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Loss of ANT1 Increases Fibrosis and Epithelial Cell Senescence in Idiopathic Pulmonary Fibrosis
Am J Respir Cell Mol Biol. 2023 Jul 24. doi: 10.1165/rcmb.2022-0315OC. Online ahead of print.ABSTRACTIdiopathic Pulmonary Fibrosis (IPF) is an interstitial lung disease characterized by progressive lung scarring and remodeling. Although treatments exist that slow disease progression, IPF is irreversible and there is no cure. Cellular senescence, a major hallmark of aging, has been implicated in IPF pathogenesis, and mitochondrial dysfunction is increasingly recognized as a driver of senescence. Adenine nucleotide translocases (ANTs) are abundant mitochondrial ATP-ADP transporters critical for regulating cell fate and maint...
Source: Am J Respir Cell Mol... - July 24, 2023 Category: Respiratory Medicine Authors: Justin Sui Jennifer C Boatz Jian Shi Qianjiang Hu Xiaoyun Li Yingze Zhang Melanie K önigshoff Corrine R Kliment Source Type: research

Cyclophilin D Contributes to Airway Epithelial Mitochondrial Damage in Chronic Obstructive Pulmonary Disease
ConclusionThese data suggest that CypD signaling pathway is involved in the pathogenesis of COPD and provide a potential therapeutic target for COPD.
Source: Lung - June 1, 2023 Category: Respiratory Medicine Source Type: research

Mitochondrial DNA stress activates MHC class I antigen presentation and CD8+ T-cell immunity: implications for pulmonary fibrosis
Mitochondrial dysfunction is a hallmark of IPF and promotes the development of fibrosis. Mitochondrial stress has been shown to activate innate immunity via mitochondrial (mt) DNA sensing. However, whether mitochondrial stress regulates adaptive immune responses is unknown. We here investigated the regulation of MHC I antigen presentation by mitochondrial stress using a chronic mitochondrial dysfunction and an acute mtDNA stress model.Mouse embryonic fibroblasts derived from the PolgA mutator mouse, which represents a system of disturbed mitochondrial function, demonstrated concerted upregulation of the MHC I antigen prese...
Source: European Respiratory Journal - November 25, 2021 Category: Respiratory Medicine Authors: Wang, X., Meul, T., Kammerl, I., Wang, Y., Mayr, C., Schiller, H. B., Meiners, S. Tags: Airway cell biology and immunopathology Source Type: research

LSC - 2020 - Epithelial-mesenchymal transition induced by cigarette smoke in lung epithelial cells is associated with metabolic reprogramming and senescence
A dysregulated epithelial–mesenchymal transition (EMT) contributes to tumor progression, fibrosis and lung tissue remodeling in Chronic Obstructive Pulmonary Disease (COPD). Cigarette smoke, a risk factor for all these processes, induces oxidative stress, mitochondrial damage and drives cell senescence by reducing FoxO3, an anti-aging factor. Mitochondrial dysfunction is involved in aging and increases lactate generation, which is correlated with EMT induction.Here, we investigated the cigarette smoke extract (CSE) effects on mitochondrial status and cell metabolism and on the expression of EMT markers in lung epithe...
Source: European Respiratory Journal - October 28, 2020 Category: Respiratory Medicine Tags: Airway cell biology and immunopathology Source Type: research

Thrombin induces stomatin-like protein 2 (STOML2) expression and IL-8/CXCL8 release by ROCK, JNK, and PEA3 pathways in human lung epithelial cells
In this study, we investigate whether Rho kinase (ROCK), JNK, and PEA3 participate in thrombin-induced STOML2 expression and IL-8/CXCL8 release in human lung epithelial cells. We found that thrombin induced increase in STOML2, but not prohibitin, expression in a time-dependent manner. Thrombin also induces STOML2-luciferase activity. Thrombin-induced STOML2 expression and IL-8/CXCL8 release were reduced by PEA3 siRNA. We also found that transfection of A549 cells with PEA3 siRNA reduced PEA3 protein expression. In addition, thrombin induced increase in PEA3 Ser phosphorylation and PEA3 translocation from the cytosol to the...
Source: European Respiratory Journal - October 28, 2020 Category: Respiratory Medicine Authors: Chen, B.-C., Lin, C.-H. Tags: Airway pharmacology and treatment Source Type: research

Sirt3-MnSOD signaling pathway attenuates airway epithelial mitochondrial oxidative stress in chronic obstructive pulmonary disease
Conclusions: The data suggest that Sirt3 attenuates CSE-induced mitochondrial oxidative stress in the airway epithelia via deacetylating MnSOD, and may provide a novel therapeutic target for COPD.
Source: European Respiratory Journal - October 28, 2020 Category: Respiratory Medicine Authors: Zhang, M., Zhang, Y., Tang, J., Shi, R., Zhang, J., Li, Y., Fang, L., Roth, M. Tags: Molecular pathology and funct. genomics Source Type: research

Extracellular mitochondrial DNA promote NLRP3 inflammasome activation and induce acute lung injury through TLR9 and NF- κB.
Conclusions: Extracellular mtDNA promote NLRP3 inflammasome activation, acute pulmonary inflammation and injury through TLR9, p38 MAPK and NF-κB pathways. PMID: 31903272 [PubMed]
Source: Journal of Thoracic Disease - January 8, 2020 Category: Respiratory Medicine Tags: J Thorac Dis Source Type: research

Cigarette smoke induces mitochondrial dysfunction via PKCd-p66Shc signaling pathway in human bronchial epithelial cells
Conclusions: These data suggest that PKC-p66Shc pathway may be involved in the pathogenesis of COPD.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Zhang, M., Li, Y., Tang, J., Zhang, J., Yang, X., Shan, H., Zhang, Q. Tags: Airway Cell Biology and Immunopathology Source Type: research

LSC Abstract - Histone deacetylase 7 mediated metabolic remodeling: A new crosslink between pulmonary hypertension and cancer
Pulmonary arterial smooth muscle cells (PASMCs) from Pulmonary Hypertension (PH) patients and several PH animal models are characterized by suppressed mitochondria-dependent apoptosis and hyperpolarization. Similarly to lung cancer (LC) cells, PH-PASMCs have reduced glucose oxidation and increased cytoplasmic glycolysis. Protein acetylation and its enzymes such as histone deacetylases (HDACs) may play a role in the control of metabolism.We assessed the regulation of Class IIa HDACs (HDAC4, 5, 7 and 9) in human and experimental models of PH and lung cancer. By using primary culture of healthy (control-PASMCs), idiopathic de...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Gamen, E., Chelladurai, P., Grimminger, F., Savai, R., Seeger, W., Savai Pullamsetti, S. Tags: 4.3 Pulmonary Circulation and Pulmonary Vascular Diseases Source Type: research

Influence of glutathione-S-transferase (GST) inhibition on lung epithelial cell injury: role of oxidative stress and metabolism.
Abstract Oxidant-mediated tissue injury is key to the pathogenesis of acute lung injury. Glutathione-S-transferases (GSTs) are important detoxifying enzymes that catalyze the conjugation of glutathione with toxic oxidant compounds and are associated with acute and chronic inflammatory lung diseases. We hypothesized that attenuation of cellular GST enzymes would augment intracellular oxidative and metabolic stress and induce lung cell injury. Treatment of murine lung epithelial cells with GST inhibitors, ethacrynic acid (EA), and caffeic acid compromised lung epithelial cell viability in a concentration-dependent m...
Source: Am J Physiol Lung Ce... - June 15, 2015 Category: Respiratory Medicine Authors: Fletcher ME, Boshier PR, Wakabayashi K, Keun HC, Smolenski RT, Kirkham PA, Adcock IM, Barton PJ, Takata M, Marczin N Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Influence of glutathione-S-transferase (GST) inhibition on lung epithelial cell injury: role of oxidative stress and metabolism
Oxidant-mediated tissue injury is key to the pathogenesis of acute lung injury. Glutathione-S-transferases (GSTs) are important detoxifying enzymes that catalyze the conjugation of glutathione with toxic oxidant compounds and are associated with acute and chronic inflammatory lung diseases. We hypothesized that attenuation of cellular GST enzymes would augment intracellular oxidative and metabolic stress and induce lung cell injury. Treatment of murine lung epithelial cells with GST inhibitors, ethacrynic acid (EA), and caffeic acid compromised lung epithelial cell viability in a concentration-dependent manner. These inhib...
Source: AJP: Lung Cellular and Molecular Physiology - June 15, 2015 Category: Respiratory Medicine Authors: Fletcher, M. E., Boshier, P. R., Wakabayashi, K., Keun, H. C., Smolenski, R. T., Kirkham, P. A., Adcock, I. M., Barton, P. J., Takata, M., Marczin, N. Tags: ARTICLES Source Type: research

Late-breaking abstract: The bromodomain-containing protein 4: The epigenetic origin of the oncogenic signature in pulmonary hypertension
Conclusion: Our study suggests an important role for BRD4 in pulmonary hypertension and opens the door to new avenues of investigation and proposes BRD4 as putative treatment for PAH.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Vaillancourt, M., Meloche, J., Ferraro, P., Provencher, S., Bonnet, S. Tags: 4.3 Pulmonary Circulation and Pulmonary Vascular Disease Source Type: research