TY - JOUR
T1 - Proliferation of mouse endometrial stromal cells in culture is highly sensitive to lysophosphatidic acid signaling
AU - Aikawa, Shizu
AU - Kano, Kuniyuki
AU - Inoue, Asuka
AU - Aoki, Junken
N1 - Funding Information:
We thank Ono pharmaceutical Co., Ltd for the gift of the ATX inhibitor ONO-8430506. The present work was supported partly by AMED-CREST (Japan Agency for Medical Research and Development, Core Research for Evolutional Science and Technology) for J.A., PRESTO (Japan Science and Technology Agency, Precursory Research for Embryonic Science and Technology) for A.I., Ministry of Education, Culture, Sports, Science and Technology (MEXT) Grant-in-Aid for Scientific Research for J.A (grant number 22116004).
Publisher Copyright:
© 2016
PY - 2017/2/26
Y1 - 2017/2/26
N2 - Endometrial stromal cells (ESCs) proliferate rapidly both in vivo and in vitro. Here we show that proliferation of ESCs in vitro is strongly dependent on lysophosphatidic acid (LPA) signaling. LPA is produced by autotaxin (ATX) and induces various kinds of cellular processes including migration, proliferation and inhibition of cell death possibly through six G protein-coupled receptors (LPA1-6). We found that ESCs proliferated rapidly in vitro in an autocrine manner and that the proliferation was prominently suppressed by either an ATX inhibitor (ONO-8430506) or an LPA1/3 antagonist (Ki16425). Among the cells lines tested, mouse ESCs were the most sensitive to these inhibitors. Proliferation of ESCs isolated from either LPA1- or LPA3-deficient mice was comparable to proliferation of ESCs isolated from control mice. An LPA receptor antagonist (AM095), which was revealed to be a dual LPA1/LPA3 antagonist, also suppressed the proliferation of ESCs. The present results show that LPA signaling has a critical role in the proliferation of ESCs, and that this role is possibly mediated redundantly by LPA1 and LPA3.
AB - Endometrial stromal cells (ESCs) proliferate rapidly both in vivo and in vitro. Here we show that proliferation of ESCs in vitro is strongly dependent on lysophosphatidic acid (LPA) signaling. LPA is produced by autotaxin (ATX) and induces various kinds of cellular processes including migration, proliferation and inhibition of cell death possibly through six G protein-coupled receptors (LPA1-6). We found that ESCs proliferated rapidly in vitro in an autocrine manner and that the proliferation was prominently suppressed by either an ATX inhibitor (ONO-8430506) or an LPA1/3 antagonist (Ki16425). Among the cells lines tested, mouse ESCs were the most sensitive to these inhibitors. Proliferation of ESCs isolated from either LPA1- or LPA3-deficient mice was comparable to proliferation of ESCs isolated from control mice. An LPA receptor antagonist (AM095), which was revealed to be a dual LPA1/LPA3 antagonist, also suppressed the proliferation of ESCs. The present results show that LPA signaling has a critical role in the proliferation of ESCs, and that this role is possibly mediated redundantly by LPA1 and LPA3.
KW - Autotaxin
KW - Endometrial stromal cell
KW - G protein-coupled receptor
KW - Lysophosphatidic acid
KW - Primary culture
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U2 - 10.1016/j.bbrc.2016.12.154
DO - 10.1016/j.bbrc.2016.12.154
M3 - Article
C2 - 28073697
AN - SCOPUS:85010928054
VL - 484
SP - 202
EP - 208
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 1
ER -