scholarly journals Cellular and Molecular Specificity of Pituitary Gland Physiology

2012 ◽  
Vol 92 (1) ◽  
pp. 1-38 ◽  
Author(s):  
Carolina Perez-Castro ◽  
Ulrich Renner ◽  
Mariana R. Haedo ◽  
Gunter K. Stalla ◽  
Eduardo Arzt

The anterior pituitary gland has the ability to respond to complex signals derived from central and peripheral systems. Perception of these signals and their integration are mediated by cell interactions and cross-talk of multiple signaling transduction pathways and transcriptional regulatory networks that cooperate for hormone secretion, cell plasticity, and ultimately specific pituitary responses that are essential for an appropriate physiological response. We discuss the physiopathological and molecular mechanisms related to this integrative regulatory system of the anterior pituitary gland and how it contributes to modulate the gland functions and impacts on body homeostasis.

2014 ◽  
Vol 53 (1) ◽  
pp. R1-R19 ◽  
Author(s):  
Tamar Eigler ◽  
Anat Ben-Shlomo

The somatostatin (SRIF) system, which includes the SRIF ligand and receptors, regulates anterior pituitary gland function, mainly inhibiting hormone secretion and to some extent pituitary tumor cell growth. SRIF-14 via its cognate G-protein-coupled receptors (subtypes 1–5) activates multiple cellular signaling pathways including adenylate cyclase/cAMP, MAPK, ion channel-dependent pathways, and others. In addition, recent data have suggested SRIF-independent constitutive SRIF receptor activity responsible for GH and ACTH inhibition in vitro. This review summarizes current knowledge on ligand-dependent and independent SRIF receptor molecular and functional effects on hormone-secreting cells in the anterior pituitary gland.


1975 ◽  
Vol 67 (2) ◽  
pp. 469-476 ◽  
Author(s):  
WH Fletcher ◽  
NC Anderson ◽  
JW Everett

The concept of "stimulus-secretion coupling" suggested by Douglas and co-workers to explain the events related to monamine discharge by the adrenal medulla (5, 7) may be applied to other endocrine tissues, such as adrenal cortex (36), pancreatic islets (4), and magnocellular hypothalamic neurons (6), which exhibit a similar ion-dependent process of hormone elaboration. In addition, they share another feature, that of joining neighbor cells via membrane junctions (12, 26, and Fletcher, unpublished observation). Given this, and the reports that hormone secretion by the pars distalis also involves a secretagogue-induced decrease in membrane bioelectric potential accompanied by a rise in cellular [Ca++] (27, 34, 41), it was appropriate to test the possibility that cells of the anterior pituitary gland are united by junctions.


Endocrine ◽  
2003 ◽  
Vol 20 (1-2) ◽  
pp. 59-66 ◽  
Author(s):  
Willis K. Samson ◽  
Cynthia Keown ◽  
Charles K. Samson ◽  
Henry W. Samson ◽  
Brian Lane ◽  
...  

Endocrinology ◽  
1999 ◽  
Vol 140 (6) ◽  
pp. 2828-2835 ◽  
Author(s):  
Thomas J. Spady ◽  
Karen L. Pennington ◽  
Rodney D. McComb ◽  
James D. Shull

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.


1982 ◽  
Vol 95 (2) ◽  
pp. 257-266 ◽  
Author(s):  
Alfredo Ulloa-Aguirre ◽  
S. C. Chappel

Anterior pituitary glands were collected from immature and mature (intact and castrated) male hamsters. The various species of FSH present within these glands were separated by Concanavalin A (Con A) chromatography and polyacrylamide gel isoelectric focusing (PAG-IEF) and measured by a specific FSH radioimmunoassay (RIA) as well as a radioreceptor assay (RRA). Two distinct forms of FSH (Con A unbound and bound) were separated by Con A chromatography and detected by both RIA and RRA. These two populations of FSH were present within anterior pituitary glands of all three animal models tested. Castration before collection of anterior pituitary glands reduced the ratio of Con A unbound: bound immunoreactive FSH. When measured by RRA this reduction was not observed. When homogenates of anterior pituitary glands obtained from mature animals were separated by PAG-IEF, six distinct species of FSH were observed by RIA with isoelectric points (pI) of 6·0, 5·7, 5·3, 5·0, 4·7 and 4·2–3·8. Homogenates of anterior pituitary glands obtained from immature male hamsters did not contain one of these species of FSH (pI value, 4·7). The relative contribution of some of the species of FSH to the total amount of detectable FSH differed depending upon the endocrine status of the animal. The species with pI value of 4·2–3·8 did not show any receptor-binding activity in any of the three models studied. The overall ratio of the activity of FSH measured by RRA compared with RIA was highest in anterior pituitary glands from intact mature and immature hamsters and lowest in anterior pituitary glands obtained from castrated animals. The RRA: RIA ratio for each species of FSH in all models tested declined as the isoelectric point of that species decreased. Thus, these results demonstrated the presence of multiple species of FSH within the anterior pituitary glands of immature and mature male hamsters. The relative proportions and receptor-binding activities of these species differed according to the isoelectric point and the pattern of hormone secretion at the time of collection of pituitary glands. Gonadal and other endocrine factors may influence not only the relative amount of each species of FSH but also the receptor-binding capacity of the FSH species synthesized by the anterior pituitary gland.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Xiuxing Liu ◽  
Binyao Chen ◽  
Zhaohao Huang ◽  
Runping Duan ◽  
He Li ◽  
...  

AbstractPoor sleep has become an important public health issue. With loss of sleep durations, poor sleep has been linked to the increased risks for diseases. Here we employed mass cytometry and single-cell RNA sequencing to obtain a comprehensive human immune cells landscape in the context of poor sleep, which was analyzed in the context of subset composition, gene signatures, enriched pathways, transcriptional regulatory networks, and intercellular interactions. Participants subjected to staying up had increased T and plasma cell frequency, along with upregulated autoimmune-related markers and pathways in CD4+ T and B cells. Additionally, staying up reduced the differentiation and immune activity of cytotoxic cells, indicative of a predisposition to infection and tumor development. Finally, staying up influenced myeloid subsets distribution and induced inflammation development and cellular senescence. These findings could potentially give high-dimensional and advanced insights for understanding the cellular and molecular mechanisms of pathologic conditions related to poor sleep.


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