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Molecular Biology of Nuclear Receptors 4.0
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Molecular Biology of Nuclear Receptors 4.0

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

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 4007

Special Issue Editor

Prof. Dr. Akira Sugawara

E-Mail Website
Guest Editor
Department of Molecular Endocrinology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan
Interests: elucidation of the involvement of nuclear receptors in the etiology of endocrine/metabolic disorders; innovation of novel drugs against endocrine/metabolic disorders by targeting nuclear receptors; identification of co-factors; post-translational modifications of nuclear receptors by LC/MS/MS
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nuclear receptors include steroid/thyroid hormone receptors, metabolic sensors and orphan receptors. Metabolic sensor-type nuclear receptors, such as liver X receptor, farnesoid X receptor and peroxisome proliferator activator receptor (PPAR), are activated by oxysterol, bile acid and fatty acid, and regulate their metabolism. These receptors, like steroid hormone receptors, also regulate cellular proliferation/differentiation, and immunity. Dysregulation in these systems has been implicated in the pathogenesis of human diseases, such as cancer, cardiovascular disease, and inflammation. Moreover, nuclear receptors including PPAR, retinoid receptors, and several orphan receptors have recently been known to be involved in the etiology of metabolic syndrome and atherosclerosis. In this Special Issue, we are pleased to invite original manuscripts focusing on the relationships between nuclear receptors and human disorders, as well as novel drug innovation.

Prof. Dr. Akira Sugawara
Guest Editor

Manuscript Submission Information

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Keywords

  • retinoid receptors
  • peroxisome proliferator activator receptor
  • orphan receptors
  • metabolic syndrome
  • endocrine disorders
  • liver X receptor
  • vitamin D receptor
  • lipid metabolism
  • bile acid metabolism
  • immunity

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Published Papers (2 papers)

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Research

19 pages, 2914 KiB  
Article
Hepatocyte Nuclear Factor 4α (HNF4α) Plays a Controlling Role in Expression of the Retinoic Acid Receptor β (RARβ) Gene in Hepatocytes
by Reza Zolfaghari, Jessica A. Bonzo, Frank J. Gonzalez and A. Catharine Ross
Int. J. Mol. Sci. 2023, 24(10), 8608; https://doi.org/10.3390/ijms24108608 - 11 May 2023
Cited by 2 | Viewed by 1769
Abstract
HNF4α, a member of the nuclear receptor superfamily, regulates the genes involved in lipid and glucose metabolism. The expression of the RARβ gene in the liver of HNF4α knock-out mice was higher versus wildtype controls, whereas oppositely, RARβ promoter activity was 50% reduced [...] Read more.
HNF4α, a member of the nuclear receptor superfamily, regulates the genes involved in lipid and glucose metabolism. The expression of the RARβ gene in the liver of HNF4α knock-out mice was higher versus wildtype controls, whereas oppositely, RARβ promoter activity was 50% reduced by the overexpression of HNF4α in HepG2 cells, and treatment with retinoic acid (RA), a major metabolite of vitamin A, increased RARβ promoter activity 15-fold. The human RARβ2 promoter contains two DR5 and one DR8 binding motifs, as RA response elements (RARE) proximal to the transcription start site. While DR5 RARE1 was previously reported to be responsive to RARs but not to other nuclear receptors, we show here that mutation in DR5 RARE2 suppresses the promoter response to HNF4α and RARα/RXRα. Mutational analysis of ligand-binding pocket amino acids shown to be critical for fatty acid (FA) binding indicated that RA may interfere with interactions of FA carboxylic acid headgroups with side chains of S190 and R235, and the aliphatic group with I355. These results could explain the partial suppression of HNF4α transcriptional activation toward gene promoters that lack RARE, including APOC3 and CYP2C9, while conversely, HNF4α may bind to RARE sequences in the promoter of the genes such as CYP26A1 and RARβ, activating these genes in the presence of RA. Thus, RA could act as either an antagonist towards HNF4α in genes lacking RAREs, or as an agonist for RARE-containing genes. Overall, RA may interfere with the function of HNF4α and deregulate HNF4α targets genes, including the genes important for lipid and glucose metabolism. Full article
(This article belongs to the Special Issue Molecular Biology of Nuclear Receptors 4.0)
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13 pages, 6172 KiB  
Article
Vitamin D Receptor Mediates Attenuating Effect of Lithocholic Acid on Dextran Sulfate Sodium Induced Colitis in Mice
by Hitomi Kubota, Michiyasu Ishizawa, Makoto Kodama, Yoshihiro Nagase, Shigeaki Kato, Makoto Makishima and Kenichi Sakurai
Int. J. Mol. Sci. 2023, 24(4), 3517; https://doi.org/10.3390/ijms24043517 - 9 Feb 2023
Cited by 8 | Viewed by 1910
Abstract
Bile acids are major components of bile; they emulsify dietary lipids for efficient digestion and absorption and act as signaling molecules that activate nuclear and membrane receptors. The vitamin D receptor (VDR) is a receptor for the active form of vitamin D and [...] Read more.
Bile acids are major components of bile; they emulsify dietary lipids for efficient digestion and absorption and act as signaling molecules that activate nuclear and membrane receptors. The vitamin D receptor (VDR) is a receptor for the active form of vitamin D and lithocholic acid (LCA), a secondary bile acid produced by the intestinal microflora. Unlike other bile acids that enter the enterohepatic circulation, LCA is poorly absorbed in the intestine. Although vitamin D signaling regulates various physiological functions, including calcium metabolism and inflammation/immunity, LCA signaling remains largely unknown. In this study, we investigated the effect of the oral administration of LCA on colitis in a mouse model using dextran sulfate sodium (DSS). Oral LCA decreased the disease activity of colitis in the early phase, which is a phenotype associated with the suppression of histological injury, such as inflammatory cell infiltration and goblet cell loss. These protective effects of LCA were abolished in VDR-deleted mice. LCA decreased the expression of inflammatory cytokine genes, but this effect was at least partly observed in VDR-deleted mice. The pharmacological effect of LCA on colitis was not associated with hypercalcemia, an adverse effect induced by vitamin D compounds. Therefore, LCA suppresses DSS-induced intestinal injury in its action as a VDR ligand. Full article
(This article belongs to the Special Issue Molecular Biology of Nuclear Receptors 4.0)
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