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Somatostatin 2.0
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Somatostatin 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 10856

Special Issue Editor

Dr. Ujendra Kumar

E-Mail Website
Guest Editor
Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC V6T 1Z3, Canada
Interests: cancer biology; neurogenerative diseases; aging; BBB; diabetes; peptide processing; G-protein coupled receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Somatostatin, a growth hormone inhibitory peptide, was first isolated from the hypothalamus in 1973. Since its discovery, this peptide has emerged not only as an inhibitor of growth hormones from the pituitary, but also as a dynamic molecule that is widely expressed in different body parts and plays a significant role in many different targets throughout the body. Taking advantage of its antiproliferative effect, SST is frequently used in different types of tumor. Recent studies have further emphasized its role in neurological diseases and neuropsychological disorders in addition to its potential therapeutic implications in acromegaly. Despite significant progress, it still remains elusive how this 14 amino acid peptide plays such a significant role in central and peripheral tissue. In this Special Issue on somatostatin, we will highlight some of the research on somatostatin biology accomplished in the last four decades.

This Special Issue of the International Journal of Molecular Sciences will focus on recent developments in the area of somatostatin. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Dr. Ujendra Kumar
Guest Editor

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 submissions that pass pre-check are 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

  • Somatostatin
  • Somatostatin receptors
  • Signaling
  • Hormones
  • Cancer
  • Neurodegeneration
  • Inflammation

Published Papers (4 papers)

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Research

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15 pages, 8186 KiB  
Article
Reassessment of SST4 Somatostatin Receptor Expression Using SST4-eGFP Knockin Mice and the Novel Rabbit Monoclonal Anti-Human SST4 Antibody 7H49L61
by Amelie Lupp, Blanca Ehms, Ralf Stumm, Johannes Göckeritz, Christian Mawrin and Stefan Schulz
Int. J. Mol. Sci. 2021, 22(23), 12981; https://doi.org/10.3390/ijms222312981 - 30 Nov 2021
Cited by 3 | Viewed by 1931
Abstract
Among the five somatostatin receptors (SST1–SST5), SST4 is the least characterized, which is in part due to the lack of specific monoclonal antibodies. We generated a knockin mouse model that expresses a carboxyl-terminal SST4-eGFP fusion protein. In addition, we extensively characterized the novel [...] Read more.
Among the five somatostatin receptors (SST1–SST5), SST4 is the least characterized, which is in part due to the lack of specific monoclonal antibodies. We generated a knockin mouse model that expresses a carboxyl-terminal SST4-eGFP fusion protein. In addition, we extensively characterized the novel rabbit monoclonal anti-human SST4 antibody 7H49L61 using transfected cells and receptor-expressing tissues. 7H49L61 was then subjected to immunohistochemical staining of a series of formalin-fixed, paraffin-embedded normal and neoplastic human tissues. Characterization of SST4-eGFP mice revealed prominent SST4 expression in cortical pyramidal cells and trigeminal ganglion cells. In the human cortex, 7H49L61 disclosed a virtually identical staining pattern. Specificity of 7H49L61 was demonstrated by detection of a broad band migrating at 50–60 kDa in immunoblots. Tissue immunostaining was abolished by preadsorption of 7H49L61 with its immunizing peptide. In the subsequent immunohistochemical study, 7H49L61 yielded a predominant plasma membrane staining in adrenal cortex, exocrine pancreas, and placenta. SST4 was also found in glioblastomas, parathyroid adenomas, gastric and pancreatic adenocarcinomas, pheochromocytomas, and lymphomas. Altogether, we provide the first unequivocal localization of SST4 in normal and neoplastic human tissues. The monoclonal antibody 7H49L61 may also prove of great value for identifying SST4-expressing tumors during routine histopathological examinations. Full article
(This article belongs to the Special Issue Somatostatin 2.0)
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17 pages, 4980 KiB  
Article
Somatostatin and Astroglial Involvement in the Human Limbic System in Alzheimer’s Disease
by Melania Gonzalez-Rodriguez, Veronica Astillero-Lopez, Patricia Villanueva-Anguita, M. Eugenia Paya-Rodriguez, Alicia Flores-Cuadrado, Sandra Villar-Conde, Isabel Ubeda-Banon, Alino Martinez-Marcos and Daniel Saiz-Sanchez
Int. J. Mol. Sci. 2021, 22(16), 8434; https://doi.org/10.3390/ijms22168434 - 05 Aug 2021
Cited by 7 | Viewed by 2458
Abstract
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease in the elderly. Progressive accumulation of insoluble isoforms of amyloid-β peptide (Aβ) and tau protein are the major neuropathologic hallmarks, and the loss of cholinergic pathways underlies cognitive deficits in patients. Recently, glial involvement [...] Read more.
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease in the elderly. Progressive accumulation of insoluble isoforms of amyloid-β peptide (Aβ) and tau protein are the major neuropathologic hallmarks, and the loss of cholinergic pathways underlies cognitive deficits in patients. Recently, glial involvement has gained interest regarding its effect on preservation and impairment of brain integrity. The limbic system, including temporal lobe regions and the olfactory bulb, is particularly affected in the early stages. In the early 1980s, the reduced expression of the somatostatin neuropeptide was described in AD. However, over the last three decades, research on somatostatin in Alzheimer’s disease has been scarce in humans. Therefore, the aim of this study was to stereologically quantify the expression of somatostatin in the human hippocampus and olfactory bulb and analyze its spatial distribution with respect to that of Aβ and au neuropathologic proteins and astroglia. The results indicate that somatostatin-expressing cells are reduced by 50% in the hippocampus but are preserved in the olfactory bulb. Interestingly, the coexpression of somatostatin with the Aβ peptide is very common but not with the tau protein. Finally, the coexpression of somatostatin with astrocytes is rare, although their spatial distribution is very similar. Altogether, we can conclude that somatostatin expression is highly reduced in the human hippocampus, but not the olfactory bulb, and may play a role in Alzheimer’s disease pathogenesis. Full article
(This article belongs to the Special Issue Somatostatin 2.0)
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Review

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13 pages, 9399 KiB  
Review
Renal and Red Marrow Dosimetry in Peptide Receptor Radionuclide Therapy: 20 Years of History and Ahead
by Stephan Walrand and François Jamar
Int. J. Mol. Sci. 2021, 22(15), 8326; https://doi.org/10.3390/ijms22158326 - 03 Aug 2021
Cited by 9 | Viewed by 2570
Abstract
The development of dosimetry and studies in peptide receptor radionuclide therapy (PRRT) over the past two decades are reviewed. Differences in kidney and bone marrow toxicity reported between 90Y, 177Lu and external beam radiotherapy (EBRT) are discussed with regard to the [...] Read more.
The development of dosimetry and studies in peptide receptor radionuclide therapy (PRRT) over the past two decades are reviewed. Differences in kidney and bone marrow toxicity reported between 90Y, 177Lu and external beam radiotherapy (EBRT) are discussed with regard to the physical properties of these beta emitter radionuclides. The impact of these properties on the response to small and large tumors is also considered. Capacities of the imaging modalities to assess the dosimetry to target tissues are evaluated. Studies published in the past two years that confirm a red marrow uptake in 177Lu-DOTATATE therapy, as already observed 20 years ago in 86Y-DOTATOC PET studies, are analyzed in light of the recent developments in the transferrin transport mechanism. The review enlightens the importance (i) of using state-of-the-art imaging modalities, (ii) of individualizing the activity to be injected with regard to the huge tissue uptake variability observed between patients, (iii) of challenging the currently used but inappropriate blood-based red marrow dosimetry and (iv) of considering individual tandem therapy. Last, a smart individually optimized tandem therapy taking benefit of the bi-orthogonal toxicity-response pattern of 177Lu-DOTATATE and of 90Y-DOTATOC is proposed. Full article
(This article belongs to the Special Issue Somatostatin 2.0)
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15 pages, 1419 KiB  
Review
Somatostatin, a Presynaptic Modulator of Glutamatergic Signal in the Central Nervous System
by Anna Pittaluga, Alessandra Roggeri, Giulia Vallarino and Guendalina Olivero
Int. J. Mol. Sci. 2021, 22(11), 5864; https://doi.org/10.3390/ijms22115864 - 30 May 2021
Cited by 13 | Viewed by 3224
Abstract
Somatostatin is widely diffused in the central nervous system, where it participates to control the efficiency of synaptic transmission. This peptide mainly colocalizes with GABA, in inhibitory, GABA-containing interneurons from which it is actively released in a Ca2+ dependent manner upon application [...] Read more.
Somatostatin is widely diffused in the central nervous system, where it participates to control the efficiency of synaptic transmission. This peptide mainly colocalizes with GABA, in inhibitory, GABA-containing interneurons from which it is actively released in a Ca2+ dependent manner upon application of depolarizing stimuli. Once released in the synaptic cleft, somatostatin acts locally, or it diffuses in the extracellular space through “volume diffusion”, a mechanism(s) of distribution which mainly operates in the cerebrospinal fluid and that assures the progression of neuronal signalling from signal-secreting sender structures towards receptor-expressing targeted neurons located extrasynaptically, in a non-synaptic, inter-neuronal form of communication. Somatostatin controls the efficiency of central glutamate transmission by either modulating presynaptically the glutamate exocytosis or by metamodulating the activity of glutamate receptors colocalized and functionally coupled with somatostatin receptors in selected subpopulations of nerve terminals. Deciphering the role of somatostatin in the mechanisms of “volume diffusion” and in the “receptor-receptor interaction” unveils new perspectives in the central role of this fine tuner of synaptic strength, paving the road to new therapeutic approaches for the cure of central disorders. Full article
(This article belongs to the Special Issue Somatostatin 2.0)
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