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Special Issue "Molecular Biology of the Pituitary"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 November 2020).

Special Issue Editors

Prof. Dr. Salvatore M. Corsello
Website
Guest Editor
Unit of Endocrinology, Università Cattolica del Sacro Cuore, Largo "A. Gemelli" 8, I-00168 Rome, Italy
Interests: pituitary, acromegaly, Cushing’s syndrome, hyerprolactinemia, TSH-secreting pituitary adenoma, syndrome of reduced sensitivity to thyroid hormones, thyroid, adrenal gland
Dr. Rosa Maria Paragliola
Website
Guest Editor
Unit of Endocrinology, Università Cattolica del Sacro Cuore, Largo "A. Gemelli" 8, I-00168 Rome, Italy
Interests: pituitary; acromegaly; Cushing’s syndrome; hyperprolactinemia; TSH-secreting pituitary adenoma; syndrome of reduced sensitivity to thyroid hormones; thyroid; adrenal gland

Special Issue Information

Dear Colleagues,

This Special Issue aims to present recent research on the molecular biology of pituitary diseases. Pituitary adenoma is a common disease, present in about 10% of the general population, which generally presents as benign tumors. However, rarely, tumors can become malignant and metastasize. Pituitary adenomas are also associated with specific syndromes (e.g., acromegaly, Cushing’s syndrome, prolactinoma, inappropriate TSH secretion syndrome) due to inappropriate hormonal secretion. The continuous development of molecular biology techniques has improved the understanding of both the pathogenesis and the biology of these tumors and this knowledge can be applied for the development of diagnostic approaches and therapeutic options. Interestingly, molecular biology techniques have led to the discovery of the pathophysiological mechanisms at the basis of non-neoplastic pituitary diseases, such as thyroid hormone resistance syndrome or non-neoplastic TSH inappropriate secretion. Regarding syndromes of reduced sensitivity to thyroid hormones, an important topic is the discovery of polymorphisms in genes which code for type 2 deiodinase. Finally, genetic analyses can identify mutations of genes coding for transcription factors involved in pituitary development, which can be involved in the pathogenesis of combined pituitary hormone deficiency.

Prof. Dr. Salvatore M. Corsello
Dr. Rosa Maria Paragliola
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • acromegaly
  • somatostatin receptor ligands
  • prolactinoma
  • Cushing’s syndrome
  • TSH-secreting adenomas
  • syndromes of reduced sensitivity to thyroid hormones
  • pituitary adenomas
  • pituitary carcinomas
  • hypopituitarism

Published Papers (4 papers)

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Research

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Open AccessArticle
Arginine Vasopressin Modulates Ion and Acid/Base Balance by Regulating Cell Numbers of Sodium Chloride Cotransporter and H+-ATPase Rich Ionocytes
Int. J. Mol. Sci. 2020, 21(11), 3957; https://doi.org/10.3390/ijms21113957 - 31 May 2020
Abstract
Arginine vasopressin (Avp) is a conserved pleiotropic hormone that is known to regulate both water reabsorption and ion balance; however, many of the mechanisms underlying its effects remain unclear. Here, we used zebrafish embryos to investigate how Avp modulates ion and acid–base homeostasis. [...] Read more.
Arginine vasopressin (Avp) is a conserved pleiotropic hormone that is known to regulate both water reabsorption and ion balance; however, many of the mechanisms underlying its effects remain unclear. Here, we used zebrafish embryos to investigate how Avp modulates ion and acid–base homeostasis. After incubating embryos in double-deionized water for 24 h, avp mRNA expression levels were significantly upregulated. Knockdown of Avp protein expression by an antisense morpholino oligonucleotide (MO) reduced the expression of ionocyte-related genes and downregulated whole-body Cl content and H+ secretion, while Na+ and Ca2+ levels were not affected. Incubation of Avp antagonist SR49059 also downregulated the mRNA expression of sodium chloride cotransporter 2b (ncc2b), which is a transporter responsible for Cl uptake. Correspondingly, avp morphants showed lower NCC and H+-ATPase rich (HR) cell numbers, but Na+/K+-ATPase rich (NaR) cell numbers remained unchanged. avp MO also downregulated the numbers of foxi3a- and p63-expressing cells. Finally, the mRNA expression levels of calcitonin gene-related peptide (cgrp) and its receptor, calcitonin receptor-like 1 (crlr1), were downregulated in avp morphants, suggesting that Avp might affect Cgrp and Crlr1 for modulating Cl balance. Together, our results reveal a molecular/cellular pathway through which Avp regulates ion and acid–base balance, providing new insights into its function. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary)
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Open AccessArticle
MSH6/2 and PD-L1 Expressions Are Associated with Tumor Growth and Invasiveness in Silent Pituitary Adenoma Subtypes
Int. J. Mol. Sci. 2020, 21(8), 2831; https://doi.org/10.3390/ijms21082831 - 18 Apr 2020
Cited by 1
Abstract
Mismatch repair genes mutS homologs 6/2 (MSH6/2) expressions are involved in tumor growth and programmed cell death 1 ligand 1 (PD-L1) expression in tumor immunity, but the direct association with pituitary adenomas (PAs) is not well understood. We aimed [...] Read more.
Mismatch repair genes mutS homologs 6/2 (MSH6/2) expressions are involved in tumor growth and programmed cell death 1 ligand 1 (PD-L1) expression in tumor immunity, but the direct association with pituitary adenomas (PAs) is not well understood. We aimed to clarify the effects of MSH6/2 and PD-L1 expression on tumor proliferation and invasiveness in nonfunctioning (NF) PAs. We performed immunohistochemistry to classify the NFPAs into gonadotroph adenoma (GAs), silent corticotroph adenomas (SCAs), null cell adenoma (NCAs), and pituitary transcription factor 1 (PIT1) lineage PAs. We evaluated MSH6/2 and PD-L1 mRNA expressions in NFPAs by real-time PCR (n = 73), and statistically analyzed the expressions and clinicopathological factors. We also investigated the effect of MSH6 knockout on PD-L1 expression in AtT-20ins and GH3. MSH6/2 expressions were significantly lower in invasive NFPAs than in non-invasive NFPAs, and lower in SCAs and NCAs than in GAs. MSH6/2 expressions were positively associated with PD-L1 expression. PD-L1 expression was significantly lower in invasive NFPAs than in non-invasive NFPAs, and lower in SCAs and NCAs than in GAs. Although MSH6/2 expressions also tended to be lower in PIT1 lineage PAs than in GAs, PIT1 lineage PAs expressed PD-L1 equivalently to GA, which was unlike SCAs and NCAs. MSH6 knockout in AtT-20ins and GH3 significantly decreased PD-L1 expression (75% and 34% reduction, respectively) with cell proliferation promotion. In conclusion, differences in MSH6/2 and PD-L1 expressions of SCAs, NCAs, and PIT1-lineage PAs from those of GAs appear to contribute to their clinically aggressive characteristics, such as more proliferation and invasiveness. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary)
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Review

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Open AccessReview
The Mechanisms Underlying Autonomous Adrenocorticotropic Hormone Secretion in Cushing’s Disease
Int. J. Mol. Sci. 2020, 21(23), 9132; https://doi.org/10.3390/ijms21239132 - 30 Nov 2020
Abstract
Cushing’s disease caused due to adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas (ACTHomas) leads to hypercortisolemia, resulting in increased morbidity and mortality. Autonomous ACTH secretion is attributed to the impaired glucocorticoid negative feedback (glucocorticoid resistance) response. Interestingly, other conditions, such as ectopic ACTH syndrome (EAS) [...] Read more.
Cushing’s disease caused due to adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas (ACTHomas) leads to hypercortisolemia, resulting in increased morbidity and mortality. Autonomous ACTH secretion is attributed to the impaired glucocorticoid negative feedback (glucocorticoid resistance) response. Interestingly, other conditions, such as ectopic ACTH syndrome (EAS) and non-neoplastic hypercortisolemia (NNH, also known as pseudo-Cushing’s syndrome) also exhibit glucocorticoid resistance. Therefore, to differentiate between these conditions, several dynamic tests, including those with desmopressin (DDAVP), corticotrophin-releasing hormone (CRH), and Dex/CRH have been developed. In normal pituitary corticotrophs, ACTH synthesis and secretion are regulated mainly by CRH and glucocorticoids, which are the ACTH secretion-stimulating and -suppressing factors, respectively. These factors regulate ACTH synthesis and secretion through genomic and non-genomic mechanisms. Conversely, glucocorticoid negative feedback is impaired in ACTHomas, which could be due to the overexpression of 11β-HSD2, HSP90, or TR4, or loss of expression of CABLES1 or nuclear BRG1 proteins. Genetic analysis has indicated the involvement of several genes in the etiology of ACTHomas, including USP8, USP48, BRAF, and TP53. However, the association between glucocorticoid resistance and these genes remains unclear. Here, we review the clinical aspects and molecular mechanisms of ACTHomas and compare them to those of other related conditions. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary)
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Open AccessReview
Pituitary Hyperplasia, Hormonal Changes and Prolactinoma Development in Males Exposed to Estrogens—An Insight From Translational Studies
Int. J. Mol. Sci. 2020, 21(6), 2024; https://doi.org/10.3390/ijms21062024 - 16 Mar 2020
Cited by 1
Abstract
Estrogen signaling plays an important role in pituitary development and function. In sensitive rat or mice strains of both sexes, estrogen treatments promote lactotropic cell proliferation and induce the formation of pituitary adenomas (dominantly prolactin or growth-hormone-secreting ones). In male patients receiving estrogen, [...] Read more.
Estrogen signaling plays an important role in pituitary development and function. In sensitive rat or mice strains of both sexes, estrogen treatments promote lactotropic cell proliferation and induce the formation of pituitary adenomas (dominantly prolactin or growth-hormone-secreting ones). In male patients receiving estrogen, treatment does not necessarily result in pituitary hyperplasia, hyperprolactinemia or adenoma development. In this review, we comprehensively analyze the mechanisms of estrogen action upon their application in male animal models comparing it with available data in human subjects. Sex-specific molecular targets of estrogen action in lactotropic (PRL) cells are highlighted in the context of their proliferative and secretory activity. In addition, putative effects of estradiol on the cellular/tumor microenvironment and the contribution of postnatal pituitary progenitor/stem cells and transdifferentiation processes to prolactinoma development have been analyzed. Finally, estrogen-induced morphological and hormone-secreting changes in pituitary thyrotropic (TSH) and adrenocorticotropic (ACTH) cells are discussed, as well as the putative role of the thyroid and/or glucocorticoid hormones in prolactinoma development, based on the current scarce literature. Full article
(This article belongs to the Special Issue Molecular Biology of the Pituitary)
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