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Special Issue "Growth Hormone (GH): Multiple Therapeutic Possibilities and Molecular Mechanisms of Action 2.0"

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

Deadline for manuscript submissions: 31 July 2021.

Special Issue Editor

Prof. Dr. Jesús Devesa
E-Mail Website
Guest Editor
Scientific Director of The Medical Center Foltra. Travesía de Montouto 24, 15886 TEO, Spain
Interests: growth hormone; growth hormone receptor; IGF-I; brain injury; stroke; cerebral palsy; hypoxia/ischemia; neurodegeneration; atherosclerosis; growth hormone and gonads; growth hormone and diabetes; growth hormone and cancer; growth hormone signaling pathway
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Special Issue Information

Dear Colleagues,

Classically, GH has been considered to be a pituitary hormone, with predominantly metabolic actions and an effect on the longitudinal growth of that organism until the end of puberty. However, today, we know that GH is expressed in virtually all tissues and organs of the human body, in which it plays a self/paracrine role—possibly, although it is not known—in cooperation with hormones from the plasma after being released by the pituitary gland. We also know that after interacting with its membrane receptor, GH is internalized together with the GHR, a mechanism that allows the GHR to be translocated to the nucleus of cells for inducing or blocking gene expression; we also know that, at least in rodents, internalized GH undergoes a proteolytic break (tissue, sex, and age-specific), giving rise to shorter peptides whose functions are still unknown. Since the beginning of the 2000s, when it was discovered that the GHR was upregulated in the brain of rodents after induced brain damage, interest in the possible actions of GH in the repair of the brain has continued to increase. The same is true with respect to the effects of the hormone on the vascular endothelium, where GH seems to have a beneficial effect, or in the gonads, where a local GH/IGF-I axis seems to play a key role in the physiological gonadal function. The effects of GH on the beta cells of the islets of Langerhans and diabetes need to be clarified, as well as the relationships between GH and cancer. Furthermore, GH signaling pathways in different tissues must be elucidated, and the same is true of the induction by GH of the expression of many different growth factors.
Giving an answer to these molecular mechanisms of action, still unknown or poorly understood, and the relationships between GH and other growth factors will provide a better understanding of the effects of this important hormone, for its therapeutic use in many different pathologies beyond its mere use for growth in GH-deficient children.
For these reasons, researchers are invited to submit their original research or reviews for this Special Issue of the International Journal of Molecular Sciences, entitled "Growth Hormone (GH): Multiple Possibilities and Molecular Mechanisms of Action", which will cover a selection of topics highlighting the role of GH and its molecular effects in health (included aging) and therapeutic possibilities.

Prof. Dr. Jesús Devesa
Guest Editor

Manuscript Submission Information

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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.

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Keywords

  • Growth Hormone
  • cancer
  • GH/IGF-I axis
  • GH-deficient

Published Papers (1 paper)

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Research

Open AccessArticle
Neuroprotective Effects of Growth Hormone (GH) and Insulin-Like Growth Factor Type 1 (IGF-1) after Hypoxic-Ischemic Injury in Chicken Cerebellar Cell Cultures
Int. J. Mol. Sci. 2021, 22(1), 256; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22010256 - 29 Dec 2020
Viewed by 536
Abstract
It has been reported that growth hormone (GH) and insulin-like growth factor 1 (IGF-1) exert protective and regenerative actions in response to neural damage. It is also known that these peptides are expressed locally in nervous tissues. When the central nervous system (CNS) [...] Read more.
It has been reported that growth hormone (GH) and insulin-like growth factor 1 (IGF-1) exert protective and regenerative actions in response to neural damage. It is also known that these peptides are expressed locally in nervous tissues. When the central nervous system (CNS) is exposed to hypoxia-ischemia (HI), both GH and IGF-1 are upregulated in several brain areas. In this study, we explored the neuroprotective effects of GH and IGF-1 administration as well as the involvement of these endogenously expressed hormones in embryonic chicken cerebellar cell cultures exposed to an acute HI injury. To induce neural damage, primary cultures were first incubated under hypoxic-ischemic (<5% O2, 1g/L glucose) conditions for 12 h (HI), and then incubated under normal oxygenation and glucose conditions (HI + Ox) for another 24 h. GH and IGF-1 were added either during or after HI, and their effect upon cell viability, apoptosis, or necrosis was evaluated. In comparison with normal controls (Nx, 100%), a significant decrease of cell viability (54.1 ± 2.1%) and substantial increases in caspase-3 activity (178.6 ± 8.7%) and LDH release (538.7 ± 87.8%) were observed in the HI + Ox group. On the other hand, both GH and IGF-1 treatments after injury (HI + Ox) significantly increased cell viability (77.2 ± 4.3% and 72.3 ± 3.9%, respectively) and decreased both caspase-3 activity (118.2 ± 3.8% and 127.5 ± 6.6%, respectively) and LDH release (180.3 ± 21.8% and 261.6 ± 33.9%, respectively). Incubation under HI + Ox conditions provoked an important increase in the local expression of GH (3.2-fold) and IGF-1 (2.5-fold) mRNAs. However, GH gene silencing with a specific small-interfering RNAs (siRNAs) decreased both GH and IGF-1 mRNA expression (1.7-fold and 0.9-fold, respectively) in the HI + Ox group, indicating that GH regulates IGF-1 expression under these incubation conditions. In addition, GH knockdown significantly reduced cell viability (35.9 ± 2.1%) and substantially increased necrosis, as determined by LDH release (1011 ± 276.6%). In contrast, treatments with GH and IGF-1 stimulated a partial recovery of cell viability (45.2 ± 3.7% and 53.7 ± 3.2%) and significantly diminished the release of LDH (320.1 ± 25.4% and 421.7 ± 62.2%), respectively. Our results show that GH, either exogenously administered and/or locally expressed, can act as a neuroprotective factor in response to hypoxic-ischemic injury, and that this effect may be mediated, at least partially, through IGF-1 expression. Full article
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