Proteomic differences with and without ozone-exposure in a smoking-induced emphysema lung model

Air pollutants include toxic particles and gases emitted in large quantities from many different combustible materials. They also include particulate matter (PM) and ozone, and biological contaminants, such as viruses and bacteria, which can penetrate the human airway and reach the bloodstream, triggering airway inflammation, dysfunction, and fibrosis. Pollutants that accumulate in the lungs exacerbate symptoms of respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD). Asthma, a heterogeneous disease with complex pathological mechanisms, is characterized by particular symptoms such as shortness of breath, a tight chest, coughing, and wheezing. Patients with COPD often experience exacerbations and worsening of symptoms, which may result in hospitalization and disease progression. PM varies in terms of composition, and can include solid and liquid particles of various sizes. PM concentrations are higher in urban areas. Ozone is one of the most toxic photochemical air pollutants. In general, air pollution decreases quality of life and life expectancy. It exacerbates acute and chronic respiratory symptoms in patients with chronic airway diseases, and increases the morbidity and risk of hospitalization associated with respiratory diseases. However, the mechanisms underlying these effects remain unclear. Therefore, we reviewed the impact of air pollutants on airway diseases such as asthma and COPD, focusing on their underlying mechanisms.

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“…treatment. Therefore, TBC1D5 may be a useful biomarker for ozone-induced lung injury in patients with emphysema [ 149 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Air Pollutants on Airway Diseases

Lee

Choi

et al. 2021

IJERPH

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“…TBC family proteins containing the TRE2/Bub2/CDC16 domain are highly conserved in eukaryotic cells [ 33 ]. Commonly, these proteins were considered as GTPase activating proteins (GAPs) of the Rab small GTPase family proteins [ 34 , 35 ]. TBC1D5 is lowly expressed in ccRCC, and the expression level is significantly associated with prognosis.…”

Section: Discussionmentioning

confidence: 99%

TBC1D5 reverses the capability of HIF-2α in tumor progression and lipid metabolism in clear cell renal cell carcinoma by regulating the autophagy

Huang,

Xiong,

Wang

et al. 2024

J Transl Med

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Background Clear cell renal cell carcinoma (ccRCC) is known for abnormal lipid metabolism and widespread activation of HIF-2α. Recently, the importance of autophagy in ccRCC has been focused, and it has potential connections with HIF-2α and lipid metabolism. However, the specific regulatory mechanism between HIF-2α, autophagy, and lipid metabolism in ccRCC is still unclear. Methods In this study, Bioinformatics Analysis and Sequencing of the whole transcriptome were used to screen our target. The expression of TBC1D5 in renal clear cell carcinoma was confirmed by database analysis, immunohistochemistry, PCR and Western blot. The effects of TBC1D5 on tumor cell growth, migration, invasion and lipid metabolism were examined by CCK8, Transwell and oil red staining, and the mechanism of TBC1D5 on autophagy was investigated by Western blot, fluorescence microscopy and electron microscopy. Chloroquine and rapamycin were used to verified the key role of autophagy in effects of TBC1D5 on tumor cell. The regulatory mechanism of TBC1D5 in renal clear cell carcinoma (RCC) was investigated by shhif-2α, shTBC1D5, mimic, inhibitor, ChIP and Luciferase experiments. The animal model of ccRCC was used to evaluate the biological function of TBC1D5 in vivo. Results In this study, TBC1D5 was found to be an important bridge between autophagy and HIF-2α. Specifically, TBC1D5 is significantly underexpressed in ccRCC, serving as a tumor suppressor which inhibits tumor progression and lipid accumulation, and is negatively regulated by HIF-2α. Further research has found that TBC1D5 regulates the autophagy pathway to reverse the biological function of HIF-2α in ccRCC. Mechanism studies have shown that HIF-2α regulates TBC1D5 through hsa-miR-7-5p in ccRCC, thereby affecting tumor progression and lipid metabolism through autophagy. Conclusions Our research reveals a completely new pathway, HIF-2α/hsa-miR-7-5p/TBC1D5 pathway affects ccRCC progression and lipid metabolism by regulating autophagy. Graphical Abstract

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“…It has been reported that Eno3 is upregulated in traumatic brain injury [44]. The expression of triosephosphate isomerase 1 (Tpi1) is low in smoking-induced emphysema lung models [45]. It is worth mentioning that Tpi1 is involved in the glycolysis or gluconeogenesis pathway in acute lung injury [46].…”

Section: Discussionmentioning

confidence: 99%

Identification of differentially expressed proteins in the injured lung from zinc chloride smoke inhalation based on proteomics analysis

Xie

Zhao²,

Xie³

et al. 2019

Respir Res

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Background Lung injury due to zinc chloride smoke inhalation is very common in military personnel and leads to a high incidence of pulmonary complications and mortality. The aim of this study was to uncover the underlying mechanisms of lung injury due to zinc chloride smoke inhalation using a rat model. Methods: Histopathology analysis of rat lungs after zinc chloride smoke inhalation was performed by using haematoxylin and eosin (H&E) and Mallory staining. A lung injury rat model of zinc chloride smoke inhalation (smoke inhalation for 1, 2, 7 and 14 days) was developed. First, isobaric tags for relative and absolute quantization (iTRAQ) and weighted gene co-expression network analysis (WGCNA) were used to identify important differentially expressed proteins. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were used to study the biological functions of differentially expressed proteins. Then, analysis of lung injury repair-related differentially expressed proteins in the early (day 1 and day 2) and middle-late stages (day 7 and day 14) of lung injury after smoke inhalation was performed, followed by the protein-protein interaction (PPI) analysis of these differentially expressed proteins. Finally, the injury repair-related proteins PARK7 and FABP5 were validated by immunohistochemistry and western blot analysis. Results Morphological changes were observed in the lung tissues after zinc chloride smoke inhalation. A total of 27 common differentially expressed proteins were obtained on days 1, 2, 7 and 14 after smoke inhalation. WGCNA showed that the turquoise module (which involved 909 proteins) was most associated with smoke inhalation time. Myl3, Ckm, Adrm1 and Igfbp7 were identified in the early stages of lung injury repair. Gapdh, Acly, Tnni2, Acta1, Actn3, Pygm, Eno3 and Tpi1 (hub proteins in the PPI network) were identified in the middle-late stages of lung injury repair. Eno3 and Tpi1 were both involved in the glycolysis/gluconeogenesis signalling pathway. The expression of PARK7 and FABP5 was validated and was consistent with the proteomics analysis. Conclusion The identified hub proteins and their related signalling pathways may play crucial roles in lung injury repair due to zinc chloride smoke inhalation.

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Proteomic differences with and without ozone-exposure in a smoking-induced emphysema lung model

Cited by 9 publications

References 35 publications

Effects of Air Pollutants on Airway Diseases

Effects of Air Pollutants on Airway Diseases

TBC1D5 reverses the capability of HIF-2α in tumor progression and lipid metabolism in clear cell renal cell carcinoma by regulating the autophagy

Identification of differentially expressed proteins in the injured lung from zinc chloride smoke inhalation based on proteomics analysis

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