scholarly journals Angiogenesis in Pituitary Adenomas and the Normal Pituitary Gland

2000 ◽  
Vol 85 (3) ◽  
pp. 1159-1162 ◽  
Author(s):  
Helen E. Turner ◽  
Zsusha Nagy ◽  
Kevin C. Gatter ◽  
Margaret M. Esiri ◽  
Adrian L. Harris ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Pituitary Adenomas ◽  
Anterior Pituitary ◽  
Pituitary Tumors ◽  
Anterior Pituitary Gland ◽  
Ulex Europaeus ◽  
Normal Pituitary Gland ◽  
Ulex Europaeus Agglutinin I ◽  
Acth Secreting ◽  
Tumor Types

Abstract Angiogenesis is essential for tumor growth beyond a few millimeters in diameter, and the intratumoral microvessel count that represents a measure of angiogenesis has been correlated with tumor behavior in a variety of different tumor types. To date no systematic study has assessed pituitary tumors of different secretory types, correlating vascular count with tumor size. The vascular densities of pituitary tumors and normal anterior pituitary were therefore assessed by counting vessels labeled using the vascular markers CD31 and ulex europaeus agglutinin I. One hundred and twelve surgically removed pituitary adenomas (30 GH-secreting, 25 prolactinomas, 15 ACTH-secreting, and 42 nonfunctioning tumors) were compared with 13 specimens of normal anterior pituitary gland. The vascular counts in the normal anterior pituitary gland were significantly higher (P < 0.05) than those in the tumors using both CD31 and ulex europaeus agglutinin I. In addition, microprolactinomas were significantly less vascular (P < 0.05) than macroprolactinomas, although there was no such difference between vascular densities of microadenomas and macroadenomas producing GH. ACTH-secreting tumors were, like microprolactinomas, of much lower vascular density than the normal pituitary and other secreting and nonsecreting tumor types. In marked contrast to other tumors, pituitary adenomas are less vascular than the normal pituitary gland, suggesting that there may be inhibitors of angiogenesis that play an important role in the behavior of these tumors.

Genetic Bases of Estrogen-Induced Pituitary Growth in an Intercross between the ACI and Copenhagen Rat Strains: Dominant Mendelian Inheritance of the ACI Phenotype*

Endocrinology ◽  
1999 ◽  
Vol 140 (6) ◽  
pp. 2828-2835 ◽  
Author(s):  
Thomas J. Spady ◽  
Karen L. Pennington ◽  
Rodney D. McComb ◽  
James D. Shull
Keyword(s):  
Cell Proliferation ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Molecular Mechanisms ◽  
Pituitary Tumors ◽  
Backcross Progeny ◽  
Anterior Pituitary Gland ◽  
Rat Strains ◽  
Genetic Trait ◽  
Inbred Rat

Abstract Estrogens stimulate cell proliferation in a variety of tissues and are widely believed to be contributing factors in the etiology of certain cancer types in humans. The molecular mechanisms through which estrogens regulate cell proliferation are currently unknown. Estrogens stimulate proliferation of the PRL-producing lactotroph of the rat anterior pituitary gland and induce development of PRL-producing pituitary tumors in several inbred rat strains. Therefore, the lactotroph provides a well defined model for identifying the mechanisms through which estrogens regulate cell proliferation and/or survival. Data from our laboratory and others indicate that the relative sensitivity to the pituitary growth-promoting actions of estrogens is highly strain specific. This allows genetics-based approaches to be used to address the molecular mechanisms through which estrogens stimulate lactotroph proliferation and induce pituitary tumor development. In the present study we have examined the ability of diethylstilbestrol (DES) to induce pituitary growth in the genetically related AxC-Irish (ACI) and Copenhagen (COP) strains and their derived F1, F2, and backcross progeny. The data presented herein indicate that the anterior pituitary gland of the ACI strain displays approximately a 2-fold greater growth response to administered DES than does the pituitary gland of the COP strain. The average pituitary weight in male ACI rats was increased from 9.2± 0.2 mg (mean ± sd) in untreated rats to 63.7± 12.6 mg in rats treated with DES for 12 weeks, whereas in male COP rats, DES increased pituitary weight from 12.7 ± 0.9 to 38.1± 8.2 mg. The ACI phenotype was inherited in the F1, F2, and backcross progeny of an ACI × COP intercross as a dominant genetic trait, and the approximately 30 mg of additional pituitary growth displayed by the DES-treated ACI rat, relative to that of the treated COP rat, appeared to result from the actions of a single locus. Moreover, in F1 progeny from an ACI × Brown Norway intercross, the ACI phenotype was inherited as a dominant or incompletely dominant genetic trait. These data, when compared with findings of previous studies using the Fischer 344 rat strain, provide the first indication that distinct genetic pathways contribute to regulation of estrogen-induced pituitary growth and induction of PRL-producing pituitary tumors in the ACI and F344 rat strains.

Enantioselective visualization of D-alanine in rat anterior pituitary gland: localization to ACTH-secreting cells

2008 ◽  
Vol 393 (1) ◽  
pp. 217-223 ◽  
Author(s):  
Sachise Etoh ◽  
Kenji Hamase ◽  
Akiko Morikawa ◽  
Tomohiro Ohgusu ◽  
Kiyoshi Zaitsu
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Acth Secreting

scholarly journals Glial-Derived Neurotropic Factor and RET Gene Expression in Normal Human Anterior Pituitary Cell Types and in Pituitary Tumors

2002 ◽  
Vol 87 (4) ◽  
pp. 1879-1884 ◽  
Author(s):  
Miguel A. Japón ◽  
Angel G. Urbano ◽  
Carmen Sáez ◽  
Dolores I. Segura ◽  
Alfonso Leal Cerro ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Pituitary Tumors ◽  
Cell Types ◽  
Anterior Pituitary Gland ◽  
Tyrosine Kinase Receptor ◽  
Positive Immunostaining ◽  
Normal Human ◽  
Human Anterior Pituitary ◽  
Neurotropic Factor

Abstract Glial-derived neurotropic factor (GDNF) signaling is mediated through a 2-component system consisting of the so-called GDNF receptor-α (GFRα1), which binds to GDNF. This complex activates the tyrosine kinase receptor RET. In this paper we demonstrate GDNF, GFRα1, and RET mRNA and protein expression in the human anterior pituitary gland. Double immunohistochemistry of anterior pituitary sections showed GDNF immunoreactivity in more than 95% of somatotrophs and to a lesser extent in corticotrophs (20%); it was almost absent in the remaining cell types. Also, although more than 95% of somatotrophs were stained for RET, no positive immunostaining could be detected in other cell types. Furthermore, we have looked for GDNF and RET in human pituitary adenomas of various hormonal phenotypes. Strong positive immunostaining was found for c-RET in all of the GH-secreting adenomas screened as well as in 50% of ACTH-producing adenomas. Positive immunostaining for GDNF was found in all of the GH-secreting adenomas and in 10% of the corticotropinomas. Lastly, we found strong positive immunostaining for GFRα1 in 90% of the somatotropinomas and 50% of the corticotropinomas as well as in 1 of 8 prolactinomas and 1 of 13 nonfunctioning adenomas. All of the remaining pituitary tumors screened were negative for RET, GDNF, and GFRα1. This study indicates that GDNF may well be acting in the regulation of somatotroph cell growth and/or cell function in the normal human anterior pituitary gland. The expression of RET in all of the somatotropinomas and in 50% of the ACTH-producing tumors implies that GDNF and RET could be involved in the pathogenesis of pituitary tumors.

Effects of estrogens on the characteristics of [3H]spiroperidol and [3H]RU24213 binding in rat anterior pituitary gland and brain

1979 ◽  
Vol 16 (2) ◽  
pp. 99-112 ◽  
Author(s):  
Thérèse Di Paolo ◽  
Réjean Carmichael ◽  
Fernand Labrie ◽  
Jean-Pierre Raynaud
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland

Effect of hypothalamic neuropeptides on corticotrophin release from quarters of rat anterior pituitary gland in vitro

1984 ◽  
Vol 100 (2) ◽  
pp. 219-226 ◽  
Author(s):  
S. A. Nicholson ◽  
T. E. Adrian ◽  
B. Gillham ◽  
M. T. Jones ◽  
S. R. Bloom
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Low Dose ◽  
Physiological Role ◽  
Anterior Pituitary Gland ◽  
High Concentration ◽  
Response Curves ◽  
Corticotrophin Releasing Factor ◽  
Basal Release

ABSTRACT The effect of six hypothalamic peptides on the basal release of ACTH and that induced by arginine vasopressin (AVP) or by ovine corticotrophin releasing factor (oCRF) from fragments of the rat anterior pituitary gland incubated in vitro was investigated. Dose–response curves to AVP and to oCRF were obtained, and the response to a low dose of oCRF was potentiated by a low dose of AVP. Basal release of ACTH was not affected by any of the peptides in concentrations in the range 10−12 to 10−6 mol/l, and only substance P (SP) and somatostatin (SRIF) inhibited significantly the response to oCRF in a dose-related manner. The responses to a range of doses of oCRF or AVP were reduced by 10−8 and 10 − 6 mol SP or SRIF/1, and to a greater extent by the higher dose. Except in the case of 10−6 mol SRIF/1 on the response to AVP, the response was not further diminished by preincubation of the tissue with the peptide before the stimulating agent was added. The inhibition of the responses to AVP or oCRF by 10−9 mol SP/1 was not potentiated by its combination with either 5 × 10−10 or 10−8 mol SRIF/1; the inhibitory effects were merely additive. The results suggest that although SRIF and SP are able to modulate the release of ACTH from the anterior pituitary gland, they do so only at a high concentration. In the case of SRIF these concentrations are several orders of magnitude higher than those reported to be present in the hypophysial portal blood and therefore a physiological role for this peptide in the control of ACTH secretion is unlikely. J. Endocr. (1984) 100, 219–226

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