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Interleukin‐1 Modulation of Human Placental Trophoblast Proliferation
Author(s) -
Athip Nilkaeo,
Suthinee Bhuvanath
Publication year - 2006
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/mi/2006/79359
Subject(s) - trophoblast , mifepristone , decidua , choriocarcinoma , cell growth , cell cycle , biology , apoptosis , microbiology and biotechnology , receptor , cell cycle checkpoint , cell culture , andrology , cancer research , placenta , pregnancy , medicine , fetus , biochemistry , genetics

During early pregnancy, interleukin-1 (IL-1) is mainly produced and secreted by maternal decidua. Yet, its biological function on placental cells is not well defined. In this study, we employed JAR choriocarcinoma cell line as a model of human placental trophoblast to study the effect of IL-1. Treatment with recombinant human IL-1 β resulted in significant inhibition of JAR proliferation ( P<.05 ) paralleled with increased cytotoxicity. The inhibitory effect was blocked by both IL-1 receptor antagonist (IL-1Ra) and antihuman IL-1 β monoclonal antibody. Analyzing the mode of action, IL-1 β was found to induce cell cycle arrest in the G0/G1 phase and triggered apoptotic cell death. These findings demonstrated that IL-1 regulates human trophoblast growth by induction of cell cycle delay and cell death.

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