Experimental Lung Research最新文献

{"title":"Melatonin attenuates lung ischemia-reperfusion injury through SIRT3 signaling-dependent mitophagy in type 2 diabetic rats.","authors":"Zhiqiang Song,&nbsp;Congmin Yan,&nbsp;Yuanbo Zhan,&nbsp;Qiujun Wang,&nbsp;Yina Zhang,&nbsp;Tao Jiang","doi":"10.1080/01902148.2023.2213335","DOIUrl":"https://doi.org/10.1080/01902148.2023.2213335","url":null,"abstract":"<p><p><b>Background:</b> Lung ischemia-reperfusion injury (LIRI) remains the major cause of primary lung dysfunction after lung transplantation. Diabetes mellitus (DM) is an independent risk factor for morbidity and mortality following lung transplantation. Mitochondrial dysfunction is recognized as a key mediator in the pathogenesis of diabetic LIRI. Melatonin has been reported to be a safe and potent preserving mitochondrial function agent. This study aimed at investigating the potential therapeutic effect and mechanisms of melatonin on diabetic LIRI. <b>Methods:</b> High-fat-diet-fed streptozotocin-induced type 2 diabetic rats were exposed to melatonin, with or without administration of the SIRT3 short hairpin ribonucleic acid (shRNA) plasmid following a surgical model of ischemia-reperfusion injury of the lung. Lung function, inflammation, oxidative stress, cell apoptosis, and mitochondrial function were examined. <b>Results:</b> The SIRT3 signaling and mitophagy were suppressed following diabetic LIRI. Treatment with melatonin markedly induced mitophagy and restored SIRT3 expression. Melatonin treatment also attenuated subsequent diabetic LIRI by improving lung functional recovery, suppressing inflammation, decreasing oxidative damage, diminishing cell apoptosis, and preserving mitochondrial function. However, either administration of <i>SIRT3</i> shRNA or an autophagy antagonist 3-methyladenine (3-MA) suppressing mitophagy, and compromised the protective action of melatonin. <b>Conclusion:</b> Data indicated that melatonin attenuates diabetic LIRI through activation of SIRT3 signaling-mediated mitophagy.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"101-115"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9598190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of hypoxia-induced pulmonary hypertension rat models caused by different hypoxia protocols.","authors":"Gexiang Cai,&nbsp;Yaxin Zhang,&nbsp;Xinghong Wang,&nbsp;Shini Li,&nbsp;Yushan Cheng,&nbsp;Xiaoying Huang","doi":"10.1080/01902148.2022.2148016","DOIUrl":"https://doi.org/10.1080/01902148.2022.2148016","url":null,"abstract":"<p><p><b>Background and aim:</b> Pulmonary hypertension (PH) is a serious and even fatal disorder with limited treatment strategies. The hypoxia-induced pulmonary hypertension (HPH) rat model is commonly used in this field. While the HPH rat model has strong predictability and repeatability, the model is a chronic model, making it time-consuming, costly, and complicated and limiting the progress of the experiments. Currently, there is no uniform international standard for the HPH model. Our study aimed to find a relatively effective and efficient HPH modeling protocol. <b>Methods:</b> We established HPH rat models with different total hypoxia periods and different daily hypoxia times, and assessed different hypoxia modeling modes in multiple dimensions, such as haemodynamics, right ventricular (RV) hypertrophy, pulmonary arterial remodeling, muscularization, inflammation, and collagen deposition. <b>Results:</b> Longer daily hypoxia time resulted in higher mean pulmonary arterial pressure (mPAP)/right ventricular systolic pressure (RVSP) and more obvious RV hypertrophy, as well as more severe pulmonary arterial remodeling and muscularization, regardless of the total period of hypoxia (3- or 4-week). Moreover, pulmonary perivascular macrophages and collagen deposition showed daily hypoxia time-dependent increases, both in 3- and 4-week hypoxia groups. <b>Conclusion:</b> Our findings showed that the 3-week continuous hypoxia mode was a relatively efficient way to reduce the time needed to induce significant disease phenotypes, which offered methodological evidence for future studies in building HPH models.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"1-11"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9732421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The multiphasic TNF-α-induced compromise of Calu-3 airway epithelial barrier function.","authors":"Katherine M DiGuilio,&nbsp;Elizabeth Rybakovsky,&nbsp;Yoongyeong Baek,&nbsp;Mary Carmen Valenzano,&nbsp;James M Mullin","doi":"10.1080/01902148.2023.2193637","DOIUrl":"https://doi.org/10.1080/01902148.2023.2193637","url":null,"abstract":"<p><p><b>Purpose:</b> Airway epithelial barrier leak and the involvement of proinflammatory cytokines play a key role in a variety of diseases. This study evaluates barrier compromise by the inflammatory mediator Tumor Necrosis Factor-α (TNF-α) in the human airway epithelial Calu-3 model. <b>Methods:</b> We examined the effects of TNF-α on barrier function in Calu-3 cell layers using Transepithelial Electrical Resistance (TER) and transepithelial diffusion of radiolabeled probe molecules. Western immunoblot analyses of tight junctional (TJ) proteins in detergent soluble fractions were performed. <b>Results:</b> TNF-α dramatically reduced TER and increased paracellular permeability of both 14C-D-mannitol and the larger 5 kDa probe, 14C-inulin. A time course of the effects shows two separate actions on barrier function. An initial compromise of barrier function occurs 2-4 hours after TNF-α exposure, followed by complete recovery of barrier function by 24 hrs. Beginning 48 hrs. post-exposure, a second more sustained barrier compromise ensues, in which leakiness persists through 144 hrs. There were no changes in TJ proteins observed at 3 hrs. post exposure, but significant increases in claudins-2, -3, -4, and -5, as well as a decrease in occludin were seen at 72 hrs. post TNF-α exposure. Both the 2-4 hr. and the 72 hr. TNF-α induced leaks are shown to be mediated by the ERK signaling pathway. <b>Conclusion:</b> TNF-α induced a multiphasic transepithelial leak in Calu-3 cell layers that was shown to be ERK mediated, as well as involve changes in the TJ complex. The micronutrients, retinoic acid and calcitriol, were effective at reducing this barrier compromise caused by TNF-α. The significance of these results for airway disease and for COVID-19 specifically are discussed.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"72-85"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9658606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of mechanical ventilation under intubation on respiratory tract change of bacterial count and alteration of bacterial flora.","authors":"Chen Xue-Meng,&nbsp;Liu Gao-Wang,&nbsp;Ling Xiao-Mei,&nbsp;Zeng Fan-Fang,&nbsp;Xiao Jin-Fang","doi":"10.1080/01902148.2023.2264947","DOIUrl":"10.1080/01902148.2023.2264947","url":null,"abstract":"<p><p><b>Background:</b> The most common 'second strike' in mechanically ventilated patients is a pulmonary infection caused by the ease with which bacteria can invade and colonize the lungs due to mechanical ventilation. At the same time, metastasis of lower airway microbiota may have significant implications in developing intubation mechanical ventilation lung inflammation. Thus, we establish a rat model of tracheal intubation with mechanical ventilation and explore the effects of mechanical ventilation on lung injury and microbiological changes in rats. To provide a reference for preventing and treating bacterial flora imbalance and pulmonary infection injury caused by mechanical ventilation of tracheal intubation. <b>Methods:</b> Sprague-Dawley rats were randomly divided into Control, Mechanical ventilation under intubation (1, 3, 6 h) groups, and Spontaneously breathing under intubation (1, 3, 6 h). Lung histopathological injury scores were evaluated. 16SrDNA sequencing was performed to explore respiratory microbiota changes, especially, changes of bacterial count and alteration of bacterial flora. <b>Results:</b> Compared to groups C and SV, critical pathological changes in pulmonary lesions occurred in the MV group after 6 h (<i>p</i> < 0.05). The Alpha diversity and Beta diversity of lower respiratory tract microbiota in MV6, SV6, and C groups were statistically significant (<i>p</i> < 0.05). The main dominant bacterial phyla in the respiratory tract of rats were <i>Proteobacteria, Firmicutes, Bacteroidetes, and Cyanobacteria. Acinetobacter radioresistens</i> in group C was significant, <i>Megaonas</i> in group MV6 was significantly increased, and <i>Parvibacter</i> in group SV6 was significantly increased. Anaerobic, biofilm formation, and Gram-negative bacteria-related functional genes were altered during mechanical ventilation with endotracheal intubation. <b>Conclusion:</b> Mechanical ventilation under intubation may cause dysregulation of lower respiratory microbiota in rats.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"165-177"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41124910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HIF and ER stress are involved in TGFβ1-mediated wound closure of alveolar epithelial cells.","authors":"Eva Delbrel,&nbsp;Nicolas Voituron,&nbsp;Emilie Boncoeur","doi":"10.1080/01902148.2023.2183996","DOIUrl":"https://doi.org/10.1080/01902148.2023.2183996","url":null,"abstract":"<p><p><b>Purpose:</b> Alveolar epithelium dysfunction is associated with a very large spectrum of disease and an abnormal repair capacity of the airway epithelium has been proposed to explain the pathogenesis of Idiopathic Pulmonary Fibrosis (IPF). Following epithelium insult, the damaged cells will activate pathways implicated in the repair process, including proliferation and acquisition of migratory capacities to cover the denuded basement membrane. Induction of Endoplasmic Reticulum stress may be implicated in this process. Interestingly, ER stress excessive activation has been proposed as a central event associated with aberrant repair process and cellular dysfunction observed in IPF. <b>Methods:</b> We study by wound healing assay the molecular targets associated with Alveolar Epithelial Cells (AEC) repair. <b>Results:</b> We demonstrate that the wound recovery of AEC is associated with TGF-β1 signaling and increased transcriptional activity of ER stress and HIF-dependent genes. We further demonstrated that inhibition of TGF-β1 signaling, CHOP expression or HIF-1 expression, limits AECs wound closure. <b>Conclusion:</b> the use of pharmacological drugs targeting the ER/HIF-1 axis could be an attractive approach to limit AEC dysregulation in pathological condition, and confirmed a critical role of theses factor in response to alveolar injury.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"63-71"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9952979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"House dust mite-induced endoplasmic reticulum stress mediates MUC5AC hypersecretion via TBK1 in airway epithelium.","authors":"Jun Deng,&nbsp;Hongmei Tang,&nbsp;Yun Zhang,&nbsp;Xiefang Yuan,&nbsp;Ning Ma,&nbsp;Hang Hu,&nbsp;Xiaoyun Wang,&nbsp;Chunfeng Liu,&nbsp;Guofeng Xu,&nbsp;Yuejiao Li,&nbsp;Songping Wang,&nbsp;Linlin Guo,&nbsp;Xing Wang","doi":"10.1080/01902148.2023.2170494","DOIUrl":"https://doi.org/10.1080/01902148.2023.2170494","url":null,"abstract":"<p><p><b>Purpose:</b> Endoplasmic reticulum (ER) stress regulates mucus hypersecretion, and may activate downstream factors via TBK1 signaling to induce gene expression. However, it remains unclear whether ER stress promotes airway mucus secretion through the TBK1 pathway. We aimed to investigate the role of the TBK1 pathway in the regulation of MUC5AC expression in a mouse model of house dust mite (HDM)-induced allergic asthma. <b>Materials and Methods:</b> Mice with HDM-induced asthma and human bronchial epithelial BEAS-2B cells were treated with amlexanox, an anti-allergy drug (25 μM), or 4-PBA (10 mM). Tissue and cell samples were collected. Tissue samples were stained with hematoxylin and eosin (H&E) or periodic acid Schiff (PAS) to evaluate pathology. Protein expression was analyzed by western blotting and immunofluorescence. <b>Results:</b> Mice exposed to HDM presented ER stress and hypersecretion of mucus Muc5ac from airway epithelial cells (<i>p</i> < 0.001). Similar results were observed in BEAS-2B cells following exposure to HDM. Both <i>in vivo</i> and <i>in vitro</i> studies revealed that HDM-induced ER stress induced MUC5AC overexpression via TBK1 signaling. Amlexanox and 4-PBA markedly reduced mucus production and weakened the TBK1 signal, which mediates MUC5AC hypersecretion. <b>Conclusion:</b> TBK1 plays a pivotal role in HDM-induced ER stress, leading to overproduction of MUC5AC in the asthmatic airway epithelium. The overproduction of MUC5AC can be significantly decreased by inhibiting TBK1 or ER stress using 4-PBA. These findings highlight potential target-specific therapies for patients with chronic allergic asthma.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"49-62"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9971416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of cGAS aggravated the host inflammatory response to <i>Aspergillus fumigatus</i>.","authors":"Mei Peng, Xiujun Li, Xiaobing Zhang, Li Peng","doi":"10.1080/01902148.2023.2211663","DOIUrl":"10.1080/01902148.2023.2211663","url":null,"abstract":"<p><p><b>Backgroud:</b> <i>Aspergillus fumigatus</i> (<i>A. fumigatus</i>) is a clinically important fungal pathogen. Invasive pulmonary aspergillosis (IPA) is the main fungal infection with increased morbidity and mortality in immunocompromised populations, although treatments are available. An innate DNA sensor known as cyclic GMP-AMP Synthase (cGAS) has recently been discovered that senses invading pathogens and has a significant impact on innate immunity. It can activate the cGAS-STING signaling pathway to stimulate downstream signals. But it is still unclear what role it plays in IPA's pathogenesis.<b>Methods:</b> An investigation into the infection of <i>A. fumigatus</i> was conducted by inhibiting cGAS activity <i>in vivo</i> and <i>in vitro</i> using siRNA and RU.521(an inhibitor of cGAS).<b>Results:</b> We discovered that suppressing cGAS increased the host's susceptibility to <i>A. fumigatus</i> and harmed those with infections by enhancing pulmonary tissue damage and edema, as well as decreasing fungal clearance. Furthermore, our findings show that inhibiting or silencing cGAS can exacerbate the inflammatory response in IPA mouse models and human bronchi epithelial cells (HBECs) treated with <i>A. fumigatus</i> by upregulating the production of inflammatory genes with non-type 1 interferon.<b>Conclusion:</b> Based on our analysis, we conclude that activating cGAS might increase host resistance to <i>A. fumigatus</i>, protect against pulmonary illnesses brought on by <i>A. fumigatus</i> and that exploring the cGAS-STING signaling pathway is beneficial not only for the immunological investigation of IPA but also may be a potential therapeutic objective.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":" ","pages":"86-100"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9463465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapamycin attenuates pyroptosis by suppressing mTOR phosphorylation and promoting autophagy in LPS-induced bronchopulmonary dysplasia.","authors":"Feng Zhang, Minrong Wang, Zhongni Li, Jiehong Deng, Yang Fan, Zhixian Gou, Yue Zhou, Li Huang, Liqun Lu","doi":"10.1080/01902148.2023.2266236","DOIUrl":"10.1080/01902148.2023.2266236","url":null,"abstract":"<p><strong>Purpose/aim: </strong>Bronchopulmonary dysplasia (BPD) is associated with poor survival in preterm infants. Intrauterine infection can aggravate the degree of obstruction of alveolar development in premature infants; however, the pathogenic mechanism remains unclear. In this study, we sought to determine whether pyroptosis could be inhibited by downregulating mammalian target of rapamycin (mTOR) activation and inducing autophagy in BPD-affected lung tissue.</p><p><strong>Materials and methods: </strong>We established a neonatal rat model of BPD induced by intrauterine infection <i>via</i> intraperitoneally injecting pregnant rats with lipopolysaccharide (LPS). Subsequently, mTOR levels and pyroptosis were evaluated using immunohistochemistry, immunofluorescence, TUNEL staining, and western blotting. The Shapiro-Wilk test was employed to assess the normality of the experimental data. Unpaired <i>t-</i>tests were used to compare the means between two groups, and comparisons between multiple groups were performed using analysis of variance.</p><p><strong>Results: </strong>Pyroptosis of lung epithelial cells increased in BPD lung tissues. After administering an mTOR phosphorylation inhibitor (rapamycin) to neonatal rats with BPD, the level of autophagy increased, while the expression of autophagy cargo adaptors, LC3 and p62, did not differ. Following rapamycin treatment, NLRP3, Pro-caspase-1, caspase-1, pro-IL-1β, IL-1β, IL-18/Pro-IL-18, N-GSDMD/GSDMD, Pro-caspase-11, and caspase-11 were negatively regulated in BPD lung tissues. The opposite results were observed after treatment with the autophagy inhibitor MHY1485, showing an increase in pyroptosis and a significant decrease in the number of alveoli in BPD.</p><p><strong>Conclusions: </strong>Rapamycin reduces pyroptosis in neonatal rats with LPS-induced BPD by inhibiting mTOR phosphorylation and inducing autophagy; hence, it may represent a potential therapeutic for treating BPD.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"49 1","pages":"178-192"},"PeriodicalIF":1.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49689470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevention of submicron aerosolized particle dispersion: evaluation of an aerosol box using a pediatric simulation model.","authors":"Laurence Tabone,&nbsp;Dominic Rivest,&nbsp;Arielle Levy,&nbsp;Michael Buyck,&nbsp;Philippe Jouvet,&nbsp;Carl-Eric Aubin,&nbsp;Tine François,&nbsp;Etienne Robert,&nbsp;Florent Baudin","doi":"10.1080/01902148.2022.2135795","DOIUrl":"https://doi.org/10.1080/01902148.2022.2135795","url":null,"abstract":"<p><p><b>Background and Aim:</b> The SplashGuard CG (SG) is a barrier enclosure developed to protect healthcare workers from SARS-CoV-2 transmission during aerosol-generating procedures. Our objective was to evaluate the protection provided by the SG against aerosolized particles (AP), using a pediatric simulation model of spontaneous ventilation (SV) and noninvasive ventilation (NIV). <b>Methods:</b> An aerosol generator was connected to the airways of a pediatric high-fidelity manikin with a breathing simulator. AP concentrations were measured both in SV and NIV in the following conditions: with and without SG, inside and outside the SG, with and without suction applied to the device. <b>Results:</b> In the SV simulated setting, AP peaks were lower with SG: 0.1 × 10⁵ particles/L compared to without: 1.6 × 10⁵, only when the ports were closed and suction applied. In the NIV simulated setting, AP peaks outside the SG were lower than without SG (20.5 × 10⁵ particles/L), whatever the situation, without suction (14.4 × 10⁵particles/L), with suction and ports open or closed: 10.3 and 0.7 × 10⁵ particles/L. In SV and NIV simulated settings, the AP peaks measured within the SG were much higher than the AP peaks measured without SG, even when suction was applied to the device. <b>Conclusions:</b> The SG seems to decrease peak AP exposure in the 2 ventilation contexts, but only with closed port and suction in SV. However, high concentrations of AP remain inside even with suction and SG should be used cautiously.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 9-10","pages":"266-274"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10440548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteomic global proteins analysis in blast lung injury reveals the altered characteristics of crucial proteins in response to oxidative stress, oxidation-reduction process and lipid metabolic process.","authors":"Peifang Cong,&nbsp;Changci Tong,&nbsp;Shun Mao,&nbsp;Xiuyun Shi,&nbsp;Ying Liu,&nbsp;Lin Shi,&nbsp;Hongxu Jin,&nbsp;Yunen Liu,&nbsp;Mingxiao Hou","doi":"10.1080/01902148.2022.2143596","DOIUrl":"https://doi.org/10.1080/01902148.2022.2143596","url":null,"abstract":"<p><p><b>Background:</b> Blast lung injury (BLI) is the most common fatal blast injury induced by overpressure wave in the events of terrorist attack, gas and underground explosion. Our previous work revealed the characteristics of inflammationrelated key proteins involved in BLI, including those regulating inflammatory response, leukocyte transendothelial migration, phagocytosis, and immune process. However, the molecular characteristics of oxidative-related proteins in BLI ar still lacking. <b>Methods:</b> In this study, protein expression profiling of the blast lungs obtained by tandem mass tag (TMT) spectrometry quantitative proteomics were re-analyzed to identify the characteristics of oxidative-related key proteins. Forty-eight male C57BL/6 mice were randomly divided into six groups: control, 12 h, 24 h, 48 h, 72 h and 1 w after blast exposure. The differential protein expression was identified by bioinformatics analysis and verified by western blotting. <b>Results:</b> The results demonstrated that thoracic blast exposure induced reactive oxygen species generation and lipid peroxidation in the lungs. Analysis of global proteins and oxidative-related proteomes showed that 62, 59, 73, 69, 27 proteins (accounted for 204 distinct proteins) were identified to be associated with oxidative stress at 12 h, 24 h, 48 h, 72 h, and 1 week after blast exposure, respectively. These 204 distinct proteins were mainly enriched in response to oxidative stress, oxidation-reduction process and lipid metabolic process. We also validated these results by western blotting. <b>Conclusions:</b> These findings provided new perspectives on blast-induced oxidative injury in lung, which may potentially benefit the development of future treatment of BLI.</p>","PeriodicalId":12206,"journal":{"name":"Experimental Lung Research","volume":"48 9-10","pages":"275-290"},"PeriodicalIF":1.7,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10441092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}