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Biomolecules
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Molecular Mechanisms of Lung Diseases
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Molecular Mechanisms of Lung Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (29 February 2020) | Viewed by 19914

Special Issue Editor

Prof. Dr. Judit E. Pongracz

E-Mail Website
Guest Editor
Pharmaceutical Biotechnology, School of Pharmacy, University of Pecs, 2 Rokus Str, H-7624 Pecs, Hungary
Interests: lung cancers; lymphangioleiomyomatosis; metabolic regulation; Wnt signaling; aging; immune system and chemotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is my great pleasure to invite you to contribute to this Special Issue of Biomolecules. This young journal has already proved worthy of scientists’ attention, reaching a first Impact Factor of (2018): 4.694, ranking 58/298 (80.70%, Q1) in 'Biochemistry and Molecular Biology'! This Special Issue: “Molecular Mechanisms of Lung Diseases” is giving us molecular researchers an opportunity to bridge various aspects of unchartered territory of molecular investigation of lung diseases. Now, here is an opportunity to connect signals delivered in extracellular vesicles that facilitate brain metastasis or systemic inflammation, or to show how metabolic changes that occur due to mutation or age modulate immune function that changes intra and intercellular communication allowing development of life-threatening lung diseases.

As the guest editor of the above Special Issue, I am looking forward to reading manuscripts with crystal-clear logic and detailed mechanistic science to draw attention to novel molecular mechanisms and drug targets that eventually lead to improved lung function or even to curing some lung diseases.

Prof. Judit Pongracz
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. Biomolecules 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 2700 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

  • COPD
  • IPF
  • Lung cancer
  • Rare lung diseases
  • Aging contributes to disease
  • Lung disease metabolism
  • Intra- and intercellular signaling

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Published Papers (5 papers)

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Research

12 pages, 1058 KiB  
Article
Increased Arginase Expression and Decreased Nitric Oxide in Pig Donor Lungs after Normothermic Ex Vivo Lung Perfusion
by Farshad Tavasoli, Mingyao Liu, Tiago Machuca, Riccardo Bonato, David R. Grant, Marcelo Cypel, Shaf Keshavjee and Hartmut Grasemann
Biomolecules 2020, 10(2), 300; https://doi.org/10.3390/biom10020300 - 14 Feb 2020
Cited by 2 | Viewed by 2382
Abstract
An established pig lung transplantation model was used to study the effects of cold ischemia time, normothermic acellular ex vivo lung perfusion (EVLP) and reperfusion after lung transplantation on l-arginine/NO metabolism in lung tissue. Lung tissue homogenates were analyzed for NO metabolite [...] Read more.
An established pig lung transplantation model was used to study the effects of cold ischemia time, normothermic acellular ex vivo lung perfusion (EVLP) and reperfusion after lung transplantation on l-arginine/NO metabolism in lung tissue. Lung tissue homogenates were analyzed for NO metabolite (NOx) concentrations by chemiluminescent NO-analyzer technique, and l-arginine, l-ornithine, l-citrulline and asymmetric dimethylarginine (ADMA) quantified using liquid chromatography-mass spectrometry (LC-MS/MS). The expression of arginase and nitric oxide synthase (NOS) isoforms in lung was measured by real-time polymerase chain reaction. EVLP preservation resulted in a significant decrease in concentrations of NOx and l-citrulline, both products of NOS, at the end of EVLP and after reperfusion following transplantation, compared to control, respectively. The ratio of l-ornithine over l-citrulline, a marker of the balance between l-arginine metabolizing enzymes, was increased in the EVLP group prior to reperfusion. The expression of both arginase isoforms was increased from baseline 1 h post reperfusion in EVLP but not in the no-EVLP group. These data suggest that EVLP results in a shift of the l-arginine balance towards arginase, leading to NO deficiency in the lung. The arginase/NOS balance may, therefore, represent a therapeutic target to improve lung quality during EVLP and, subsequently, transplant outcomes. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Lung Diseases)
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19 pages, 985 KiB  
Article
IL10 rs1800872 Is Associated with Non-Steroidal Anti-Inflammatory Drugs Exacerbated Respiratory Disease in Mexican-Mestizo Patients
by Gandhi Fernando Pavón-Romero, Gloria Pérez-Rubio, Fernando Ramírez-Jiménez, Enrique Ambrocio-Ortiz, Cristian Rubén Merino-Camacho, Ramcés Falfán-Valencia and Luis M. Teran
Biomolecules 2020, 10(1), 104; https://doi.org/10.3390/biom10010104 - 7 Jan 2020
Cited by 6 | Viewed by 3011
Abstract
Non-steroidal anti-inflammatory drugs (NSAID) exacerbated respiratory disease (N-ERD) is a disease integrated by asthma, nasal polyps, and hypersensitivity to non-steroidal anti-inflammatory drugs (NSAID). Genetic association studies have explored single nucleotide polymorphisms (SNPs) in genes involved in theoretical pathophysiological mechanisms, but most of these [...] Read more.
Non-steroidal anti-inflammatory drugs (NSAID) exacerbated respiratory disease (N-ERD) is a disease integrated by asthma, nasal polyps, and hypersensitivity to non-steroidal anti-inflammatory drugs (NSAID). Genetic association studies have explored single nucleotide polymorphisms (SNPs) in genes involved in theoretical pathophysiological mechanisms, but most of these lack replication of findings in second populations. Our objective was to evaluate the association of SNPs in candidate genomic regions described in Asian and European subjects with N-ERD in Mexican-mestizo patients. We designed a replicative study in two stages. We included 381 SNPs selected by fine mapping of associated genes in a microarray, which were tested in three groups: N-ERD (N), asthma (A), and control group (CG); by means of GoldenGate array, positive results by genetic models were validated in the second stage in another population through qPCR with the same methodology. In the allelic model, we identified 11 SNPs in N vs. CG comparison, and five in N vs. A and A vs. CG, respectively. By genetics models, all SNPs in PPARG, rs13239058 in TBXAS1, and rs1554286 and rs1800872 in IL10 were associated in both models. In the second stage, only rs1800872CC showed an association in the dominant model comparing N vs. GC, p = 0.004, OR = 0.44. In conclusion, rs1800872 in IL10 was the only associated with N-ERD in Mexican-mestizo patients. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Lung Diseases)
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12 pages, 3316 KiB  
Article
Inhibition of Growth of TSC2-Null Cells by a PI3K/mTOR Inhibitor but Not by a Selective MNK1/2 Inhibitor
by Jilly F. Evans, Ryan W. Rue, Alexander R. Mukhitov, Kseniya Obraztsova, Carly J. Smith and Vera P. Krymskaya
Biomolecules 2020, 10(1), 28; https://doi.org/10.3390/biom10010028 - 24 Dec 2019
Cited by 3 | Viewed by 4050
Abstract
Lymphangioleiomyomatosis (LAM) is a rare metastatic cystic lung disease due to a mutation in a TSC tumor suppressor, resulting in hyperactive mTOR growth pathways. Sirolimus (rapamycin), an allosteric mTORC1 inhibitor, is a therapeutic option for women with LAM but it only maintains lung [...] Read more.
Lymphangioleiomyomatosis (LAM) is a rare metastatic cystic lung disease due to a mutation in a TSC tumor suppressor, resulting in hyperactive mTOR growth pathways. Sirolimus (rapamycin), an allosteric mTORC1 inhibitor, is a therapeutic option for women with LAM but it only maintains lung volume during treatment and does not provide benefit for all LAM patients. The two major mTORC1 protein synthesis pathways are via S6K/S6 or 4E-BP/eIF4E activation. We aimed to investigate rapamycin in combination with compounds that target associated growth pathways, with the potential to be additive to rapamycin. In this study we demonstrated that rapamycin, at a clinically tolerable concentration (10 nM), inhibited the phosphorylation of S6, but not the critical eIF4E releasing Thr 37/46 phosphorylation sites of 4E-BP1 in TSC2-deficient LAM-derived cells. We also characterized the abundant protein expression of peIF4E within LAM lesions. A selective MNK1/2 inhibitor eFT508 inhibited the phosphorylation of eIF4E but did not reduce TSC2-null cell growth. In contrast, a PI3K/mTOR inhibitor omipalisib blocked the phosphorylation of Akt and both S6K/S6 and 4E-BP/eIF4E branches, and additively decreased the growth of TSC2-null cells with rapamycin. Omipalisib, or another inhibitor of both major mTORC1 growth pathways and pAkt, might provide therapeutic options for TSC2-deficient cancers including, but not limited to, LAM. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Lung Diseases)
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9 pages, 833 KiB  
Article
Participation of the miR-22-HDAC4-DLCO Axis in Patients with COPD by Tobacco and Biomass
by Yadira Velasco-Torres, Víctor Ruiz, Martha Montaño, Rogelio Pérez-Padilla, Ramcés Falfán-Valencia, Julia Pérez-Ramos, Oliver Pérez-Bautista and Carlos Ramos
Biomolecules 2019, 9(12), 837; https://doi.org/10.3390/biom9120837 - 6 Dec 2019
Cited by 12 | Viewed by 3666
Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation and systemic inflammation. The main causes of COPD include interaction between genetic and environmental factors associated with tobacco smoking (COPD-TS) and/or exposure to biomass smoke (COPD-BS). Several microRNAs (miRNAs) control posttranscriptional regulation of [...] Read more.
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation and systemic inflammation. The main causes of COPD include interaction between genetic and environmental factors associated with tobacco smoking (COPD-TS) and/or exposure to biomass smoke (COPD-BS). Several microRNAs (miRNAs) control posttranscriptional regulation of COPD-TS associated gene expression. The miR-22-HDAC4-IL-17 axis was recently characterized. It is still unknown, however, whether this axis, participates in COPD-BS. To investigate, 50 patients diagnosed with severe-to-very severe COPD GOLD (Global Initiative for Chronic Obstructive Lung Disease) stages III/IV, were recruited, 25 women had COPD-BS (never smokers, exposed heavily to BS) and 25 had COPD-TS. Serum levels of miRNA-22-3p were measured by RT (Reverse Transcription)-qPCR, while the concentration of HDAC4 (Histone deacetylase 4) was detected by ELISA. Additionally, we looked for association between serum HDAC4 and DLCOsb (Single-breath diffusing capacity of the lung for carbon monoxide), as % of predicted by age, height, and gender, one of the main differences described between COPD-BS and COPD-TS. Women with COPD-BS were older and shorter and had a higher DLCOsb %P (percent predicted) compared to COPD-TS. Serum miR-22-3p was downregulated in COPD-BS relative to COPD-TS. In contrast, the concentration of HDAC4 was higher in COPD-BS compared to COPD-TS. Furthermore, a positive correlation between serum HDAC4 levels and DLCOsb %P was observed. We concluded that the miR-22-HDAC4-DLCO axis behaves differently in patients with COPD-BS and COPD-TS. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Lung Diseases)
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16 pages, 1329 KiB  
Article
Non-Invasive Approach for Evaluation of Pulmonary Hypertension Using Extracellular Vesicle-Associated Small Non-Coding RNA
by Christoph Lipps, Philipp Northe, Ricardo Figueiredo, Manfred Rohde, Alexandra Brahmer, Eva-Maria Krämer-Albers, Christoph Liebetrau, Christoph B. Wiedenroth, Eckhard Mayer, Steffen D. Kriechbaum, Oliver Dörr, Holger Nef, Christian W. Hamm, Till Keller and Christian Troidl
Biomolecules 2019, 9(11), 666; https://doi.org/10.3390/biom9110666 - 29 Oct 2019
Cited by 34 | Viewed by 6263
Abstract
Extracellular vesicles are released by numerous cell types of the human body under physiological but also under pathophysiological conditions. They are important for cell–cell communication and carry specific signatures of peptides and RNAs. In this study, we aimed to determine whether extracellular vesicles [...] Read more.
Extracellular vesicles are released by numerous cell types of the human body under physiological but also under pathophysiological conditions. They are important for cell–cell communication and carry specific signatures of peptides and RNAs. In this study, we aimed to determine whether extracellular vesicles isolated from patients with pulmonary hypertension show a disease specific signature of small non-coding RNAs and thus have the potential to serve as diagnostic and prognostic biomarkers. Extracellular vesicles were isolated from the serum of 23 patients with chronic thromboembolic pulmonary hypertension (CTEPH) and 23 controls using two individual methods: a column-based method or by precipitation. Extracellular vesicle- associated RNAs were analyzed by next-generation sequencing applying molecular barcoding, and differentially expressed small non-coding RNAs were validated by quantitative real-time polymerase chain reaction (qRT-PCR). We identified 18 microRNAs and 21 P-element induced wimpy testis (PIWI)-interacting RNAs (piRNAs) or piRNA clusters that were differentially expressed in CTEPH patients compared with controls. Bioinformatic analysis predicted a contribution of these piRNAs to the progression of cardiac and vascular remodeling. Expression levels of DQ593039 correlated with clinically meaningful parameters such as mean pulmonary arterial pressure, pulmonary vascular resistance, right ventricular systolic pressure, and levels of N-terminal pro-brain natriuretic peptide. Thus, we identified the extracellular vesicle- derived piRNA, DQ593039, as a potential biomarker for pulmonary hypertension and right heart disease. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Lung Diseases)
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