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Article ; Online: Extracellular vesicles in acute respiratory distress syndrome: Understanding protective and harmful signaling for the development of new therapeutics.

Bavuso, Matthew / Miller, Noel / Sill, Joshua M / Dobrian, Anca / Colunga Biancatelli, Ruben M L

2023 Volume 39, Issue 2, Page(s) 131–144

Abstract: Acute respiratory distress syndrome (ARDS) is a severe respiratory condition characterized by increased lung permeability, hyper-inflammatory state, and fluid leak into the alveolar spaces. ARDS is a heterogeneous disease, with multiple direct and ... ...

Abstract	Acute respiratory distress syndrome (ARDS) is a severe respiratory condition characterized by increased lung permeability, hyper-inflammatory state, and fluid leak into the alveolar spaces. ARDS is a heterogeneous disease, with multiple direct and indirect causes that result in a mortality of up to 40%. Due to the ongoing Covid-19 pandemic, its incidence has increased up to ten-fold. Extracellular vesicles (EVs) are small liposome-like particles that mediate intercellular communication and play a major role in ARDS pathophysiology. Indeed, they participate in endothelial barrier dysfunction and permeability, neutrophil, and macrophage activation, and also in the development of a hypercoagulable state. A more thorough understanding of the variegated and cell-specific functions of EVs may lead to the development of safe and effective therapeutics. In this review, we have collected evidence of EVs role in ARDS, revise the main mechanisms of production and internalization and summarize the current therapeutical approaches that have shown the ability to modulate EV signaling.
MeSH term(s)	Humans ; Pandemics ; Respiratory Distress Syndrome/therapy ; Lung ; Signal Transduction ; Extracellular Vesicles
Language	English
Publishing date	2023-09-01
Publishing country	Spain
Document type	Journal Article ; Review
ZDB-ID	83911-5
ISSN	1699-5848 ; 0213-3911
ISSN (online)	1699-5848
ISSN	0213-3911
DOI	10.14670/HH-18-659
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Article ; Online: An acute respiratory distress syndrome drug development collaboration stimulated by the Virginia Drug Discovery Consortium.

Lazo, John S / Colunga-Biancatelli, Ruben M L / Solopov, Pavel A / Catravas, John D

SLAS discovery : advancing life sciences R & D

2023 Volume 28, Issue 6, Page(s) 249–254

Abstract: The genesis of most older medicinal agents has generally been empirical. During the past one and a half centuries, at least in the Western countries, discovering and developing drugs has been primarily the domain of pharmaceutical companies largely built ...

Abstract	The genesis of most older medicinal agents has generally been empirical. During the past one and a half centuries, at least in the Western countries, discovering and developing drugs has been primarily the domain of pharmaceutical companies largely built upon concepts emerging from organic chemistry. Public sector funding for the discovery of new therapeutics has more recently stimulated local, national, and international groups to band together and focus on new human disease targets and novel treatment approaches. This Perspective describes one contemporary example of a newly formed collaboration that was simulated by a regional drug discovery consortium. University of Virginia, Old Dominion University, and a university spinout company, KeViRx, Inc., partnered under a NIH Small Business Innovation Research grant, to produce potential therapeutics for acute respiratory distress syndrome resulting from the ongoing COVID-19 pandemic.
MeSH term(s)	Humans ; COVID-19 ; SARS-CoV-2 ; Pandemics ; Virginia ; Drug Development ; Drug Discovery ; Respiratory Distress Syndrome/drug therapy
Language	English
Publishing date	2023-02-15
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2885123-7
ISSN	2472-5560 ; 2472-5552
ISSN (online)	2472-5560
ISSN	2472-5552
DOI	10.1016/j.slasd.2023.02.001
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Article ; Online: HSP70 Is a Critical Regulator of HSP90 Inhibitor's Effectiveness in Preventing HCl-Induced Chronic Lung Injury and Pulmonary Fibrosis.

Colunga Biancatelli, Ruben M L / Solopov, Pavel A / Day, Tierney / Gregory, Betsy / Osei-Nkansah, Michael / Dimitropoulou, Christiana / Catravas, John D

International journal of molecular sciences

2024 Volume 25, Issue 3

Abstract: Exposure to hydrochloric acid (HCl) can provoke acute and chronic lung injury. Because of its extensive production for industrial use, frequent accidental exposures occur, making HCl one of the top five chemicals causing inhalation injuries. There are no ...

Abstract	Exposure to hydrochloric acid (HCl) can provoke acute and chronic lung injury. Because of its extensive production for industrial use, frequent accidental exposures occur, making HCl one of the top five chemicals causing inhalation injuries. There are no Food and Drug Administration (FDA)-approved treatments for HCl exposure. Heat shock protein 90 (HSP90) inhibitors modulate transforming growth factor-β (TGF-β) signaling and the development of chemical-induced pulmonary fibrosis. However, little is known on the role of Heat Shock Protein 70 (HSP70) during injury and treatment with HSP90 inhibitors. We hypothesized that administration of geranylgeranyl-acetone (GGA), an HSP70 inducer, or gefitinib (GFT), an HSP70 suppressant, alone or in combination with the HSP90 inhibitor, TAS-116, would improve or worsen, respectively, HCl-induced chronic lung injury in vivo and endothelial barrier dysfunction in vitro. GGA, alone, improved HCl-induced human lung microvascular endothelial cells (HLMVEC) barrier dysfunction and, in combination with TAS-116, improved the protective effect of TAS-116. In mice, GGA reduced HCl toxicity and while TAS-116 alone blocked HCl-induced chronic lung injury, co-administration with GGA, resulted in further improvement. Conversely, GFT potentiated HCl-induced barrier dysfunction and impaired the antidotal effects of TAS-116. We conclude that combined treatments with HSP90 inhibitors and HSP70 inducers may represent a novel therapeutic approach to manage HCl-induced chronic lung injury and pulmonary fibrosis.
MeSH term(s)	Mice ; Humans ; Animals ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/metabolism ; Lung Injury/chemically induced ; Lung Injury/drug therapy ; Hydrochloric Acid/toxicity ; HSP70 Heat-Shock Proteins/metabolism ; Endothelial Cells/metabolism ; Antineoplastic Agents/adverse effects ; Gefitinib/adverse effects ; HSP90 Heat-Shock Proteins/metabolism ; Benzamides ; Pyrazoles
Chemical Substances	TAS-116 ; Hydrochloric Acid (QTT17582CB) ; HSP70 Heat-Shock Proteins ; Antineoplastic Agents ; Gefitinib (S65743JHBS) ; HSP90 Heat-Shock Proteins ; Benzamides ; Pyrazoles
Language	English
Publishing date	2024-02-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25031920
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Article ; Online: The Inflammasome NLR Family Pyrin Domain-Containing Protein 3 (NLRP3) as a Novel Therapeutic Target for Idiopathic Pulmonary Fibrosis.

Colunga Biancatelli, Ruben M L / Solopov, Pavel A / Catravas, John D

The American journal of pathology

2022 Volume 192, Issue 6, Page(s) 837–846

Abstract: Idiopathic pulmonary fibrosis (IPF) is a dramatic disease without cure. The US Food and Drug Administration-approved drugs, pirfenidone and nintedanib, only slow disease progression. The clinical investigation of novel therapeutic approaches for IPF is ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a dramatic disease without cure. The US Food and Drug Administration-approved drugs, pirfenidone and nintedanib, only slow disease progression. The clinical investigation of novel therapeutic approaches for IPF is an unmet clinical need. Nucleotide-binding oligomerization domain-like receptor or NOD-like receptors are pattern recognition receptors capable of binding a large variety of stress factors. NLR family pyrin domain-containing protein 3 (NLRP3), once activated, promotes IL-1β, IL-18 production, and innate immune responses. Multiple reports indicate that the inflammasome NLRP3 is overactivated in IPF patients, leading to increased production of class I IL and collagens. Similarly, data from animal models of pulmonary fibrosis confirm the role of NLRP3 in the development of chronic lung injury and pulmonary fibrosis. This report provides a review of the evidence of NLRP3 activation in IPF and of NLRP3 inhibition in different animal models of fibrosis, and highlights the recent advances in direct and indirect NLRP3 inhibitors.
MeSH term(s)	Animals ; Carrier Proteins/metabolism ; Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; Inflammasomes/metabolism ; Interleukin-1beta/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pyrin Domain
Chemical Substances	Carrier Proteins ; Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human
Language	English
Publishing date	2022-03-26
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2022.03.003
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Article ; Online: Alcohol Increases Lung Angiotensin-Converting Enzyme 2 Expression and Exacerbates Severe Acute Respiratory Syndrome Coronavirus 2 Spike Protein Subunit 1-Induced Acute Lung Injury in K18-hACE2 Transgenic Mice.

Solopov, Pavel A / Colunga Biancatelli, Ruben M L / Catravas, John D

The American journal of pathology

2022 Volume 192, Issue 7, Page(s) 990–1000

Abstract: During the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, alcohol consumption increased markedly. Nearly one in four adults reported drinking more alcohol to cope with stress. Chronic alcohol abuse is now recognized as a factor ... ...

Abstract	During the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, alcohol consumption increased markedly. Nearly one in four adults reported drinking more alcohol to cope with stress. Chronic alcohol abuse is now recognized as a factor complicating the course of acute respiratory distress syndrome and increasing mortality. To investigate the mechanisms behind this interaction, a combined acute respiratory distress syndrome and chronic alcohol abuse mouse model was developed by intratracheally instilling the subunit 1 (S1) of SARS-CoV-2 spike protein (S1SP) in K18-human angiotensin-converting enzyme 2 (ACE2) transgenic mice that express the human ACE2 receptor for SARS-CoV-2 and were kept on an ethanol diet. Seventy-two hours after S1SP instillation, mice on an ethanol diet showed a strong decrease in body weight, a dramatic increase in white blood cell content of bronchoalveolar lavage fluid, and an augmented cytokine storm, compared with S1SP-treated mice on a control diet. Histologic examination of lung tissue showed abnormal recruitment of immune cells in the alveolar space, abnormal parenchymal architecture, and worsening Ashcroft score in S1SP- and alcohol-treated animals. Along with the activation of proinflammatory biomarkers [NF-κB, STAT3, NLR family pyrin domain-containing protein 3 (NLRP3) inflammasome], lung tissue homogenates from mice on an alcohol diet showed overexpression of ACE2 compared with mice on a control diet. This model could be useful for the development of therapeutic approaches against alcohol-exacerbated coronavirus disease 2019.
MeSH term(s)	Acute Lung Injury/pathology ; Acute Lung Injury/virology ; Alcoholism ; Angiotensin-Converting Enzyme 2 ; Animals ; COVID-19/pathology ; Ethanol/adverse effects ; Humans ; Lung/pathology ; Mice ; Mice, Transgenic ; Peptidyl-Dipeptidase A/metabolism ; Respiratory Distress Syndrome/virology ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/genetics
Chemical Substances	Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; Ethanol (3K9958V90M) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2022-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2022.03.012
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Article ; Online: Synergistic effects of nanosecond pulsed plasma and electric field on inactivation of pancreatic cancer cells in vitro.

Oshin, Edwin A / Minhas, Zobia / Biancatelli, Ruben M L Colunga / Catravas, John D / Heller, Richard / Guo, Siqi / Jiang, Chunqi

Scientific reports

2024 Volume 14, Issue 1, Page(s) 885

Abstract: Nanosecond pulsed atmospheric pressure plasma jets (ns-APPJs) produce reactive plasma species, including charged particles and reactive oxygen and nitrogen species (RONS), which can induce oxidative stress in biological cells. Nanosecond pulsed electric ... ...

Abstract	Nanosecond pulsed atmospheric pressure plasma jets (ns-APPJs) produce reactive plasma species, including charged particles and reactive oxygen and nitrogen species (RONS), which can induce oxidative stress in biological cells. Nanosecond pulsed electric field (nsPEF) has also been found to cause permeabilization of cell membranes and induce apoptosis or cell death. Combining the treatment of ns-APPJ and nsPEF may enhance the effectiveness of cancer cell inactivation with only moderate doses of both treatments. Employing ns-APPJ powered by 9 kV, 200 ns pulses at 2 kHz and 60-nsPEF of 50 kV/cm at 1 Hz, the synergistic effects on pancreatic cancer cells (Pan02) in vitro were evaluated on the metabolic activities of cells and transcellular electrical resistance (TER). It was observed that treatment with ns-APPJ for > 2 min disrupts Pan02 cell stability and resulted in over 30% cell death. Similarly, applying nsPEF alone, > 20 pulses resulted in over 15% cell death. While the inactivation activity from the individual treatment is moderate, combined treatments resulted in 80% cell death, approximately 3-to-fivefold increase compared to the individual treatment. In addition, reactive oxygen species such as OH and O were identified at the plasma-liquid interface. The gas temperature of the plasma and the temperature of the cell solution during treatments were determined to be near room temperature.
MeSH term(s)	Humans ; Pancreas ; Pancreatic Neoplasms/therapy ; Cell Membrane ; Apoptosis ; Cell Death
Language	English
Publishing date	2024-01-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-51298-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Synergistic effects of nanosecond pulsed plasma and electric field on inactivation of pancreatic cancer cells in vitro

Edwin A. Oshin / Zobia Minhas / Ruben M. L. Colunga Biancatelli / John D. Catravas / Richard Heller / Siqi Guo / Chunqi Jiang

Scientific Reports, Vol 14, Iss 1, Pp 1-

2024 Volume 12

Abstract: Abstract Nanosecond pulsed atmospheric pressure plasma jets (ns-APPJs) produce reactive plasma species, including charged particles and reactive oxygen and nitrogen species (RONS), which can induce oxidative stress in biological cells. Nanosecond pulsed ... ...

Abstract	Abstract Nanosecond pulsed atmospheric pressure plasma jets (ns-APPJs) produce reactive plasma species, including charged particles and reactive oxygen and nitrogen species (RONS), which can induce oxidative stress in biological cells. Nanosecond pulsed electric field (nsPEF) has also been found to cause permeabilization of cell membranes and induce apoptosis or cell death. Combining the treatment of ns-APPJ and nsPEF may enhance the effectiveness of cancer cell inactivation with only moderate doses of both treatments. Employing ns-APPJ powered by 9 kV, 200 ns pulses at 2 kHz and 60-nsPEF of 50 kV/cm at 1 Hz, the synergistic effects on pancreatic cancer cells (Pan02) in vitro were evaluated on the metabolic activities of cells and transcellular electrical resistance (TER). It was observed that treatment with ns-APPJ for > 2 min disrupts Pan02 cell stability and resulted in over 30% cell death. Similarly, applying nsPEF alone, > 20 pulses resulted in over 15% cell death. While the inactivation activity from the individual treatment is moderate, combined treatments resulted in 80% cell death, approximately 3-to-fivefold increase compared to the individual treatment. In addition, reactive oxygen species such as OH and O were identified at the plasma-liquid interface. The gas temperature of the plasma and the temperature of the cell solution during treatments were determined to be near room temperature.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Synergistic effects of nanosecond pulsed plasma and electric field on inactivation of pancreatic cancer cells in vitro.

Oshin, Edwin A / Minhas, Zobia / Biancatelli, Ruben M L Colunga / Catravas, John D / Heller, Richard / Guo, Siqi / Jiang, Chunqi

Research square

2023

Abstract	Nanosecond pulsed atmospheric pressure plasma jets (ns-APPJs) produce reactive plasma species, including charged particles and reactive oxygen and nitrogen species (RONS), which can induce oxidative stress in biological cells. Nanosecond pulsed electric field (nsPEF) has also been found to cause permeabilization of cell membranes and induce apoptosis or cell death. Combining the treatment of ns-APPJ and nsPEF may enhance the effectiveness of cancer cell inactivation with only moderate doses of both treatments. Employing ns-APPJ powered by 9 kV, 200 ns pulses at 2 kHz and 60-nsPEF of 50 kV/cm at 1 Hz, the synergistic effects on pancreatic cancer cells (Pan02)
Language	English
Publishing date	2023-07-25
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3143506/v1
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Article: Endothelial cell-derived extracellular vesicles impair the angiogenic response of coronary artery endothelial cells.

Carter, Nigeste / Mathiesen, Allison H / Miller, Noel / Brown, Michael / Colunga Biancatelli, Ruben M L / Catravas, John D / Dobrian, Anca D

Frontiers in cardiovascular medicine

2022 Volume 9, Page(s) 923081

Abstract: Cardiovascular disease (CVD) is the most prominent cause of death of adults in the United States with coronary artery disease being the most common type of CVD. Following a myocardial event, the coronary endothelium plays an important role in the ... ...

Abstract	Cardiovascular disease (CVD) is the most prominent cause of death of adults in the United States with coronary artery disease being the most common type of CVD. Following a myocardial event, the coronary endothelium plays an important role in the recovery of the ischemic myocardium. Specifically, endothelial cells (EC) must be able to elicit a robust angiogenic response necessary for tissue revascularization and repair. However, local or distant cues may prevent effective revascularization. Extracellular vesicles (EV) are produced by all cells and endothelium is a rich source of EVs that have access to the main circulation thereby potentially impacting local and distant tissue function. Systemic inflammation associated with conditions such as obesity as well as the acute inflammatory response elicited by a cardiac event can significantly increase the EV release by endothelium and alter their miRNA, protein or lipid cargo. Our laboratory has previously shown that EVs released by adipose tissue endothelial cells exposed to chronic inflammation have angiostatic effects on naïve adipose tissue EC
Language	English
Publishing date	2022-07-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2022.923081
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Article ; Online: Age-Dependent Chronic Lung Injury and Pulmonary Fibrosis following Single Exposure to Hydrochloric Acid.

Colunga Biancatelli, Ruben M L / Solopov, Pavel / Dimitropoulou, Christiana / Catravas, John D

International journal of molecular sciences

2021 Volume 22, Issue 16

Abstract: Exposure to hydrochloric acid (HCl) represents a threat to public health. Children may inhale higher doses and develop greater injury because of their smaller airways and faster respiratory rate. We have developed a mouse model of pediatric exposure to ... ...

Abstract	Exposure to hydrochloric acid (HCl) represents a threat to public health. Children may inhale higher doses and develop greater injury because of their smaller airways and faster respiratory rate. We have developed a mouse model of pediatric exposure to HCl by intratracheally instilling p24 mice (mice 24 days old; 8-10 g) with 2 µL/g 0.1 N HCl, and compared the profile of lung injury to that in HCl-instilled adults (10 weeks old; 25-30 g) and their age-matched saline controls. After 30 days, alveolar inflammation was observed with increased proteinosis and mononuclear cells in the bronchoalveolar lavage fluid (BALF) in both HCl-instilled groups. Young p24 animals-but not adults-exhibited higher NLR family pyrin domain containing 3 (NLRP3) inflammasome levels. Increased amounts of Transforming Growth Factor-β (TGF-β) mRNA and its intracellular canonical and non-canonical pathways (p-Smad2 and p-ERK) were found in the lungs of both young and adult HCl-instilled mice. Constitutive age-related differences were observed in the levels of heat shock protein family (HSP70 and HSP90). HCl equally provoked the deposition of collagen and fibronectin; however, significant age-dependent differences were observed in the increase in elastin and tenascin C mRNA. HCl induced pulmonary fibrosis with an increased Ashcroft score, which was higher in adults, and a reduction in alveolar Mean Alveolar Linear Intercept (MALI). Young mice developed increased Newtonian resistance (Rn) and lower PV loops, while adults showed a higher respiratory system resistance and elastance. This data indicate that young p24 mice can suffer long-term complications from a single exposure to HCl, and can develop chronic lung injury characterized by a stronger persistent inflammation and lesser fibrotic pattern, mostly in the airways, differently from adults. Further data are required to characterize HCl time- and dose-dependent injury in young animals and to identify new key-molecular targets.
MeSH term(s)	Acute Lung Injury/chemically induced ; Acute Lung Injury/pathology ; Aging ; Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Hydrochloric Acid/toxicity ; Inflammation/chemically induced ; Inflammation/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/pathology
Chemical Substances	Hydrochloric Acid (QTT17582CB)
Language	English
Publishing date	2021-08-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22168833
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