Cells of the anterior pituitary

Yeung, Chung-Man; Chan, Chi-Bun; Leung, Po Sing; Chen, Cheng

doi:10.1016/j.biocel.2006.02.012

Cited by 54 publications

(53 citation statements)

References 43 publications

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“…Strong cytoplasmic immunopositivity for FSH, LH and TSH was seen in the majority of cells in PT. The percentages of adenohypophyseal hormone-immunopositive cells were calculated, after screening the entire adenohypophyseal tissue section, as follows: GH (50% of the adenohypophyseal cell population), FSH (10%), LH (10%), TSH (10%), ACTH (10%), and prolactin (10%), and were consistent with those previously described [30]. In PT, FSH-immunopositive cells accounted for approximately 40%, LH for 40% and TSH for 5%.…”

Section: Resultssupporting

confidence: 61%

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Expression of Adiponectin and Adiponectin Receptors in Human Pituitary Gland and Brain

Psilopanagioti¹,

Papadaki²,

et al. 2008

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Background/Aims: Adiponectin and its receptors, AdipoR1 and AdipoR2, constitute integral components of energy homeostatic mechanism in peripheral tissues. Recent studies have implicated adiponectin in central neural networks regulating food intake and energy expenditure. The present study aimed at investigating the possible expression and distribution of adiponectin and its receptors in human pituitary gland, hypothalamus and different brain areas. Methods: Sections of the pituitary gland, hypothalamus and adjacent basal forebrain area, cerebrum and cerebellum from 35 autopsy cases, were examined using HE, PAS-Orange G, luxol fast blue/cresyl violet stains and single and double immunohistochemistry using adiponectin, AdipoR1, AdipoR2, choline acetyltransferase, FSH, LH, TSH, GH, ACTH and prolactin-specific antibodies. Age and BMI mean values ± SD of the autopsy cases were 56 ± 18 years and 27 ± 5 kg/m², respectively. Results: Strong adiponectin expression was observed in pituitary gland. In pars distalis (PD), adiponectin localized in GH, FSH, LH and TSH-producing cells and in pars tuberalis (PT) in FSH, LH and TSH-producing cells. Strong to moderate expression of AdipoR1 and AdipoR2 was observed in PD by the same cell types as adiponectin. No immunoreactivity for adiponectin receptors was noted in cells of PT. Intense AdipoR1 immunostaining was observed in neurons of lateral hypothalamic area and of nucleus basalis of Meynert (NBM). Conclusions: Adiponectin and its receptors expression in human pituitary might indicate the existence of a local system, modulating endocrine axes. Furthermore, the presence of AdipoR1 in hypothalamus and NBM suggests that adiponectin may participate in central neural signaling pathways controlling energy homeostasis and higher brain functions.

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Section: Resultssupporting

confidence: 61%

“…It is known that many adenohypophyseal cells are multifunctional, expressing various hormones [30], including peripheral hormones, i.e. leptin [31] and ghrelin [32].…”

Section: Discussionmentioning

confidence: 99%

Expression of Adiponectin and Adiponectin Receptors in Human Pituitary Gland and Brain

Psilopanagioti¹,

Papadaki²,

et al. 2008

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“…Within the anterior pituitary gland (AP), somatotrophs comprise w50% of the cells with the remaining cells, lactotrophs, gonadotrophs, corticotrophs and thyrotrophs comprising w10-20% each (Horvath & Kovacs 1988, Yeung et al 2006. Irrespective of hormonal status of individual cells, w40% of cells within the AP-stained positive for NNAT protein (Fig.…”

Section: Ihc Localization Of Nnat In Normal Pituitarymentioning

confidence: 99%

Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma

Revill¹,

Dudley²,

Clayton³

et al. 2009

Endocrine-Related Cancer

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The imprinted gene, neuronatin (NNAT), is one of the most abundant transcripts in the pituitary and is thought to be involved in the development and maturation of this gland. In a recent whole-genome approach, exploiting a pituitary tumour cell line, we identified hypermethylation associated loss of NNAT. In this report, we determined the expression pattern of NNAT in individual cell types of the normal gland and within each of the different pituitary adenoma subtypes. In addition, we determined associations between expression and CpG island methylation and used colony forming efficiency assays (CFE) to gain further insight into the tumour-suppressor function of this gene. Immunohistochemical (IHC) co-localization studies of normal pituitaries showed that each of the hormone secreting cells (GH, PRL, ACTH, FSH and TSH) expressed NNAT. However, 33 out of 47 adenomas comprising, 11 somatotrophinomas, 10 prolactinomas, 12 corticotrophinomas and 14 non-functioning tumours, irrespective of subtype failed to express either NNAT transcript or protein as determined by quantitative real-time RT-PCR and IHC respectively. In normal pituitaries and adenomas that expressed NNAT the promoter-associated CpG island showed characteristics of an imprinted gene where w50% of molecules were densely methylated. However, in the majority of adenomas that showed loss or significantly reduced expression of NNAT, relative to normal pituitaries, the gene-associated CpG island showed significantly increased methylation.

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“…Uma pequena população de mamossomatotrófos também existe, a qual produz tanto GH quanto PRL (Yeung et al, 2006).…”

Section: Acthunclassified

“…Os somatotrófos representam o maior tipo celular do lobo, constituindo aproximadamente 50% da população celular, seguido pelos lactotrófos (10-25%), corticotrófos (10-20%), tireotrófos (10%) e gonadotrófos (10%) (Yeung et al, 2006). …”

Section: Acthunclassified

Análise da expressão dos genes CRABP1, CRABP2, GRP e RERG em adenomas hipofisários funcionantes e clinicamente não funcionantes

Chile¹

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DEDICATÓRIADedico esta dissertação aos meus pais, exemplos de fé e perseverança, por me ensinarem a sonhar e a persistir em todos os momentos de minha vida. AGRADECIMENTOS AgradecimentosA Deus, fonte de sabedoria, pela força, iluminação e por nunca deixar faltar coragem em minha caminhada.Aos meus pais, José Roberto e Auzenir, pelo amor incondicional, dedicação e incentivo.Ao meu irmão, Felipe, pelo afeto e apoio demonstrados.Aos meus avós, José (in memorian) e Aramita, pelo carinho e preocupação durante esta jornada.Às amigas Maria Auxiliadora Higa e Patrícia Lopes Pereira por, simplesmente, existirem em minha vida.Ao meu orientador e amigo, Prof. Dr. Ricardo Rodrigues Giorgi, pelos ensinamentos, apoio e esforço demonstrados durante o desenvolvimento deste trabalho e pela confiança em mim depositada.À bióloga Maria Angela Zanella Fortes pela colaboração fundamental neste estudo, pela amizade e pelos momentos de descontração que tornaram meus dias mais alegres.À biomédica Ana Mercedes Cavaleiro pela convivência e incentivo. ...................................................................................................................61 5.1.1.1 CRABP1................................................................................................................63 5.1.1.2 CRABP2................................................................................................................65 5.1.2 GRP.........................................................................................................................68 5.1.3 RERG..................................................................................................................... Tumores hipofisáriosOs tumores hipofisários são adenomas monoclonais e representam 10% a 15% das neoplasias intracranianas. Embora benignos e raramente metastáticos, podem apresentar comportamento invasivo estando associados à alta morbidade e mortalidade (Kovacs e Horvarth, 1987;Herman et al., 1990;Faglia, 1993 Bases molecularesO entendimento sobre os mecanismos moleculares responsáveis pela formação e progressão dos adenomas hipofisários ainda permanece incompleto, contudo, algumas informações têm sido acumuladas nos últimos anos. Foi demonstrado, por inativação do cromossomo X, que os adenomas hipofisários possuem origem monoclonal (Herman et al., 1990). Assim, embora um papel permissivo do hipotálamo não possa ser desconsiderado, as evidências apontam um mecanismo hipofisário primário para o desenvolvimento tumoral, como a replicação de uma única célula mutada na qual a vantagem de proliferação resulta ou da ativação de um proto-oncogene ou da inativação de genes supressores tumorais (Melmed, 2003). Ativação de proto-oncogenesProto-oncogenes são genes que codificam proteínas envolvidas no controle da Zhang et al., 1999a;Heaney et al., 2000). Adenomas hipofisários testados por RT-PCR demonstraram expressão aumentada dePTTG quando comparados aos tecidos hipofisários normais, havendo, inclusive, correlação positiva entre o grau de expressão e o grau...

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Cells of the anterior pituitary

Cited by 54 publications

References 43 publications

Expression of Adiponectin and Adiponectin Receptors in Human Pituitary Gland and Brain

Expression of Adiponectin and Adiponectin Receptors in Human Pituitary Gland and Brain

Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma

Análise da expressão dos genes CRABP1, CRABP2, GRP e RERG em adenomas hipofisários funcionantes e clinicamente não funcionantes

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