Identification of Epidermal Growth Factor mRNA-Expressing Cells in the Mouse Anterior Pituitary

Honda, Junichi; Oomizu, Souichi; Kiuchi, Yuko; Komatsu, Noriko; Tanaka, Sakae; Takahashi, Sumio

doi:10.1159/000054532

Cited by 23 publications

(21 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, EGF increased BrdU uptake (indicative of replicating cells) in ACTH enriched dispersed anterior pituitary cells (48,49). In primary cultures of male mouse anterior pituitaries, EGF treatment enhanced BrdU uptake in ACTH-(as well as in PRL-) immunopositive cells, but not in other pituitary cell subpopulations (37). The EGFR inhibitor RG-13022 decreased the percentage of BrdU labeled cells immunoreactive for ACTH (and PRL), providing functional evidence for the presence of active receptors on corticotroph (and lactotroph) populations (50).…”

Section: Egfr and Corticotroph Functionmentioning

confidence: 92%

Decoding the genetic basis of Cushing's disease: USP8 in the spotlight

Theodoropoulou

Reincke

Faßnacht

et al. 2015

European Journal of Endocrinology

View full text Add to dashboard Cite

Cushing's disease (CD) arises from pituitary-dependent glucocorticoid excess due to an ACTH-secreting corticotroph tumor. Genetic hits in oncogenes and tumor suppressor genes that afflict other pituitary tumor subtypes are not found in corticotrophinomas. Recently, a somatic mutational hotspot was found in up to half of corticotrophinomas in the USP8 gene that encodes a protein that impairs the downregulation of the epidermal growth factor receptor (EGFR) and enables its constitutive signaling. EGF is an important regulator of corticotroph function and its receptor is highly expressed in Cushing's pituitary tumors, where it leads to increased ACTH synthesis in vitro and in vivo. The mutational hotspot found in corticotrophinomas hyper-activates USP8, enabling it to rescue EGFR from lysosomal degradation and ensure its stimulatory signaling. This review presents new developments in the study of the genetics of CD and focuses on the USP8-EGFR system as trigger and target of corticotroph tumorigenesis.

show abstract

Section: Egfr and Corticotroph Functionmentioning

confidence: 92%

Decoding the genetic basis of Cushing's disease: USP8 in the spotlight

Theodoropoulou

Reincke

Faßnacht

et al. 2015

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…The pituitary cells were incubated with one of the antibodies to PRL and GH at room temperature for 2 h. The primary antibodies were localized with fluorescein-labelled antibodies (1:200; EY Laboratories, San Mateo, Calif., USA). Immunostaining was abolished by omission of each primary antibody or by the use of primary antibodies (working dilution, 100 µl) preabsorbed with 10 µg of each highly purified pituitary hormone (rat PRL and rat GH, respectively) at 4°C for 24 h [16]. …”

Section: Methodsmentioning

confidence: 99%

α-Melanocyte-Stimulating Hormone Stimulates Prolactin Secretion through Melanocortin-3 Receptors Expressed in Mammotropes in the Mouse Pituitary

et al. 2003

Self Cite

View full text Add to dashboard Cite

The intermediate lobe of rodent pituitaries is involved in the regulation of prolactin (PRL) secretion from the anterior lobe. In a previous study, we demonstrated the stimulatory effect of α-melanocyte-stimulating hormone (α-MSH) on PRL release and the expression of melanocortin-3 receptors (MC3-Rs) in cultured mouse pituitary cells. The aim of the present study was to clarify whether α-MSH directly stimulates PRL release through the MC3-Rs by determining the cell type of MC3-R-expressing cells in the mouse pituitary anterior lobe. Northern blot analysis revealed a 2.7-kb transcript for MC3-R mRNA in the anterior and neurointermediate lobes of pituitary glands of adult male and female mice. Dual cellular localization of MC3-R mRNA and PRL or growth hormone (GH) in the mouse pituitary glands was performed by in situ hybridization analysis of MC3-R mRNA followed by immunocytochemical detection of PRL or GH. MC3-R mRNA was detected in most mammotropes and some somatotropes. α-MSH increased PRL release and stimulated DNA replication in mammotropes, and these effects were blocked by SHU9119, an antagonist of MC3-R and MC4-R. These results indicate that α-MSH stimulates PRL release and proliferation of mammotropes through MC3-Rs, and suggest that α-MSH from intermediate lobes can regulate mammotrope functions in the mouse pituitary.

show abstract

“…Since EGF or TGF-α are expressed in the pituitary of different species including human (172–175), more precisely in gonadotrophs (176), somatotrophs and lactotrophs (173, 174, 176), and since these growth factors are mitogenic for these cell types (171, 173, 175, 177, 178) and stimulate PRL gene expression and production (179, 180), these growth factors may have a permissive function in the paracrine action of gonadotrophs. This is supported by other findings.…”

Section: Gonadotrophs Signal To Lactotrophs Somatotrophs and Corticomentioning

confidence: 99%

Endogenous Cannabinoids: Structure and Metabolism

Bisogno

2008

J Neuroendocrinology

144

View full text Add to dashboard Cite

D9 -Tetrahydrocannabinol (THC), the main psychoactive compound extracted from Cannabis sativa, is the most representative component of the mixture of therapeutic substances that are communally referred to as cannabinoids (1). It acts as an agonist at specific G-protein-coupled receptors, cannabinoid receptor subtypes CB 1 and CB 2 (2). The discovery of cannabinoid receptors has driven the investigation of the existence of their natural ligands and, soon after, endocannabinoids were identified. N-arachidonoyl-ethanolamine (AEA, anandamide) and 2-arachidonoyl glycerol (2-AG) are the two most studied endocannabinoids. They are biosynthesised 'on demand' by cleavage of their membrane lipid precursors N-arachidonoyl-phosphatidylethanolamine (N-ArPE) and sn-1-acyl-2-arachidonoylglycerols (DAGs) respectively, and then inactivated by intracellular hydrolysing enzymes. Cannabinoid receptors, endocannabinoids and enzymes that biosynthesise [N-acyl-phosphatidylethanolamine-selective phospholipase D (NAPE-PLD) and diacylglycerol lipase (DAGL)] and degrade [fatty acid amide hydrolase (FAAH) and the monoacylglycerol lipases (MAGL)] AEA and 2-AG, respectively, are key components in the endocannabinoid system (3). Despite a large number of excellent studies having contributed to the current understanding of the endocannabinoid regulation and function, further efforts are necessary to fully comprehend this signalling system. Here, a review on the current knowledge on structure and metabolism of the best studied endogenous cannabinoids is presented. In particular, this review concentrates on the mechanisms responsible for the biosynthesis and inactivation of the endocannabinoids, as well as on the several inhibitors of their metabolism identified to date. Endocannabinoids and related N-acyl-ethanolaminesEndocannabinoids are defined as endogenous compounds capable of binding to and functionally activating cannabinoid receptors. At least five endocannabinoids have been identified to date (Fig. 1). Anandamide, the amide between arachidonic acid and ethanolamine, was the first endogenous ligand to be reported at the end of 1992 (4) and additional polyunsaturated ethanolamines that bind to cannabinoid receptors, homolinolenylethanolamide and docosatetraenylethanolamide, have been isolated in the brain. Other endocannabinoids, all derived from arachidonic acid, were identified. The identification of 2-AG, the ester of arachidonic acid with glycerol, isolated from canine gut and brain has also been reported (5, 6). Subsequently, the first endocannabinoid characterised by ether bond, 2-arachidonyl glyceryl ether or noladin ether, was isolated from porcine brain (7) and N-arachidonoyldopamine (NADA), a selective CB 1 agonist and a potent agonist of vanilloid receptors, was discovered (8, 9). O-arachidonoylethanolamine, the ester derivative of ethanolamine with arachidonic acid, with the same molecular weight as anandamide but with opposite orientation of the polar ethanolamine moiety, was named virodhamine from the Sanskrit word virodha, ...

show abstract

Identification of Epidermal Growth Factor mRNA-Expressing Cells in the Mouse Anterior Pituitary

Cited by 23 publications

References 26 publications

Decoding the genetic basis of Cushing's disease: USP8 in the spotlight

Decoding the genetic basis of Cushing's disease: USP8 in the spotlight

α-Melanocyte-Stimulating Hormone Stimulates Prolactin Secretion through Melanocortin-3 Receptors Expressed in Mammotropes in the Mouse Pituitary

Endogenous Cannabinoids: Structure and Metabolism

Contact Info

Product

Resources

About