Cigarette smoke exposure enhances transforming acidic coiled-coil–containing protein 2 turnover and thereby promotes emphysema

Mallampalli, Rama K.; Li, Xiuying; Jang, Ji-Young; Kamiński, Tomasz W.; Hoji, Aki; Coon, Tiffany A.; Chandra, Divay; Welty, Starr; Teng, Yaqun; Sembrat, John; Rojas, Mauricio; Zhao, Yutong; Lafyatis, Robert; Zou, Chunbin; Sciurba, Frank C.; Sundd, Prithu; Lan, Li; Nyunoya, Toru

doi:10.1172/jci.insight.125895

Cited by 14 publications

(14 citation statements)

References 43 publications

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“…A centrosome-and microtubule-interacting protein, involved in homologous recombination repair [22], attenuates DNA damage and cytotoxicity in immortalized human bronchial epithelial cells [23].…”

Section: Tacc2mentioning

confidence: 99%

Reticular Basement Membrane Thickness Is Associated with Growth- and Fibrosis-Promoting Airway Transcriptome Profile-Study in Asthma Patients

Bazan-Socha

Buregwa-Czuma

Jakieła

et al. 2021

IJMS

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Airway remodeling in asthma is characterized by reticular basement membrane (RBM) thickening, likely related to epithelial structural and functional changes. Gene expression profiling of the airway epithelium might identify genes involved in bronchial structural alterations. We analyzed bronchial wall geometry (computed tomography (CT)), RBM thickness (histology), and the bronchial epithelium transcriptome profile (gene expression array) in moderate to severe persistent (n = 21) vs. no persistent (n = 19) airflow limitation asthmatics. RBM thickness was similar in the two studied subgroups. Among the genes associated with increased RBM thickness, the most essential were those engaged in cell activation, proliferation, and growth (e.g., CDK20, TACC2, ORC5, and NEK5) and inhibiting apoptosis (e.g., higher mRNA expression of RFN34, BIRC3, NAA16, and lower of RNF13, MRPL37, CACNA1G). Additionally, RBM thickness correlated with the expression of genes encoding extracellular matrix (ECM) components (LAMA3, USH2A), involved in ECM remodeling (LTBP1), neovascularization (FGD5, HPRT1), nerve functioning (TPH1, PCDHGC4), oxidative stress adaptation (RIT1, HSP90AB1), epigenetic modifications (OLMALINC, DNMT3A), and the innate immune response (STAP1, OAS2). Cluster analysis revealed that genes linked with RBM thickness were also related to thicker bronchial walls in CT. Our study suggests that the pro-fibrotic profile in the airway epithelial cell transcriptome is associated with a thicker RBM, and thus, may contribute to asthma airway remodeling.

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Section: Tacc2mentioning

confidence: 99%

Reticular Basement Membrane Thickness Is Associated with Growth- and Fibrosis-Promoting Airway Transcriptome Profile-Study in Asthma Patients

Bazan-Socha

Buregwa-Czuma

Jakieła

et al. 2021

IJMS

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“…Cigarette smoke is composed of more than 7,000 chemicals, including nicotine, carbon monoxide, nitrogen oxides, and heavy metals (Gunes et al, 2018;Rennard, 2004;Talhout et al, 2011). Numerous studies have suggested that cigarette smoke extract (CSE) enhances or suppresses the expression of many genes in human epithelial cells (Mallampalli et al, 2020;Zeng et al, 2019). However, CSE-associated production of IL-36 in human epithelial cells has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Cigarette Smoke Underlies the Pathogenesis of Palmoplantar Pustulosis via an IL-17A–Induced Production of IL-36γ in Tonsillar Epithelial Cells

Kobayashi

Kamekura

Kato

et al. 2021

Journal of Investigative Dermatology

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“…Cigarette smoke induced aberrant activation of proteasome (Kim et al, 2011). F-Box proteins were suggested to be enrolled in cigarette smoke-stimulated protein degradation, indicating the potential roles of F-box protein in COPD development (Mallampalli et al, 2020). Combined with the above data, we hypothesized that CSE-induced lung inflammation and apoptosis may be regulated by FBXW17/ PRMT6 signaling.…”

Section: Fbxw17/prmt6 Signaling Involves In Cse-induced Lung Epithelimentioning

confidence: 81%

F-Box Protein FBXW17-Mediated Proteasomal Degradation of Protein Methyltransferase PRMT6 Exaggerates CSE-Induced Lung Epithelial Inflammation and Apoptosis

Luo

et al. 2021

Front. Cell Dev. Biol.

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Chronic obstructive pulmonary disease (COPD) is a chronic debilitating lung disease, characterized by progressive airway inflammation and lung structural cell death. Cigarette smoke is considered the most common risk factor of COPD pathogenesis. Understanding the molecular mechanisms of persistent inflammation and epithelial apoptosis induced by cigarette smoke would be extremely beneficial for improving the treatment and prevention of COPD. A histone methyl modifier, protein arginine N-methyltransferase 6 (PRMT6), is reported to alleviate cigarette smoke extract (CSE)-induced emphysema through inhibiting inflammation and cell apoptosis. However, few studies have focused on the modulation of PRMT6 in regulating inflammation and cell apoptosis. In this study, we showed that protein expression of PRMT6 was aberrantly decreased in the lung tissue of COPD patients and CSE-treated epithelial cells. FBXW17, a member of the Skp1-Cullin-F-box (SCF) family of E3 ubiquitin ligases, selectively bound to PRMT6 in nuclei to modulate its elimination in the proteasome system. Proteasome inhibitor or silencing of FBXW17 abrogated CSE-induced PRMT6 protein degradation. Furthermore, negative alteration of FBXW17/PRMT6 signaling lessened the proapoptotic and proinflammatory effects of CSE in lung epithelial cells. Our study, therefore, provides a potential therapeutic target against the airway inflammation and cell death in CS-induced COPD.

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Cigarette smoke exposure enhances transforming acidic coiled-coil–containing protein 2 turnover and thereby promotes emphysema

Cited by 14 publications

References 43 publications

Reticular Basement Membrane Thickness Is Associated with Growth- and Fibrosis-Promoting Airway Transcriptome Profile-Study in Asthma Patients

Reticular Basement Membrane Thickness Is Associated with Growth- and Fibrosis-Promoting Airway Transcriptome Profile-Study in Asthma Patients

Cigarette Smoke Underlies the Pathogenesis of Palmoplantar Pustulosis via an IL-17A–Induced Production of IL-36γ in Tonsillar Epithelial Cells

F-Box Protein FBXW17-Mediated Proteasomal Degradation of Protein Methyltransferase PRMT6 Exaggerates CSE-Induced Lung Epithelial Inflammation and Apoptosis

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