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Steroids and Lipophilic Hormones, and Their Actions

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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 October 2019) | Viewed by 31592

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Special Issue Editor

Prof. Dr. Noriyuki Koibuchi

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Guest Editor

Department of Integrative Physiology, Gunma University Graduate School of Medicine, 3-39-22, Showa-machi, Maebashi, Gunma 371-8511, Japan
Interests: steroid/thyroid hormone in CNS; neuroendocrine; cerebellum; trophic factors in brain development and organ metabolism; nuclear receptor; endocrine disrupting chemicals; epigenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Small lipophilic hormones such as steroid, thyroid, retinoids, vitamin D, and other endogenous substances play an important role in signal transduction pathway across various organs. Their action is mainly exerted by biding to nuclear hormone receptors, which are the ligand-activated transcription factors. These nuclear receptors are indispensible for epigenetic programmig of the cell. Disruption of this hormone signaling may cause a varois disorders.

In this Special Issue, we call for manuscripts on various aspects of the celllular and molecular biology of steroids and other lipohilic hormones, including the regulation of synthesis, secretion, and their actions. We also accept manuscripts dealing with the disruption of hormone actions by environmental chemicals and xenobiotics. Through this Special Issue, we would like to provide excellent articles in this research field to a broad range of readers.

Prof. Dr. Noriyuki Koibuchi
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

steroid
thyroid
retinoid
vitamin D
neurosteroid
nuclear receptor
endocrine disruption

Published Papers (6 papers)

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Research

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16 pages, 1538 KiB

Open AccessArticle

Single-Cell Gene Profiling Reveals Social Status-Dependent Modulation of Nuclear Hormone Receptors in GnRH Neurons in a Male Cichlid Fish

by Satoshi Ogawa and Ishwar S. Parhar

Int. J. Mol. Sci. 2020, 21(8), 2724; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082724 - 15 Apr 2020

Cited by 16 | Viewed by 2714

Abstract

Gonadotropin-releasing hormone (GnRH) is essential for the initiation and maintenance of reproductive functions in vertebrates. To date, three distinct paralogue lineages, GnRH1, GnRH2, and GnRH3, have been identified with different functions and regulatory mechanisms. Among them, hypothalamic GnRH1 neurons are classically known as the hypophysiotropic form that is regulated by estrogen feedback. However, the mechanism of action underlying the estrogen-dependent regulation of GnRH1 has been debated, mainly due to the coexpression of low levels of estrogen receptor (ER) genes. In addition, the role of sex steroids in the modulation of GnRH2 and GnRH3 neurons has not been fully elucidated. Using single-cell real-time PCR, we revealed the expression of genes for estrogen, androgen, glucocorticoid, thyroid, and xenobiotic receptors in GnRH1, GnRH2, and GnRH3 neurons in the male Nile tilapia Oreochromis niloticus. We further quantified expression levels of estrogen receptor genes (ERα, ERβ, and ERγ) in three GnRH neuron types in male tilapia of two different social statuses (dominant and subordinate) at the single cell level. In dominant males, GnRH1 mRNA levels were positively proportional to ERγ mRNA levels, while in subordinate males, GnRH2 mRNA levels were positively proportional to ERβ mRNA levels. These results indicate that variations in the expression of nuclear receptors (and possibly steroid sensitivities) among individual GnRH cells may facilitate different physiological processes, such as the promotion of reproductive activities through GnRH1 neurons, and the inhibition of feeding and sexual behaviors through GnRH2 neurons. Full article

(This article belongs to the Special Issue Steroids and Lipophilic Hormones, and Their Actions)

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19 pages, 18524 KiB

Open AccessArticle

Neurochemical Characterization of Neurons Expressing Estrogen Receptor β in the Hypothalamic Nuclei of Rats Using in Situ Hybridization and Immunofluorescence

by Moeko Kanaya, Shimpei Higo and Hitoshi Ozawa

Int. J. Mol. Sci. 2020, 21(1), 115; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21010115 - 23 Dec 2019

Cited by 18 | Viewed by 5657

Abstract

Estrogens play an essential role in multiple physiological functions in the brain, including reproductive neuroendocrine, learning and memory, and anxiety-related behaviors. To determine these estrogen functions, many studies have tried to characterize neurons expressing estrogen receptors known as ERα and ERβ. However, the characteristics of ERβ-expressing neurons in the rat brain still remain poorly understood compared to that of ERα-expressing neurons. The main aim of this study is to determine the neurochemical characteristics of ERβ-expressing neurons in the rat hypothalamus using RNAscope in situ hybridization (ISH) combined with immunofluorescence. Strong Esr2 signals were observed especially in the anteroventral periventricular nucleus (AVPV), bed nucleus of stria terminalis, hypothalamic paraventricular nucleus (PVN), supraoptic nucleus, and medial amygdala, as previously reported. RNAscope ISH with immunofluorescence revealed that more than half of kisspeptin neurons in female AVPV expressed Esr2, whereas few kisspeptin neurons were found to co-express Esr2 in the arcuate nucleus. In the PVN, we observed a high ratio of Esr2 co-expression in arginine-vasopressin neurons and a low ratio in oxytocin and corticotropin-releasing factor neurons. The detailed neurochemical characteristics of ERβ-expressing neurons identified in the current study can be very essential to understand the estrogen signaling via ERβ. Full article

(This article belongs to the Special Issue Steroids and Lipophilic Hormones, and Their Actions)

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16 pages, 5667 KiB

Open AccessArticle

Applicability of Anti-Human Estrogen Receptor β Antibody PPZ0506 for the Immunodetection of Rodent Estrogen Receptor β Proteins

by Hirotaka Ishii, Mai Otsuka, Moeko Kanaya, Shimpei Higo, Yujiro Hattori and Hitoshi Ozawa

Int. J. Mol. Sci. 2019, 20(24), 6312; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20246312 - 13 Dec 2019

Cited by 15 | Viewed by 2937

Abstract

Several lines of controversial evidence concerning estrogen receptor β (ERβ) remain to be solved because of the unavailability of specific antibodies against ERβ. The recent validation analysis identified a monoclonal antibody (PPZ0506) with sufficient specificity against human ERβ. However, the specificity and cross-reactivity of PPZ0506 antibody against ERβ proteins from laboratory animals have not been confirmed. In the present study, we aimed to validate the applicability of PPZ0506 to rodent studies. The antibody exhibited specific cross-reactivity against mouse and rat ERβ proteins in immunoblot and immunocytochemical experiments using transfected cells. In immunohistochemistry for rat tissue sections, PPZ0506 showed immunoreactive signals in the ovary, prostate, and brain. These immunohistochemical profiles of rat ERβ proteins in rat tissues accord well with its mRNA expression patterns. Although the antibody was reported to show the moderate signals in human testis, no immunoreactive signals were observed in rat testis. Subsequent RT-PCR analysis revealed that this species difference in ERβ expression resulted from different expression profiles related to the alternative promoter usage between humans and rats. In conclusion, we confirmed applicability of PPZ0506 for rodent ERβ studies, and our results provide a fundamental basis for further examination of ERβ functions. Full article

(This article belongs to the Special Issue Steroids and Lipophilic Hormones, and Their Actions)

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14 pages, 14825 KiB

Open AccessArticle

A Novel Mechanism of S-equol Action in Neurons and Astrocytes: The Possible Involvement of GPR30/GPER1

by Winda Ariyani, Wataru Miyazaki and Noriyuki Koibuchi

Int. J. Mol. Sci. 2019, 20(20), 5178; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20205178 - 18 Oct 2019

Cited by 17 | Viewed by 3774

Abstract

S-equol is a major bacterial metabolite of the soy isoflavone daidzein. It is known to be a phytoestrogen that acts by binding to the nuclear estrogen receptors (ERs) that are expressed in various brain regions, including the cerebellum. However, the effects of S-equol on cerebellar development and function have not yet been extensively studied. In this study, the effects of S-equol were evaluated using a mouse primary cerebellar culture, Neuro-2A clonal cells, and an astrocyte-enriched culture. S-equol augmented the dendrite arborization of Purkinje cells induced by triiodothyronine (T₃) and the neurite growth of Neuro-2A cell differentiation. Such augmentation was suppressed by G15, a selective G-protein coupled ER (GPR30) antagonist, and ICI 182,780, an antagonist for ERs in both cultures. On the other hand, in astrocytes, S-equol induced cell proliferation and cell migration with an increase in the phosphorylated extracellular-signal-regulated kinase 1/2 and F-actin rearrangements. Such effects were suppressed by G15, but not by ICI. These findings indicated that S-equol may enhanced cerebellar development by affecting both neurons and astrocytes through several signaling pathways, including GPR30 and ERs. We here report a novel mechanism of S-equol in cerebellar development that may provide a novel possibility to use S-equol supplementation during development. Full article

(This article belongs to the Special Issue Steroids and Lipophilic Hormones, and Their Actions)

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Review

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21 pages, 3288 KiB

Open AccessReview

Steroid Therapy and Steroid Response in Autoimmune Pancreatitis

by Hiroyuki Matsubayashi, Hirotoshi Ishiwatari, Kenichiro Imai, Yoshihiro Kishida, Sayo Ito, Kinichi Hotta, Yohei Yabuuchi, Masao Yoshida, Naomi Kakushima, Kohei Takizawa, Noboru Kawata and Hiroyuki Ono

Int. J. Mol. Sci. 2020, 21(1), 257; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21010257 - 30 Dec 2019

Cited by 26 | Viewed by 7631

Abstract

Autoimmune pancreatitis (AIP), a unique subtype of pancreatitis, is often accompanied by systemic inflammatory disorders. AIP is classified into two distinct subtypes on the basis of the histological subtype: immunoglobulin G4 (IgG4)-related lymphoplasmacytic sclerosing pancreatitis (type 1) and idiopathic duct-centric pancreatitis (type 2). Type 1 AIP is often accompanied by systemic lesions, biliary strictures, hepatic inflammatory pseudotumors, interstitial pneumonia and nephritis, dacryoadenitis, and sialadenitis. Type 2 AIP is associated with inflammatory bowel diseases in approximately 30% of cases. Standard therapy for AIP is oral corticosteroid administration. Steroid treatment is generally indicated for symptomatic cases and is exceptionally applied for cases with diagnostic difficulty (diagnostic steroid trial) after a negative workup for malignancy. More than 90% of patients respond to steroid treatment within 1 month, and most within 2 weeks. The steroid response can be confirmed on clinical images (computed tomography, ultrasonography, endoscopic ultrasonography, magnetic resonance imaging, and ¹⁸F-fluorodeoxyglucose-positron emission tomography). Hence, the steroid response is included as an optional diagnostic item of AIP. Steroid treatment results in normalization of serological markers, including IgG4. Short- and long-term corticosteroid treatment may induce adverse events, including chronic glycometabolism, obesity, an immunocompromised status against infection, cataracts, glaucoma, osteoporosis, and myopathy. AIP is common in old age and is often associated with diabetes mellitus (33–78%). Thus, there is an argument for corticosteroid therapy in diabetes patients with no symptoms. With low-dose steroid treatment or treatment withdrawal, there is a high incidence of AIP recurrence (24–52%). Therefore, there is a need for long-term steroid maintenance therapy and/or steroid-sparing agents (immunomodulators and rituximab). Corticosteroids play a critical role in the diagnosis and treatment of AIP. Full article

(This article belongs to the Special Issue Steroids and Lipophilic Hormones, and Their Actions)

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15 pages, 930 KiB

Open AccessReview

Growth Hormone Deficiency Following Traumatic Brain Injury

by Oratile Kgosidialwa, Osamah Hakami, Hafiz Muhammad Zia-Ul-Hussnain and Amar Agha

Int. J. Mol. Sci. 2019, 20(13), 3323; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20133323 - 06 Jul 2019

Cited by 28 | Viewed by 7418

Abstract

Traumatic brain injury (TBI) is fairly common and annually affects millions of people worldwide. Post traumatic hypopituitarism (PTHP) has been increasingly recognized as an important and prevalent clinical entity. Growth hormone deficiency (GHD) is the most common pituitary hormone deficit in long-term survivors of TBI. The pathophysiology of GHD post TBI is thought to be multifactorial including primary and secondary mechanisms. An interplay of ischemia, cytotoxicity, and inflammation post TBI have been suggested, resulting in pituitary hormone deficits. Signs and symptoms of GHD can overlap with those of TBI and may delay rehabilitation/recovery if not recognized and treated. Screening for GHD is recommended in the chronic phase, at least six months to a year after TBI as GH may recover in those with GHD in the acute phase; conversely, it may manifest in those with a previously intact GH axis. Dynamic testing is the standard method to diagnose GHD in this population. GHD is associated with long-term poor medical outcomes. Treatment with recombinant human growth hormone (rhGH) seems to ameliorate some of these features. This review will discuss the frequency and pathophysiology of GHD post TBI, its clinical consequences, and the outcomes of treatment with GH replacement. Full article

(This article belongs to the Special Issue Steroids and Lipophilic Hormones, and Their Actions)

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