title: The 17-β-oestradiol inhibits osteoclast activity by increasing the cannabinoid CB2 receptor expression.
abstract: Bone is a highly metabolically active tissue and its formation and resorption is at the base of bone remodelling. The critical importance of a balanced bone remodelling is demonstrated by human diseases, i.e. osteoporosis, in which a net increase in bone resorption is responsible of skeleton weakening and fracture risk. Oestrogens display anti-resorptive properties on bone metabolism. Indeed, the so-called post-menopausal osteoporosis occurs after interruption of gonad function and benefits from hormonal replacement treatment. Recently, an important role for the endocannabinoid system in the regulation of skeletal remodelling in human has also been shown. In particular, we showed that CB2 stimulation is able to reduce the number of human OCs in vitro. Here, we provide unprecedented evidence that 17-β-oestradiol administration inhibits activity and formation of human OCs in vitro, demonstrating that oestrogens are able to induce an increase of CB2 expression probably through the recruitment of a putative oestrogens responsive element in the CB2 encoding for gene.
authors.affiliation: Department of Pediatrics, Second University of Naples, 80138 Naples, Italy.
authors.forename: Francesca
authors.initials: F
authors.lastname: Rossi
authors.forename: Giulia
authors.initials: G
authors.lastname: Bellini
authors.forename: Livio
authors.initials: L
authors.lastname: Luongo
authors.forename: Silvia
authors.initials: S
authors.lastname: Mancusi
authors.forename: Marco
authors.initials: M
authors.lastname: Torella
authors.forename: Chiara
authors.initials: C
authors.lastname: Tortora
authors.forename: Iolanda
authors.initials: I
authors.lastname: Manzo
authors.forename: Francesca
authors.initials: F
authors.lastname: Guida
authors.forename: Bruno
authors.initials: B
authors.lastname: Nobili
authors.forename: Vito
authors.initials: V
authors.lastname: de Novellis
authors.forename: Sabatino
authors.initials: S
authors.lastname: Maione
mesh_terms: D000135:Acid Phosphatase / Q000235:genetics; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002478:Cells, Cultured; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D000077267:Fulvestrant; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D007527:Isoenzymes / Q000235:genetics; D008875:Middle Aged; D010010:Osteoclasts / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D017698:Postmenopause / Q000502:physiology; D017697:Premenopause / Q000502:physiology; D043884:Receptor, Cannabinoid, CB1 / Q000037:antagonists & inhibitors / Q000235:genetics; D043885:Receptor, Cannabinoid, CB2 / Q000037:antagonists & inhibitors / Q000235:genetics*; D020218:Response Elements; D050916:TRPV Cation Channels / Q000235:genetics; D000071681:Tartrate-Resistant Acid Phosphatase; D055815:Young Adult
chemical_list: D004965:Estrogen Antagonists; D004967:Estrogens; D007211:Indoles; D007527:Isoenzymes; D043884:Receptor, Cannabinoid, CB1; D043885:Receptor, Cannabinoid, CB2; D050916:TRPV Cation Channels; C494482:TRPV1 protein, human; D000077267:Fulvestrant; D004958:Estradiol; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; C094023:iodopravadoline