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Phosphodiesterases and cAMP pathway in pituitary diseases
Authors
Aflorei
Ang
+96 more
Baciu
Baciu
Beard
Beard
Beckers
Bell
Bizzi
Bolger
Bolger
Bolger
Bolger
Bolger
Bolger
Buchbinder
Cai
Caimari
Cazabat
Cazabat
Chahal
Conti
Conti
Cuny
Daly
Daly
de
De
de
Dinesen
Dénes
Farrugia
Formosa
Formosa
Formosa
Francis
Gadelha
Georgitsi
Georgitsi
Georgitsi
Guaraldi
Guaraldi
Hamilton
Hernández-Ramírez
Hernández-Ramírez
Hernández-Ramírez
Hernández-Ramírez
Houslay
Houslay
Huston
Igreja
Imran
Iwata
Jennings
Karaca
Kazlauskas
Lania
Leontiou
Libé
Mackenzie
Mantovani
Martinez
Maurice
McPhee
Mokra
Morgan
Mothojakan
Moustafa
Nikodemova
Niyazoglu
Occhi
Occhi
Oriola
Pardi
Persani
Pertuit
Peverelli
Peverelli
Radian
Raitila
Rena
Richards
Salvatori
Salvatori
Schernthaner-Reiter
Stratakis
Tian
Tichomirowa
Toledo
Trivellin
Trivellin
Tuominen
Vargiolu
Vezzosi
Vierimaa
Wallace
Williams
Zatelli
Publication date
1 March 2019
Publisher
'Frontiers Media SA'
Doi
Cite
Abstract
© 2019 Bizzi, Bolger, Korbonits and Ribeiro-Oliveira. Human phosphodiesterases (PDEs) comprise a complex superfamily of enzymes derived from 24 genes separated into 11 PDE gene families (PDEs 1-11), expressed in different tissues and cells, including heart and brain. The isoforms PDE4, PDE7, and PDE8 are specific for the second messenger cAMP, which is responsible for mediating diverse physiological actions involving different hormones and neurotransmitters. The cAMP pathway plays an important role in the development and function of endocrine tissues while phosphodiesterases are responsible for ensuring the appropriate intensity of the actions of this pathway by hydrolyzing cAMP to its inactive form 5'-AMP. PDE1, PDE2, PDE4, and PDE11A are highly expressed in the pituitary, and overexpression of some PDE4 isoforms have been demonstrated in different pituitary adenoma subtypes. This observed over-expression in pituitary adenomas, although of unknown etiology, has been considered a compensatory response to tumorigenesis. PDE4A4/5 has a unique interaction with the co-chaperone aryl hydrocarbon receptor-interacting protein (AIP), a protein implicated in somatotroph tumorigenesis via germline loss-of-function mutations. Based on the association of low PDE4A4 expression with germline AIP-mutation-positive samples, the available data suggest that lack of AIP hinders the upregulation of PDE4A4 protein seen in sporadic somatotrophinomas. This unique disturbance of the cAMP-PDE pathway observed in the majority of AIP-mutation positive adenomas could contribute to their well-described poor response to somatostatin analogs and may support a role in tumorigenesis.We are grateful for the support by Fundação de Amparo à Pesquisa de Minas Gerais—Fapemig (AR-O), Conselho Nacional de Desenvolvimento Científico e Tecnológico—CNPq (AR-O, MB) and the Medical Research Council UK (MK), and the NIH, USA (GB)
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