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Artikel ; Online: Is there a role for specialized pro-resolving mediators in pulmonary fibrosis?

Thatcher, Thomas H / Freeberg, Margaret A T / Myo, Yu Par Aung / Sime, Patricia J

2023 Band 247, Seite(n) 108460

Abstract: Pulmonary fibrotic diseases are characterized by proliferation of lung fibroblasts and myofibroblasts and excessive deposition of extracellular matrix proteins. Depending on the specific form of lung fibrosis, there can be progressive scarring of the ... ...

Abstract	Pulmonary fibrotic diseases are characterized by proliferation of lung fibroblasts and myofibroblasts and excessive deposition of extracellular matrix proteins. Depending on the specific form of lung fibrosis, there can be progressive scarring of the lung, leading in some cases to respiratory failure and/or death. Recent and ongoing research has demonstrated that resolution of inflammation is an active process regulated by families of small bioactive lipid mediators termed "specialized pro-resolving mediators." While there are many reports of beneficial effects of SPMs in animal and cell culture models of acute and chronic inflammatory and immune diseases, there have been fewer reports investigating SPMs and fibrosis, especially pulmonary fibrosis. Here, we will review evidence that resolution pathways are impaired in interstitial lung disease, and that SPMs and other similar bioactive lipid mediators can inhibit fibroblast proliferation, myofibroblast differentiation, and accumulation of excess extracellular matrix in cell culture and animal models of pulmonary fibrosis, and we will consider future therapeutic implications of SPMs in fibrosis.
Mesh-Begriff(e)	Animals ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/metabolism ; Pulmonary Fibrosis/pathology ; Lung/metabolism ; Fibrosis ; Cell Differentiation ; Inflammation/drug therapy ; Lipids ; Inflammation Mediators/metabolism
Chemische Substanzen	Lipids ; Inflammation Mediators
Sprache	Englisch
Erscheinungsdatum	2023-05-26
Erscheinungsland	England
Dokumenttyp	Journal Article ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2023.108460
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Dickkopf1 Promotes Pulmonary Fibrosis upon Bleomycin-Induced Lung Injury.

Sung, Eun-Ah / Park, Min Hee / Henegariu, Octavian / Sime, Patricia J / Chae, Wook-Jin

The American journal of pathology

2023 Band 193, Heft 9, Seite(n) 1130–1142

Abstract: Orchestration of inflammation and tissue repair processes is critical to maintaining homeostasis upon tissue injury. Tissue fibrosis is a pathological process characterized by aberrant accumulation of extracellular matrix proteins, such as collagen, upon ...

Abstract	Orchestration of inflammation and tissue repair processes is critical to maintaining homeostasis upon tissue injury. Tissue fibrosis is a pathological process characterized by aberrant accumulation of extracellular matrix proteins, such as collagen, upon injury. Dickkopf1 (DKK1) is a quintessential Wnt antagonist. The role of DKK1 in bleomycin (BLM)-induced lung injury and fibrosis model remains elusive. This study shows that BLM-induced lung injury markedly elevated DKK1 protein expressions in the lungs in mice, consistent with human pulmonary fibrosis patient lung tissues. The elevated DKK1 levels coincided with immune cell infiltration and collagen deposition. Notably, the reduced expression of DKK1 in Dkk1 hypomorphic doubleridge (Dkk1
Mesh-Begriff(e)	Humans ; Mice ; Animals ; Pulmonary Fibrosis/pathology ; Bleomycin/toxicity ; Lung Injury/pathology ; Lung/pathology ; Transforming Growth Factor beta1/metabolism ; Collagen/metabolism ; Pneumonia/metabolism ; Inflammation/pathology
Chemische Substanzen	Bleomycin (11056-06-7) ; Transforming Growth Factor beta1 ; Collagen (9007-34-5)
Sprache	Englisch
Erscheinungsdatum	2023-05-30
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2023.05.009
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Potential late effects of SARS-CoV-2 (COVID-19) infection: parallels to cancer late effects.

Phipps, Richard P / Sime, Patricia J / Phipps, Connor R

Cancer metastasis reviews

2021 Band 40, Heft 1, Seite(n) 1–2

Mesh-Begriff(e)	COVID-19/epidemiology ; COVID-19/prevention & control ; COVID-19/virology ; Epidemics ; Humans ; Neoplasms/diagnosis ; Neoplasms/therapy ; SARS-CoV-2/isolation & purification ; SARS-CoV-2/physiology ; Time Factors
Sprache	Englisch
Erscheinungsdatum	2021-02-04
Erscheinungsland	Netherlands
Dokumenttyp	Editorial
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1007/s10555-021-09954-6
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Watching an Evolution in Progress, Cutting-Edge Research Transforming Outcomes in Interstitial Lung Disease: Introduction to an

Maher, Toby M / Podolanczuk, Anna J / Drake, Wonder P / Sime, Patricia J / Eickelberg, Oliver / DeMeo, Dawn L / Richeldi, Luca

American journal of respiratory and critical care medicine

2024 Band 209, Heft 9, Seite(n) 1049–1050

Mesh-Begriff(e)	Humans ; Lung Diseases, Interstitial/therapy ; Lung Diseases, Interstitial/physiopathology ; Biomedical Research
Sprache	Englisch
Erscheinungsdatum	2024-03-04
Erscheinungsland	United States
Dokumenttyp	Introductory Journal Article ; Editorial
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202404-0675ED
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Reproducible Single-Cell Genomic Research in Pulmonary and Critical Care Medicine.

Eickelberg, Oliver / Misharin, Alexander V / Sime, Patricia J

American journal of respiratory and critical care medicine

2020 Band 202, Heft 11, Seite(n) 1495–1497

Mesh-Begriff(e)	Critical Care ; Genomics ; Humans ; Idiopathic Pulmonary Fibrosis ; Lung ; Medicine ; Research
Sprache	Englisch
Erscheinungsdatum	2020-09-10
Erscheinungsland	United States
Dokumenttyp	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202008-3073ED
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The Future of Endowed Chairs in Academic Medicine.

Buckley, Peter F / Sime, Patricia J / Collins, Love / Eggleston, Niles / Davenport, Jay E

Academic medicine : journal of the Association of American Medical Colleges

2022 Band 97, Heft 11, Seite(n) 1583–1586

Abstract: As the landscape of philanthropy changes following the COVID-19 pandemic, this commentary considers the future of endowed chairs in academic medicine in the light of articles by Thorndyke and colleagues and by Chin-Hong and colleagues in this issue. The ... ...

Abstract	As the landscape of philanthropy changes following the COVID-19 pandemic, this commentary considers the future of endowed chairs in academic medicine in the light of articles by Thorndyke and colleagues and by Chin-Hong and colleagues in this issue. The authors evaluate the traditional allocation of endowed chairs, which can attract and retain talented faculty and can support focused research far into the future, while other gifts may support more timely concerns, but over a shorter term. The authors weigh the benefits and challenges of allocation of endowed chairs, such as the need to improve representation, diversity, equity, and inclusion, and opportunities to support early-career investigators or research teams. New endowed positions can be challenging to establish, as there may be competition with learner scholarship programs and programmatic support. Leadership turnover of university presidents and deans can slow philanthropic growth and make recruitment and fundraising for new positions even more challenging. The authors discuss the balance of institutional priorities and ways to use endowed chairs for scholarship in evolving areas of medicine and science. They further suggest working with donors to develop more adaptable gift agreements, which will allow institutions to transform endowed positions to meet changing needs while preserving the intentions of the donor. To maintain endowed chairs as a worthwhile and relevant outlet for philanthropy, one which donors will enthusiastically support, it is essential to align them with the changing needs of the institution and the broader environment of academic medicine.
Mesh-Begriff(e)	Humans ; Faculty, Medical ; Academic Medical Centers ; Pandemics ; COVID-19/epidemiology ; Leadership ; Emergency Medicine
Sprache	Englisch
Erscheinungsdatum	2022-08-30
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Comment
ZDB-ID	96192-9
ISSN	1938-808X ; 1040-2446
ISSN (online)	1938-808X
ISSN	1040-2446
DOI	10.1097/ACM.0000000000004960
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: miR-338-3p blocks TGFβ-induced myofibroblast differentiation through the induction of PTEN.

Rackow, Ashley R / Judge, Jennifer L / Woeller, Collynn F / Sime, Patricia J / Kottmann, Robert M

American journal of physiology. Lung cellular and molecular physiology

2022 Band 322, Heft 3, Seite(n) L385–L400

Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease. The pathogenesis of IPF is not completely understood. However, numerous genes are associated with the development and progression of pulmonary fibrosis, indicating there is a ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease. The pathogenesis of IPF is not completely understood. However, numerous genes are associated with the development and progression of pulmonary fibrosis, indicating there is a significant genetic component to the pathogenesis of IPF. Epigenetic influences on the development of human disease, including pulmonary fibrosis, remain to be fully elucidated. In this paper, we identify miR-338-3p as a microRNA severely downregulated in the lungs of patients with pulmonary fibrosis and in experimental models of pulmonary fibrosis. Treatment of primary human lung fibroblasts with miR-338-3p inhibits myofibroblast differentiation and matrix protein production. Published and proposed targets of miR-338-3p such as TGFβ receptor 1, MEK/ERK 1/2, Cdk4, and Cyclin D are also not responsible for the regulation of pulmonary fibroblast behavior by miR-338-3p. miR-338-3p inhibits myofibroblast differentiation by preventing TGFβ-mediated downregulation of phosphatase and tensin homolog (PTEN), a known antifibrotic mediator.
Mesh-Begriff(e)	Fibroblasts/metabolism ; Humans ; Idiopathic Pulmonary Fibrosis/pathology ; Lung/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myofibroblasts/metabolism ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Transforming Growth Factor beta/metabolism
Chemische Substanzen	MIRN338 microRNA, human ; MicroRNAs ; Transforming Growth Factor beta ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67)
Sprache	Englisch
Erscheinungsdatum	2022-01-05
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00251.2021
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Decline in forced vital capacity as a surrogate for mortality in patients with pulmonary fibrosis.

Maher, Toby M / Stowasser, Susanne / Voss, Florian / Bendstrup, Elisabeth / Kreuter, Michael / Martinez, Fernando J / Sime, Patricia J / Stock, Christian

Respirology (Carlton, Vic.)

2023 Band 28, Heft 12, Seite(n) 1147–1153

Abstract: Background and objective: Surrogate endpoints enable determination of meaningful treatment effects more efficiently than applying the endpoint of ultimate interest. We used data from trials of nintedanib in subjects with pulmonary fibrosis to assess ... ...

Abstract	Background and objective: Surrogate endpoints enable determination of meaningful treatment effects more efficiently than applying the endpoint of ultimate interest. We used data from trials of nintedanib in subjects with pulmonary fibrosis to assess decline in forced vital capacity (FVC) as a surrogate for mortality. Methods: Data from the nintedanib and placebo groups of trials in subjects with idiopathic pulmonary fibrosis, other forms of progressive pulmonary fibrosis, and pulmonary fibrosis due to systemic sclerosis (NCT00514683, NCT01335464, NCT01335477, NCT01979952, NCT02999178, NCT02597933) were pooled. Using joint models for longitudinal and time-to-event data, we assessed the association between decline in FVC % predicted and time to death over 52 weeks. The rate of change in FVC % predicted and the current value of FVC % predicted were modelled longitudinally and estimates applied as predictors in time-to-event models. Results: Among 2583 subjects with pulmonary fibrosis, both a greater rate of decline in FVC % predicted and a lower current value of FVC % predicted were associated with an increased risk of death over 52 weeks (HR 1.79 [95% CI: 1.57, 2.03] and HR 1.24 [1.17, 1.32] per 5-percentage point decrease, respectively). Associations between the rate of change in FVC % predicted and the risk of death were consistent between patients with IPF and other ILDs. Conclusion: Data from clinical trials in subjects with pulmonary fibrosis of diverse aetiology demonstrate a strong association between decline in FVC % predicted and mortality over 52 weeks, supporting FVC decline as a surrogate for mortality in these patients.
Mesh-Begriff(e)	Humans ; Treatment Outcome ; Vital Capacity ; Idiopathic Pulmonary Fibrosis/drug therapy ; Biomarkers ; Disease Progression
Chemische Substanzen	Biomarkers
Sprache	Englisch
Erscheinungsdatum	2023-08-30
Erscheinungsland	Australia
Dokumenttyp	Journal Article
ZDB-ID	1435849-9
ISSN	1440-1843 ; 1323-7799
ISSN (online)	1440-1843
ISSN	1323-7799
DOI	10.1111/resp.14579
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The Novel Small Molecule BTB Inhibits Pro-Fibrotic Fibroblast Behavior though Inhibition of RhoA Activity.

Rackow, Ashley R / Nagel, David J / Zapas, Gregory / Clough, Ryan S / Sime, Patricia J / Kottmann, R Matthew

International journal of molecular sciences

2022 Band 23, Heft 19

Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic, interstitial lung disease with a poor prognosis. Although specific anti-fibrotic medications are now available, the median survival time following diagnosis remains very low, and new ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic, interstitial lung disease with a poor prognosis. Although specific anti-fibrotic medications are now available, the median survival time following diagnosis remains very low, and new therapies are urgently needed. To uncover novel therapeutic targets, we examined how biochemical properties of the fibrotic lung are different from the healthy lung. Previous work identified lactate as a metabolite that is upregulated in IPF lung tissue. Importantly, inhibition of the enzyme responsible for lactate production prevents fibrosis in vivo. Further studies revealed that fibrotic lesions of the lung experience a significant decline in tissue pH, likely due to the overproduction of lactate. It is not entirely clear how cells in the lung respond to changes in extracellular pH, but a family of proton sensing G-protein coupled receptors has been shown to be activated by reductions in extracellular pH. This work examines the expression profiles of proton sensing GPCRs in non-fibrotic and IPF-derived primary human lung fibroblasts. We identify TDAG8 as a proton sensing GPCR that is upregulated in IPF fibroblasts and that knockdown of TDAG8 dampens myofibroblast differentiation. To our surprise, BTB, a proposed positive allosteric modulator of TDAG8, inhibits myofibroblast differentiation. Our data suggest that BTB does not require TDAG8 to inhibit myofibroblast differentiation, but rather inhibits myofibroblast differentiation through suppression of RhoA mediated signaling. Our work highlights the therapeutic potential of BTB as an anti-fibrotic treatment and expands upon the importance of RhoA-mediated signaling pathways in the context of myofibroblast differentiation. Furthermore, this works also suggests that TDAG8 inhibition may have therapeutic relevance in the treatment of IPF.
Mesh-Begriff(e)	Cell Differentiation/physiology ; Fibroblasts/metabolism ; Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis/metabolism ; Lactates/metabolism ; Lung/pathology ; Myofibroblasts/metabolism ; Protons ; rhoA GTP-Binding Protein/metabolism
Chemische Substanzen	Lactates ; Protons ; RHOA protein, human (124671-05-2) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Sprache	Englisch
Erscheinungsdatum	2022-10-08
Erscheinungsland	Switzerland
Dokumenttyp	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/ijms231911946
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Cell-Type-Specific Effects of the Ovarian Cancer G-Protein Coupled Receptor (OGR1) on Inflammation and Fibrosis; Potential Implications for Idiopathic Pulmonary Fibrosis.

Nagel, David J / Rackow, Ashley R / Ku, Wei-Yao / Bell, Tyler J / Sime, Patricia J / Kottmann, Robert Matthew

Cells

2022 Band 11, Heft 16

Abstract: Idiopathic pulmonary fibrosis (IPF) is a disease characterized by irreversible lung scarring. The pathophysiology is not fully understood, but the working hypothesis postulates that a combination of epithelial injury and myofibroblast differentiation ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a disease characterized by irreversible lung scarring. The pathophysiology is not fully understood, but the working hypothesis postulates that a combination of epithelial injury and myofibroblast differentiation drives progressive pulmonary fibrosis. We previously demonstrated that a reduction in extracellular pH activates latent TGF-β1, and that TGF-β1 then drives its own activation, creating a feed-forward mechanism that propagates myofibroblast differentiation. Given the important roles of extracellular pH in the progression of pulmonary fibrosis, we sought to identify whether pH mediates other cellular phenotypes independent of TGF-β1. Proton-sensing G-protein coupled receptors are activated by acidic environments, but their role in fibrosis has not been studied. Here, we report that the Ovarian Cancer G-Protein Coupled Receptor1 (OGR1 or GPR68) has dual roles in both promoting and mitigating pulmonary fibrosis. We demonstrate that OGR1 protein expression is significantly reduced in lung tissue from patients with IPF and that TGF-β1 decreases OGR1 expression. In fibroblasts, OGR1 inhibits myofibroblast differentiation and does not contribute to inflammation. However, in epithelial cells, OGR1 promotes epithelial to mesenchymal transition (EMT) and inflammation. We then demonstrate that sub-cellular localization and alternative signaling pathways may be responsible for the differential effect of OGR1 in each cell type. Our results suggest that strategies to selectively target OGR1 expression may represent a novel therapeutic strategy for pulmonary fibrosis.
Mesh-Begriff(e)	Carcinoma, Ovarian Epithelial ; Epithelial-Mesenchymal Transition ; Female ; Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis/metabolism ; Inflammation ; Ovarian Neoplasms ; Receptors, G-Protein-Coupled/metabolism ; Transforming Growth Factor beta1/pharmacology
Chemische Substanzen	GPR68 protein, human ; Receptors, G-Protein-Coupled ; Transforming Growth Factor beta1
Sprache	Englisch
Erscheinungsdatum	2022-08-16
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11162540
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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