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. 2005 Jan 14;229(1-2):65-74.
doi: 10.1016/j.mce.2004.09.007.

Cannabinoid receptor I activation markedly inhibits human decidualization

Kenneth K Moghadam  1 , Cherie A Kessler, Jennifer K Schroeder, Arthur R Buckley, Anoop K Brar, Stuart Handwerger
Affiliations

Cannabinoid receptor I activation markedly inhibits human decidualization

Kenneth K Moghadam et al. Mol Cell Endocrinol. .

Erratum in

  • Mol Cell Endocrinol. 2009 Apr 10;302(1):108

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.

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