Anandamide restricts uterine stromal differentiation and is critical for complete decidualization

• Type: Article in International Scientific Journal
• Date: 2015

Authors

Fonseca, SM (Author) Other; Correia da Silva, G (Author) FFUP; Teixeira, NA (Author) FFUP

Journal

Title: Molecular and Cellular Endocrinology

Vol. 411

Pages: 167-176

ISSN: 0303-7207

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 9 Citations

Scopus - 15 Citations

Scientific classification

FOS: Medical and Health sciences > Clinical medicine

Other information

Authenticus ID: P-00G-5T2

DOI: 10.1016/j.mce.2015.04.024

Abstract (EN): The major endocannabinoid, anandamide (AEA), is widely distributed in the body, especially in the reproductive tissues, where it is implicated in early pregnancy events, particularly during implantation period. Although AEA is synthesized in decidual cells and showed to induce apoptosis through CBI receptor, its roles in decidualization remain to be elucidated. This study examined the effect of AEA in the progression of decidualization both in vitro and in vivo and explored the involvement of COX-2 in its action. To determine the function of AEA during this differentiation process, we employed a primary culture system in which undifferentiated stromal cells isolated from pregnant rat uterus undergo decidualization. AEA treatment markedly interfered with the differentiation program, as revealed by alpha 2-macroglobulin (alpha 2-MG) expression and alkaline phosphatase activity. Additionally, it was evaluated the effects of AEA in decidual establishment in the pseudopregnant rat model. The abundance of AEA in the uterine lumen disrupted the decidualization process accompanied by a decreased expression of COX-2 and VEGF. It was also observed that uterine lumen, which failed the progression of decidualization in response to AEA, also presented lower expression of NAPE-PLD and FAAH. Thus, the mechanisms by which AEA inhibits decidualization can be either via direct actions on stromal cell differentiation within the reproductive tract system or by the inhibition of COX-2 derived products and, consequently, the vascular remodeling required to proper decidualization. In addition, the previous observations showing that higher AEA levels in pre-implantation sites are hostile to blastocyst survival may result from problems in decidual cell reaction more than with implantation failure.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 10