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Environmental Medicine and Human Diseases: Molecular Insight

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 14003

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Special Issue Editor

Dr. Hong Sun

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Guest Editor

Department of Environmental Medicine, New York University School of Medicine, 341 East 25 Street, New York, NY 10010, USA
Interests: environmental medicine; human disease; epigenetics

Special Issue Information

Dear Colleagues,

Human health can be influenced by physical, chemical, biological, and radiological contaminants in our air, water, and diet. Direct and indirect exposures to environmental toxicants possess a greater risk for onset and progression of leading diseases, such as cardiovascular disease, chronic obstructive pulmonary disease, asthma, diabetes, obesity, and cancer. Environmental medicine is a multidisciplinary field that aims to identify human diseases associated with environmental exposure and determine underlying mechanisms of adverse health outcomes. It is essential to consider fundamental cellular and molecular processes that drive the initiation and progression of diseases, some of which may include regulation of gene expression, DNA replication and repair, epigenetic modifications, and cellular homeostasis.

This Special Issue will focus on research that further enhances our understanding of environmental exposures and human disease. It aims to encompass a diversity of fields, such as molecular and cellular biology, medicine, toxicology, and environmental science.

We kindly invite researchers working in these fields to submit their original research or review manuscripts to this Special Issue on environmental medicine.

Dr. Hong Sun
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

contaminants
human disease
environmental exposure
environmental medicine
gene expression
DNA replication and repair
epigenetic modifications
cellular homeostasis

Published Papers (5 papers)

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Research

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21 pages, 9230 KiB

Open AccessArticle

The Oncogenic and Tumor Suppressive Long Non-Coding RNA–microRNA–Messenger RNA Regulatory Axes Identified by Analyzing Multiple Platform Omics Data from Cr(VI)-Transformed Cells and Their Implications in Lung Cancer

by Osama Sweef, Chengfeng Yang and Zhishan Wang

Biomedicines 2022, 10(10), 2334; https://doi.org/10.3390/biomedicines10102334 - 20 Sep 2022

Cited by 5 | Viewed by 1596

Abstract

Chronic exposure to hexavalent chromium (Cr(VI)) causes lung cancer in humans, however, the underlying mechanism has not been well understood. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are commonly studied non-coding RNAs. miRNAs function mainly through interaction with the 3′-untranslated regions of messenger RNAs (mRNAs) to down-regulate gene expression. LncRNAs have been shown to function as competing endogenous RNAs (ceRNAs) to sponge miRNAs and regulate gene expression. It is now well accepted that lncRNAs and miRNAs could function as oncogenes or tumor suppressors. Dysregulations of lncRNAs and miRNAs have been shown to play important roles in cancer initiation, progression, and prognosis. To explore the mechanism of Cr(VI) lung carcinogenesis, we performed lncRNA, mRNA, and miRNA microarray analysis using total RNAs from our previously established chronic Cr(VI) exposure malignantly transformed and passage-matched control human bronchial epithelial BEAS-2B cells. Based on the differentially expressed lncRNAs, miRNAs, and mRNAs between the control (BEAS-2B-Control) and Cr(VI)-transformed (BEAS-Cr(VI)) cells and by using the lncRNA–miRNA interaction and miRNA target prediction algorithms, we identified three oncogenic (HOTAIRM1/miR-182-5p/ERO1A, GOLGA8B/miR-30d-5p/RUNX2, and PDCD6IPP2/miR-23a-3p/HOXA1) and three tumor suppressive (ANXA2P1/miR-20b-5p/FAM241A (C4orf32), MIR99AHG/miR-218-5p/GPM6A, and SH3RF3-AS1/miR-34a-5p/HECW2) lncRNA–miRNA–mRNA regulatory axes. Moreover, the relevance of these three oncogenic and three tumor suppressive lncRNA–miRNA–mRNA regulatory axes in lung cancer was explored by analyzing publicly available human lung cancer omics datasets. It was found that the identified three oncogenic lncRNA–miRNA–mRNA regulatory axes (HOTAIRM1/miR-182-5p/ERO1A, GOLGA8B/miR-30d-5p/RUNX2, and PDCD6IPP2/miR-23a-3p/HOXA1) and the three tumor suppressive lncRNA–miRNA–mRNA regulatory axes (ANXA2P1/miR-20b-5p/FAM241A (C4orf32), MIR99AHG/miR-218-5p/GPM6A, and SH3RF3-AS1/miR-34a-5p/HECW2) have significant diagnostic and prognosis prediction values in human lung cancer. In addition, our recent studies showed that Cr(VI)-transformed cells display cancer stem cell (CSC)-like properties. Further bioinformatics analysis identified the oncogenic lncRNA–miRNA–mRNA regulatory axes as the potential regulators of cancer stemness. In summary, our comprehensive analysis of multiple platform omics datasets obtained from Cr(VI)-transformed human bronchial epithelial cells identified several oncogenic and tumor suppressive lncRNA–miRNA–mRNA regulatory axes, which may play important roles in Cr(VI) carcinogenesis and lung cancer in general. Full article

(This article belongs to the Special Issue Environmental Medicine and Human Diseases: Molecular Insight)

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17 pages, 18511 KiB

Open AccessArticle

Depletion of Mdig Changes Proteomic Profiling in Triple Negative Breast Cancer Cells

by Chitra Thakur, Nicholas J. Carruthers, Qian Zhang, Liping Xu, Yao Fu, Zhuoyue Bi, Yiran Qiu, Wenxuan Zhang, Priya Wadgaonkar, Bandar Almutairy, Chunna Guo, Paul M. Stemmer and Fei Chen

Biomedicines 2022, 10(8), 2021; https://doi.org/10.3390/biomedicines10082021 - 19 Aug 2022

Viewed by 1892

Abstract

Triple-negative breast cancers are highly aggressive with an overall poor prognosis and limited therapeutic options. We had previously investigated the role of mdig, an oncogenic gene induced by some environmental risk factors, on the pathogenesis of breast cancer. However, a comprehensive analysis of the proteomic profile affected by mdig in triple-negative breast cancer has not been determined yet. Using label-free bottom-up quantitative proteomics, we compared wildtype control and mdig knockout MDA-MB-231 cells and identified the proteins and pathways that are significantly altered with mdig deletion. A total of 904 differentially expressed (p < 0.005) proteins were identified in the KO cells. Approximately 30 pathways and networks linked to the pathogenicity of breast cancer were either up- or downregulated, such as EIF2 signaling, the unfolded protein response, and isoleucine degradation I. Ingenuity Pathway Analysis established that the differentially expressed proteins have relevant biological actions in cell growth, motility, and malignancy. These data provide the first insight into protein expression patterns in breast cancer associated with a complete disruption of the mdig gene and yielded substantial information on the key proteins, biological processes, and pathways modulated by mdig that contribute to breast cancer tumorigenicity and invasiveness. Full article

(This article belongs to the Special Issue Environmental Medicine and Human Diseases: Molecular Insight)

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14 pages, 16489 KiB

Open AccessArticle

Arsenic Activates the ER Stress-Associated Unfolded Protein Response via the Activating Transcription Factor 6 in Human Bronchial Epithelial Cells

by Priya Wadgaonkar, Zhuoyue Bi, Junmei Wan, Yao Fu, Qian Zhang, Bandar Almutairy, Wenxuan Zhang, Yiran Qiu, Chitra Thakur, Maik Hüttemann and Fei Chen

Biomedicines 2022, 10(5), 967; https://doi.org/10.3390/biomedicines10050967 - 22 Apr 2022

Cited by 4 | Viewed by 2160

Abstract

Arsenic is a well-known human carcinogen associated with a number of cancers, including lung cancers. We have previously shown that long-term exposure to an environmentally relevant concentration of inorganic arsenic (As³⁺) leads to the malignant transformation of the BEAS2B cells, and some of the transformed cells show cancer stem-like features (CSCs) with a significant upregulation of glycolysis and downregulation of mitochondrial oxidative phosphorylation. In the present report, we investigate the short-term effect of As³⁺ on the endoplasmic reticulum (ER) stress response—the “unfolded protein response (UPR)” and metabolism in human bronchial epithelial cell line BEAS-2B cells. Treatment of the cells with inorganic As³⁺ upregulated both glycolysis and mitochondrial respiration. Analysis of ER UPR signaling pathway using a real-time human UPR array revealed that As³⁺ induced a significant up-regulation of some UPR genes, including ATF6, CEBPB, MAPK10, Hsp70, and UBE2G2. Additional tests confirmed that the induction of ATF6, ATF6B and UBE2G2 mRNAs and/or proteins by As³⁺ is dose dependent. Chromosome immunoprecipitation and global sequencing indicated a critical role of Nrf2 in mediating As³⁺-induced expression of these UPR genes. In summary, our data suggest that As³⁺ is able to regulate the ER stress response, possibly through activating the ATF6 signaling. Full article

(This article belongs to the Special Issue Environmental Medicine and Human Diseases: Molecular Insight)

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19 pages, 51271 KiB

Open AccessArticle

Environmental Nanoparticles Reach Human Fetal Brains

by Lilian Calderón-Garcidueñas, Ángel Augusto Pérez-Calatayud, Angélica González-Maciel, Rafael Reynoso-Robles, Héctor G. Silva-Pereyra, Andrea Ramos-Morales, Ricardo Torres-Jardón, Candelario de Jesús Soberanes-Cerino, Raúl Carrillo-Esper, Jesús Carlos Briones-Garduño and Yazmín del Socorro Conde-Gutiérrez

Biomedicines 2022, 10(2), 410; https://doi.org/10.3390/biomedicines10020410 - 9 Feb 2022

Cited by 22 | Viewed by 2637

Abstract

Anthropogenic ultrafine particulate matter (UFPM) and industrial and natural nanoparticles (NPs) are ubiquitous. Normal term, preeclamptic, and postconceptional weeks(PCW) 8–15 human placentas and brains from polluted Mexican cities were analyzed by TEM and energy-dispersive X-ray spectroscopy. We documented NPs in maternal erythrocytes, early syncytiotrophoblast, Hofbauer cells, and fetal endothelium (ECs). Fetal ECs exhibited caveolar NP activity and widespread erythroblast contact. Brain ECs displayed micropodial extensions reaching luminal NP-loaded erythroblasts. Neurons and primitive glia displayed nuclear, organelle, and cytoplasmic NPs in both singles and conglomerates. Nanoscale Fe, Ti, and Al alloys, Hg, Cu, Ca, Sn, and Si were detected in placentas and fetal brains. Preeclamptic fetal blood NP vesicles are prospective neonate UFPM exposure biomarkers. NPs are reaching brain tissues at the early developmental PCW 8–15 stage, and NPs in maternal and fetal placental tissue compartments strongly suggests the placental barrier is not limiting the access of environmental NPs. Erythroblasts are the main early NP carriers to fetal tissues. The passage of UFPM/NPs from mothers to fetuses is documented and fingerprinting placental single particle composition could be useful for postnatal risk assessments. Fetal brain combustion and industrial NPs raise medical concerns about prenatal and postnatal health, including neurological and neurodegenerative lifelong consequences. Full article

(This article belongs to the Special Issue Environmental Medicine and Human Diseases: Molecular Insight)

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Review

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17 pages, 2184 KiB

Open AccessReview

Microplastics: A Matter of the Heart (and Vascular System)

by Elisa Persiani, Antonella Cecchettini, Elisa Ceccherini, Ilaria Gisone, Maria Aurora Morales and Federico Vozzi

Biomedicines 2023, 11(2), 264; https://doi.org/10.3390/biomedicines11020264 - 18 Jan 2023

Cited by 15 | Viewed by 4754

Abstract

Plastic use dramatically increased over the past few years. Besides obvious benefits, the consequent plastic waste and mismanagement in disposal have caused ecological problems. Plastic abandoned in the environment is prone to segregation, leading to the generation of microplastics (MPs) and nanoplastics (NPs), which can reach aquatic and terrestrial organisms. MPs/NPs in water can access fish’s bodies through the gills, triggering an inflammatory response in loco. Furthermore, from the gills, plastic fragments can be transported within the circulatory system altering blood biochemical parameters and hormone levels and leading to compromised immunocompetence and angiogenesis. In addition, it was also possible to observe an unbalanced ROS production, damage in vascular structure, and enhanced thrombosis. MPs/NPs led to cardiotoxicity, pericardial oedema, and impaired heart rate in fish cardiac tissue. MPs/NPs effects on aquatic organisms pose serious health hazards and ecological consequences because they constitute the food chain for humans. Once present in the mammalian body, plastic particles can interact with circulating cells, eliciting an inflammatory response, with genotoxicity and cytotoxicity of immune cells, enhanced haemolysis, and endothelium adhesion. The interaction of MPs/NPs with plasma proteins allows their transport to distant organs, including the heart. As a consequence of plastic fragment internalisation into cardiomyocytes, oxidative stress was increased, and metabolic parameters were altered. In this scenario, myocardial damage, fibrosis and impaired electrophysiological values were observed. In summary, MPs/NPs are an environmental stressor for cardiac function in living organisms, and a risk assessment of their influence on the cardiovascular system certainly merits further analysis. Full article

(This article belongs to the Special Issue Environmental Medicine and Human Diseases: Molecular Insight)

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