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Cannabinoid receptor I activation markedly inhibits human decidualization.

Abstract：

:The role of cannabinoid receptor I (CBR-1) in the induction of decidualization was examined using decidual fibroblasts and human endometrial stromal cells as model systems. Decidual fibroblasts decidualized in vitro for 3 and 6 days in the presence of the CBR-1 agonist R(+)-WIN 55,212-2 mesylate (WIN, 0.1-10 microM) expressed less of the decidualization-specific markers prolactin, CBR-1, forkhead (FKHR), TIMP-3, laminin, endometrial bleeding associated factor (EBAF), decorin and insulin-like growth factor binding protein-1 (IGFBP-1) mRNA levels compared to control cells. The maximal decrease for each transcript was in the range of 50-99%. In contrast, cells exposed to the CBR-1 inhibitor AM-251 (1 microM) expressed about two-fold higher levels of the decidualization-specific marker gene mRNAs. The WIN-exposed cells showed a marked decrease in intracellular cAMP levels and a progressive, concentration-dependent increase in DNA fragmentation (TUNEL assay) and caspase 3 levels during decidualization compared to control cells. These studies strongly suggest that activation of CBR-1 inhibits human decidualization and stimulates apoptosis by a cAMP-dependent mechanism.

journal_name

Mol Cell Endocrinol

journal_title

Molecular and cellular endocrinology

authors

Moghadam KK,Kessler CA,Schroeder JK,Buckley AR,Brar AK,Handwerger S

doi

10.1016/j.mce.2004.09.007

keywords:

subject

Has Abstract

pub_date

2005-01-14 00:00:00

pages

65-74

issue

1-2

eissn

0303-7207

issn

1872-8057

pii

S0303-7207(04)00376-4

journal_volume

229

pub_type

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