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Molecular Toxicology

A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Toxicology and Public Health".

Deadline for manuscript submissions: closed (31 May 2020) | Viewed by 6105

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Department of Biology, College of Science, Engineering, and Technology, Jackson State University, Jackson, MS 39217, USA
Interests: lung cancer; lung fibrosis; nanotoxicogenomics; endothelial dysfunction; molecular network interactions
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Special Issue Information

Dear Colleagues,


This Special Issue is intended to cover the mechanisms that regulate microRNAs (miRNAs). The discovery of miRNAs has tremendously advanced the understanding of signal transduction, not only during normal development, but also in pathological conditions. Studies have shown the critical role of miRNAs in many biological processes, including proliferation, differentiation, migration and invasion, apoptosis, and transformation. Moreover, recent studies also show a role of miRNAs in host–pathogen interactions. Therefore, this Special Issue is dedicated to understanding how these miRNAs are regulated, such as how their aberrant expression contributes to the development of disease. This being said, in this Special Issue, we invite the scientific community to address the mechanisms that regulate miRNAs in organ injury, cancer, cardiovascular disease, and diabetes. We invite both original articles and reviews on the future of translation medicine. In this Special Issue, we are excited to address such a small molecule, with sucha giant switch with profound biological effects.

Dr. Maricica Pacurari
Guest Editor

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Keywords

  • microRNA
  • signal transduction
  • regulation
  • hormones
  • disease
  • development
  • inflammation
  • oxidative stress
  • cytokines
  • organ injury
  • cancer
  • diabetes

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Published Papers (2 papers)

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Research

18 pages, 8000 KiB  
Article
The Effects of Long-Term Immunosuppressive Therapies on the Structure of the Rat Prostate
by Marta Grabowska, Maria Laszczyńska, Karolina Kędzierska-Kapuza, Andrzej Kram, Kamil Gill and Małgorzata Piasecka
Int. J. Environ. Res. Public Health 2020, 17(12), 4614; https://doi.org/10.3390/ijerph17124614 - 26 Jun 2020
Cited by 3 | Viewed by 2971
Abstract
Background: Little is known about the overall impact of immunosuppressive drugs on the prostate. The study aimed to determine the impact of different protocols of immunosuppressive treatment on the structure of the rat ventral prostate. Methods: For 6 months, 48 male Wistar [...] Read more.
Background: Little is known about the overall impact of immunosuppressive drugs on the prostate. The study aimed to determine the impact of different protocols of immunosuppressive treatment on the structure of the rat ventral prostate. Methods: For 6 months, 48 male Wistar rats received immunosuppressive drugs: cyclosporin A, tacrolimus, mycophenolate mofetil, rapamycin, and prednisone, according to three-drug protocols. Light and transmission electron microscopic studies, and quantitative evaluation of immunohistochemical expression of selected intermediate filaments, CD117+ mast cells, and CD138+ plasma cells were performed in the rat ventral prostate. Results: In all experimental groups, acini focal hyperplasia, changes to the ultrastructure of the glandular epithelium, changes in the expression of cytokeratins and desmin, and numerous mast and plasma cells in the prostate stroma were found. In cyclosporine-A-based groups, atrophy and numerous intracellular vacuoles were observed. In groups where a three-drug treatment was replaced with rapamycin, morphological alterations were less severe compared to those without conversion. Conclusions: In the rat ventral prostate, (1) immunosuppressive protocols affect the morphology and immunohistochemical expression of intermediate filaments, (2) morphological alterations, expression, and localization of selected proteins are not connected with adenocarcinoma development, and (3) conversion of the treatment to rapamycin may prevent hyperplastic abnormalities. Full article
(This article belongs to the Special Issue Molecular Toxicology)
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14 pages, 2094 KiB  
Article
Effects of Gintonin-Enriched Fraction on Methylmercury-Induced Neurotoxicity and Organ Methylmercury Elimination
by Hyeon-Joong Kim, Sun-Hye Choi, Na-Eun Lee, Hee-Jung Cho, Hyewhon Rhim, Hyoung-Chun Kim, Sung-Hee Hwang and Seung-Yeol Nah
Int. J. Environ. Res. Public Health 2020, 17(3), 838; https://doi.org/10.3390/ijerph17030838 - 29 Jan 2020
Cited by 6 | Viewed by 2727
Abstract
Gintonin is a newly discovered ingredient of ginseng and plays an exogenous ligand for G protein-coupled lysophosphatidic acid receptors. We previously showed that gintonin exhibits diverse effects from neurotransmitter release to improvement of Alzheimer’s disease-related cognitive dysfunctions. However, previous studies did not show [...] Read more.
Gintonin is a newly discovered ingredient of ginseng and plays an exogenous ligand for G protein-coupled lysophosphatidic acid receptors. We previously showed that gintonin exhibits diverse effects from neurotransmitter release to improvement of Alzheimer’s disease-related cognitive dysfunctions. However, previous studies did not show whether gintonin has protective effects against environmental heavy metal. We investigated the effects of gintonin-enriched fraction (GEF) on methylmercury (MeHg)-induced neurotoxicity and learning and memory dysfunction and on organ MeHg elimination. Using hippocampal neural progenitor cells (hNPCs) and mice we examined the effects of GEF on MeHg-induced hippocampal NPC neurotoxicity, on formation of reactive oxygen species (ROS), and on in vivo learning and memory functions after acute MeHg exposure. Treatment of GEF to hNPCs attenuated MeHg-induced neurotoxicity with concentration- and time-dependent manner. GEF treatment inhibited MeHg- and ROS inducer-induced ROS formations. Long-term treatment of GEF also improved MeHg-induced learning and memory dysfunctions. Oral administration of GEF decreased the concentrations of MeHg in blood, brain, liver, and kidney. This is the first report that GEF attenuated MeHg-induced in vitro and in vivo neurotoxicities through LPA (lysophosphatidic acids) receptor-independent manner and increased organ MeHg elimination. GEF-mediated neuroprotection might achieve via inhibition of ROS formation and facilitation of MeHg elimination from body. Full article
(This article belongs to the Special Issue Molecular Toxicology)
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