Phospholipase D1 as a key enzyme for decidualization in human endometrial stromal cellsopen access
- Authors
- Yoon, Mee-Sup; Koo, Jun Bon; Jeong, Yong Geon; Kim, Yong Seok; Lee, Jung Han; Yun, Hyae Jin; Lee, Ki Sung; Han, Joong-Soo
- Issue Date
- Feb-2007
- Publisher
- OXFORD UNIV PRESS INC
- Keywords
- 8-Br-cAMP; developmental biology; decidualization; human endometrial stromal cell; phospholipase
- Citation
- BIOLOGY OF REPRODUCTION, v.76, no.2, pp.250 - 258
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOLOGY OF REPRODUCTION
- Volume
- 76
- Number
- 2
- Start Page
- 250
- End Page
- 258
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/180504
- DOI
- 10.1095/biolreprod.106.056226
- ISSN
- 0006-3363
- Abstract
- Using primary cell cultures of human endometrial stromal cells (ES cells), we investigated the role of phospholipase D (PLD) in 8-Br-cAMP-induced decidualization, which involves morphological and biological differentiation processes. When treated with 0.5 mM 8-Br-cAMP for 12 days, ES cells were transformed into a decidualized morphology and produced significant amounts of prolactin (PRL) and insulin-like growth factor-binding protein 1 (IGFBP1). Simultaneously, the activity and expression levels of PLD1 increased. In addition, removal of 8-Br-cAMP from decidualized ES cells restored the undifferentiated state, and this was accompanied by decreases in PLD1 promoter activity and PLD1 expression. Overexpression of dominant negative (DN)-PLD1 inhibited the morphological changes induced by 0.5 mM 8-Br-cAMP, whereas PLD1 overexpression induced morphological changes in the absence of 0.5 mM 8-Br-cAMP treatment. Moreover, knockdown of PLD1 by siRNA and blockage of PLD by treatment with 0.3 % 1-butanol decreased PRL/IGFBP1 mRNA expression, whereas PLD1 overexpression increased PRL/IGFBP1 mRNA expression. Treatment of ES cells with phosphatidic acid (PA) for 3 days induced PRL mRNA expression and morphological changes, which implies that PA is an end-product of PLD activation-induced decidualization. In addition, pretreatment of ES cells with mepacrine decreased PRL/IGFBP1 expression and inhibited morphological change, whereas pretreatment with propranolol caused no changes, as compared to cAMP-treated cells, which suggests that PA induces decidualization through phospholipase A2 (PLA2G1B). Taken together, these results suggest that PLD1 regulates 8-Br-cAMP-induced decidualization through PLA2G1B, and that PLD1 upregulation is essential for the decidualization of ES cells.
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