine, Reproductive Biology Unit, Medical University of Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't