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Anandamide restricts uterine stromal differentiation and is critical for complete decidualization.
Mol Cell Endocrinol. 2015 Aug 15; 411:167-76.MC

Abstract

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 CB1 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 α2-macroglobulin (α2-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.

Authors+Show Affiliations

UCIBIO, REQUIMTE, Laboratório de Bioquímica, Departamento Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal.UCIBIO, REQUIMTE, Laboratório de Bioquímica, Departamento Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal.UCIBIO, REQUIMTE, Laboratório de Bioquímica, Departamento Ciências Biológicas, Faculdade de Farmácia, Universidade do Porto, Porto, Portugal. Electronic address: natercia@ff.up.pt.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25960165

Citation

Fonseca, B M., et al. "Anandamide Restricts Uterine Stromal Differentiation and Is Critical for Complete Decidualization." Molecular and Cellular Endocrinology, vol. 411, 2015, pp. 167-76.
Fonseca BM, Correia-da-Silva G, Teixeira NA. Anandamide restricts uterine stromal differentiation and is critical for complete decidualization. Mol Cell Endocrinol. 2015;411:167-76.
Fonseca, B. M., Correia-da-Silva, G., & Teixeira, N. A. (2015). Anandamide restricts uterine stromal differentiation and is critical for complete decidualization. Molecular and Cellular Endocrinology, 411, 167-76. https://doi.org/10.1016/j.mce.2015.04.024
Fonseca BM, Correia-da-Silva G, Teixeira NA. Anandamide Restricts Uterine Stromal Differentiation and Is Critical for Complete Decidualization. Mol Cell Endocrinol. 2015 Aug 15;411:167-76. PubMed PMID: 25960165.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anandamide restricts uterine stromal differentiation and is critical for complete decidualization. AU - Fonseca,B M, AU - Correia-da-Silva,G, AU - Teixeira,N A, Y1 - 2015/05/07/ PY - 2014/11/06/received PY - 2015/03/24/revised PY - 2015/04/27/accepted PY - 2015/5/12/entrez PY - 2015/5/12/pubmed PY - 2016/3/24/medline KW - Anandamide KW - Decidualization KW - Pseudopregnancy KW - Uterus SP - 167 EP - 76 JF - Molecular and cellular endocrinology JO - Mol Cell Endocrinol VL - 411 N2 - 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 CB1 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 α2-macroglobulin (α2-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. SN - 1872-8057 UR - https://www.unboundmedicine.com/medline/citation/25960165/Anandamide_restricts_uterine_stromal_differentiation_and_is_critical_for_complete_decidualization_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0303-7207(15)00225-7 DB - PRIME DP - Unbound Medicine ER -