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    Leukemia inhibitory factor promotes human first trimester extravillous trophoblast adhesion to extracellular matrix and secretion of tissue inhibitor of metalloproteinases-1 and -2

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    Author
    Tapia, A; Salamonsen, LA; Manuelpillai, U; Dimitriadis, E
    Date
    2008-08-01
    Source Title
    Human Reproduction
    Publisher
    OXFORD UNIV PRESS
    University of Melbourne Author/s
    Dimitriadis, Evdokia
    Affiliation
    Obstetrics and Gynaecology
    Metadata
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    Document Type
    Journal Article
    Citations
    Tapia, A., Salamonsen, L. A., Manuelpillai, U. & Dimitriadis, E. (2008). Leukemia inhibitory factor promotes human first trimester extravillous trophoblast adhesion to extracellular matrix and secretion of tissue inhibitor of metalloproteinases-1 and -2. HUMAN REPRODUCTION, 23 (8), pp.1724-1732. https://doi.org/10.1093/humrep/den121.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257241
    DOI
    10.1093/humrep/den121
    Abstract
    BACKGROUND: Leukemia inhibitory factor (LIF) is a pleiotropic cytokine that is essential for blastocyst implantation in mice. It has been suggested that LIF may play a role in human first trimester extravillous trophoblast (EVT) invasion. The aim of the present study was to establish whether LIF induces changes in EVT function related to invasiveness. METHODS: Primary first trimester human EVT cell cultures were treated with/without LIF and the effects on cell adhesion to fibronectin (FN), vitronectin (VN) and laminin (LN) were assessed. Transcript levels of integrin subunits that mediate cell adhesion to these extracellular matrix (ECM) elements were determined by real-time RT-PCR. Matrix metalloproteinase (MMP)2 and MMP9 secretion was assessed by gelatine zymography and tissue inhibitors matrix metalloproteinase (TIMP) -1 and TIMP-2 secretion by enzyme-linked immunosorbent assay. RESULTS: EVT cells showed increased adhesion to FN, VN and LN ECM elements in response to LIF (20, 20 and 29%, respectively, P < 0.05 FN and VN compared to control; and P < 0.001 LN compared to control). Integrin beta(4) mRNA levels decreased by 50% following LIF treatment (P < 0.001 versus control). MMP2 and MMP9 secretion was not affected by LIF but LIF did increase secretion of TIMP-1 and -2 (P < 0.001 versus control). LIF stimulated the phosphorylation of signal transducer and activator of transcription (STAT) 3 protein while it did not affect STAT3 protein abundance. The addition of a LIF inhibitor attenuated the LIF-induced STAT3 phosphorylation in EVT. CONCLUSION: The results suggest that LIF can regulate EVT invasion, suggesting an important role in early placental development.

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