title: Expression and thyroid hormone regulation of annexins in the anterior pituitary.
abstract: Due to their property to bind to phospholipids in a Ca(2)(+)-dependent manner, proteins of the annexin superfamily are involved in many membrane-related events and thus in various forms of physiological and pathological processes. We were therefore interested in analyzing the mRNA expression of the annexins in the severely disorganized pituitaries of the athyroid Pax8(-/-) mice in comparison with that of control animals. In neither condition was mRNA expression of the annexins A3, A7, A8, A9, A11, and A13 detectable. The annexins A2, A4, and A6 were equally expressed in wild-type and Pax8(-/-) mice. Transcript levels of A1 and A10 were highly increased and those of A5 were significantly decreased in the athyroid mutants compared with controls. Treatment of Pax8(-/-) mice with physiological doses of thyroxine for 3 days normalized the mRNA expression of A1, A5, and A10 indicating that the expression of these annexins is directly regulated by thyroid hormone (TH). Since A5 exhibits by far the highest transcript levels of all annexins in the pituitary and its regulation by TH could be also confirmed at the protein level, we analyzed the mRNA expression of pituitary hormones in A5(-/-) mice. In these mutants, only the beta-FSH mRNA expression was found to be significantly reduced, while the mRNA expression levels of the other pituitary hormones were not altered. These results support the concept that annexins might serve important albeit redundant functions as modulators of pituitary hormone secretion.
authors.affiliation: Max Planck Institute for Experimental Endocrinology, Feodor-Lynen-Str. 7, D-30625 Hannover, Germany. jens.mittag@ki.se
authors.forename: Jens
authors.initials: J
authors.lastname: Mittag
authors.forename: Wiebke
authors.initials: W
authors.lastname: Oehr
authors.forename: Heike
authors.initials: H
authors.lastname: Heuer
authors.forename: Tuula
authors.initials: T
authors.lastname: Hämäläinen
authors.forename: Bent
authors.initials: B
authors.lastname: Brachvogel
authors.forename: Ernst
authors.initials: E
authors.lastname: Pöschl
authors.forename: Karl
authors.initials: K
authors.lastname: Bauer
mesh_terms: D000818:Animals; D017305:Annexin A1 / Q000235:genetics / Q000378:metabolism; D017304:Annexin A5 / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D017302:Annexins / Q000235:genetics / Q000378:metabolism*; D037201:Follicle Stimulating Hormone, beta Subunit / Q000235:genetics; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D000072636:PAX8 Transcription Factor; D051761:Paired Box Transcription Factors / Q000172:deficiency; D010903:Pituitary Gland, Anterior / Q000378:metabolism*; D010907:Pituitary Hormones / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D013961:Thyroid Gland / Q000002:abnormalities; D013963:Thyroid Hormones / Q000502:physiology*; D013974:Thyroxine / Q000494:pharmacology
chemical_list: D017305:Annexin A1; D017304:Annexin A5; D017302:Annexins; C485665:Anxa10 protein, mouse; D037201:Follicle Stimulating Hormone, beta Subunit; D000072636:PAX8 Transcription Factor; D051761:Paired Box Transcription Factors; C499496:Pax8 protein, mouse; D010907:Pituitary Hormones; D012333:RNA, Messenger; D013963:Thyroid Hormones; D013974:Thyroxine