Tags

Type your tag names separated by a space and hit enter

Anandamide and decidual remodelling: COX-2 oxidative metabolism as a key regulator.
Biochim Biophys Acta. 2015 Nov; 1851(11):1473-81.BB

Abstract

Recently, endocannabinoids have emerged as signalling mediators in reproduction. It is widely accepted that anandamide (AEA) levels must be tightly regulated, and that a disturbance in AEA levels may impact decidual stability and regression. We have previously characterized the endocannabinoid machinery in rat decidual tissue and reported the pro-apoptotic action of AEA on rat decidual cells. Cyclooxygenase-2 (COX-2) is an inducible enzyme that plays a crucial role in early pregnancy, and is also a key modulator in the crosstalk between endocannabinoids and prostaglandins. On the other hand, AEA-oxidative metabolism by COX-2 is not merely a mean to inactivate its action, but it yields the formation of a new class of mediators, named prostaglandin-ethanolamides, or prostamides. In this study we found that AEA-induced apoptosis in decidual cells involves COX-2 metabolic pathway. AEA induced COX-2 expression through p38 MAPK, resulting in the formation of prostamide E2 (PME2). Our findings also suggest that AEA-induced effect is associated with NF-kB activation. Finally, we describe the involvement of PME2 in the induction of the intrinsic apoptotic pathway in rat decidual cells. Altogether, our findings highlight the role of COX-2 as a gatekeeper in the uterine environment and clarify the impact of the deregulation of AEA levels on the decidual remodelling process.

Authors+Show Affiliations

UCIBIO, REQUIMTE, Laboratory of Biochemistry, Biological Sciences Department, Faculty of Pharmacy, University of Porto, Portugal.Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Consiglio Nazionale delle Ricerche, Pozzuoli, Naples, Italy.UCIBIO, REQUIMTE, Laboratory of Biochemistry, Biological Sciences Department, Faculty of Pharmacy, University of Porto, Portugal.Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Consiglio Nazionale delle Ricerche, Pozzuoli, Naples, Italy.UCIBIO, REQUIMTE, Laboratory of Biochemistry, Biological Sciences Department, Faculty of Pharmacy, University of Porto, Portugal.UCIBIO, REQUIMTE, Laboratory of Biochemistry, Biological Sciences Department, Faculty of Pharmacy, University of Porto, Portugal.

Pub Type(s)

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

Language

eng

PubMed ID

26335727

Citation

Almada, M, et al. "Anandamide and Decidual Remodelling: COX-2 Oxidative Metabolism as a Key Regulator." Biochimica Et Biophysica Acta, vol. 1851, no. 11, 2015, pp. 1473-81.
Almada M, Piscitelli F, Fonseca BM, et al. Anandamide and decidual remodelling: COX-2 oxidative metabolism as a key regulator. Biochim Biophys Acta. 2015;1851(11):1473-81.
Almada, M., Piscitelli, F., Fonseca, B. M., Di Marzo, V., Correia-da-Silva, G., & Teixeira, N. (2015). Anandamide and decidual remodelling: COX-2 oxidative metabolism as a key regulator. Biochimica Et Biophysica Acta, 1851(11), 1473-81. https://doi.org/10.1016/j.bbalip.2015.08.011
Almada M, et al. Anandamide and Decidual Remodelling: COX-2 Oxidative Metabolism as a Key Regulator. Biochim Biophys Acta. 2015;1851(11):1473-81. PubMed PMID: 26335727.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anandamide and decidual remodelling: COX-2 oxidative metabolism as a key regulator. AU - Almada,M, AU - Piscitelli,F, AU - Fonseca,B M, AU - Di Marzo,V, AU - Correia-da-Silva,G, AU - Teixeira,N, Y1 - 2015/09/01/ PY - 2015/04/13/received PY - 2015/08/24/revised PY - 2015/08/28/accepted PY - 2015/9/4/entrez PY - 2015/9/4/pubmed PY - 2015/12/15/medline KW - Anandamide KW - Apoptosis KW - COX-2 KW - Decidualization KW - Prostamide E2 KW - Signalling pathway SP - 1473 EP - 81 JF - Biochimica et biophysica acta JO - Biochim Biophys Acta VL - 1851 IS - 11 N2 - Recently, endocannabinoids have emerged as signalling mediators in reproduction. It is widely accepted that anandamide (AEA) levels must be tightly regulated, and that a disturbance in AEA levels may impact decidual stability and regression. We have previously characterized the endocannabinoid machinery in rat decidual tissue and reported the pro-apoptotic action of AEA on rat decidual cells. Cyclooxygenase-2 (COX-2) is an inducible enzyme that plays a crucial role in early pregnancy, and is also a key modulator in the crosstalk between endocannabinoids and prostaglandins. On the other hand, AEA-oxidative metabolism by COX-2 is not merely a mean to inactivate its action, but it yields the formation of a new class of mediators, named prostaglandin-ethanolamides, or prostamides. In this study we found that AEA-induced apoptosis in decidual cells involves COX-2 metabolic pathway. AEA induced COX-2 expression through p38 MAPK, resulting in the formation of prostamide E2 (PME2). Our findings also suggest that AEA-induced effect is associated with NF-kB activation. Finally, we describe the involvement of PME2 in the induction of the intrinsic apoptotic pathway in rat decidual cells. Altogether, our findings highlight the role of COX-2 as a gatekeeper in the uterine environment and clarify the impact of the deregulation of AEA levels on the decidual remodelling process. SN - 0006-3002 UR - https://www.unboundmedicine.com/medline/citation/26335727/Anandamide_and_decidual_remodelling:_COX_2_oxidative_metabolism_as_a_key_regulator_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1388-1981(15)00165-1 DB - PRIME DP - Unbound Medicine ER -