Protein carbonylation in human bronchial epithelial cells exposed to cigarette smoke extract

Colombo, Graziano; Garavaglia, Maria Lisa; Astori, Emanuela; Giustarini, Daniela; Rossi, Ranieri; Milzani, Aldo; Dalle‐Donne, Isabella

doi:10.1007/s10565-019-09460-0

Cited by 30 publications

(18 citation statements)

References 76 publications

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“…The 2 -ΔΔCt method was applied to calculate the expression of each gene relative to the expression of β-actin. The primer sequences used for PCR were: Mfn1 forward: 5'-CTGGAGC ACGTTCCTTCCTC-3', reverse: 5'-ACAGTGCGAAC TGCCTCTTG-3'; Mfn2 forward: 5'-AGG CGAAACCAGGAGAGAC-3', reverse: 5'-CCTCCCCGATCAG AGTGAA-3'; Opa1 forward: 5'-TTATAGAGCGATACAAGGGG GAG-3', reverse: 5'-CGCCGTCTGATTATCTTGATGAG-3'; β-actin forward: 5'-GGGAAATCGTG CG TGACATTAAGG-3', reverse: 5'-CAGGAAGGAAGGCTGGA AGAGTG-3' (Avalle et al, 2019;Cao et al, 2019;Colombo et al, 2019).…”

Section: Qrt-pcr Analysismentioning

confidence: 99%

RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion

et al. 2021

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Matrine, an active component of Sophora flavescens Ait root extracts, has been used in China for years to treat cancer and viral hepatitis. In the present study, we explored the effects of matrine on hyperglycemia-treated cardiomyocytes. Cardiomyocyte function, oxidative stress, cellular viability, and mitochondrial fusion were assessed through immunofluorescence, quantitative real-time PCR (qRT-PCR), enzyme-linked immunosorbent assays, and RNA interference. Matrine treatment suppressed hyperglycemia-induced oxidative stress in cardiomyocytes by upregulating transcription of nuclear factor erythroid 2-like 2 and heme oxygenase-1. Matrine also improved cardiomyocyte contractile and relaxation function during hyperglycemia, and it reduced hyperglycemia-induced cardiomyocyte death by inhibiting mitochondrial apoptosis. Matrine treatment increased the transcription of mitochondrial fusion-related genes and thus attenuated the proportion of fragmented mitochondria in cardiomyocytes. Inhibiting mitochondrial fusion by knocking down mitofusin 2 (Mfn2) abolished the cardioprotective effects of matrine during hyperglycemia. These results demonstrate that matrine could be an effective drug to alleviate hyperglycemia-induced cardiomyocyte damage by activating Mfn2-induced mitochondrial fusion.

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Section: Qrt-pcr Analysismentioning

confidence: 99%

RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion

et al. 2021

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“…There is growing evidence to support a link between smoking-induced oxidative stress and protein carbonylation [114,116,117]. Colombo et al [118] have shown that treatment of human bronchial epithelial cells with increasing concentrations of cigarette-smoke concentrate induces oxidative stress and increases protein carbonylation in a concentration-dependent manner. Also, Sumanasekera et al [61] have reported that cardiac stem cells treated with cigarette-smoke concentrate exhibit increased oxidative modification of proteins via carbonylation.…”

Section: Oxidative Damage To Proteins: Connection With Smoking and Cancermentioning

confidence: 99%

Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer

Caliri

Tommasi

Besaratinia

2021

Mutation Research/Reviews in Mutation Research

313

139

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Smoking is a major risk factor for a variety of diseases, including cancer and immune-mediated inflammatory diseases. Tobacco smoke contains a mixture of chemicals, including a host of reactive oxygen-and nitrogen species (ROS and RNS), among others, that can damage cellular and sub-cellular targets, such as lipids, proteins, and nucleic acids. A growing body of evidence supports a key role for smoking-induced ROS and the resulting oxidative stress in inflammation and carcinogenesis. This comprehensive and up-to-date review covers four interrelated topics, including 'smoking', 'oxidative stress', 'inflammation', and 'cancer'. The review discusses each of the four topics, while exploring the intersections among the topics by highlighting the macromolecular damage attributable to ROS. Specifically, oxidative damage to macromolecular targets, such as lipid peroxidation, post-translational modification of proteins, and DNA adduction, as well as enzymatic and non-enzymatic antioxidant defense mechanisms, and the multi-faceted repair pathways of oxidized lesions are described. Also discussed are the biological consequences of oxidative damage to macromolecules if they evade the defense mechanisms and/or are not repaired properly or in time. Emphasis is placed on the genetic-and epigenetic alterations that may lead to transcriptional deregulation of functionally-important genes and disruption of regulatory elements. Smoking-associated oxidative stress also activates the inflammatory response pathway, which triggers a cascade of events of which ROS production is an initial yet indispensable step. The release of ROS at the site of damage and inflammation helps combat foreign pathogens and restores the injured tissue, while simultaneously increasing the burden of oxidative stress. This creates a vicious cycle in which smoking-related oxidative stress causes inflammation, which in turn, results in further generation of ROS, and potentially increased oxidative damage to macromolecular targets that may lead to cancer initiation and/or progression.

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“…ROS generation caused by ADR administration would disturb the normal redox balance and produce huge oxidative stress, which subsequently stimulates the carbonylation of specific groups of proteins involved in physiological dysfunction and induces cardiomyocyte apoptosis [ 14 – 16 ]. The most largely studied oxidative stress–caused by a modification of proteins is the formation of carbonyl groups which can react with 2,4-dinitrophenylhydrazine (DNP) and are discovered by redox proteomics [ 17 , 18 ]. The appearance of carbonylated proteins has been considered as a hallmark of ROS-induced change of protein which might be helpful to predict novel targets for the diagnosis and prognosis of diseases.…”

Section: Introductionmentioning

confidence: 99%

Functional Redox Proteomics Reveal That Salvia miltiorrhiza Aqueous Extract Alleviates Adriamycin-Induced Cardiomyopathy via Inhibiting ROS-Dependent Apoptosis

Hung

Wang

Lin

et al. 2020

Oxidative Medicine and Cellular Longevity

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The anticancer agent adriamycin (ADR) has long been recognized to induce a dose-limiting cardiotoxicity, while Salvia miltiorrhiza (SM) is a Chinese herb widely used for the treatment of cardiovascular disorders and its aqueous extract (SMAE) has shown anticancer as well as antioxidant effects. In the current study, we aimed at investigating the synergistic effect and potent molecular mechanisms of SMAE with a focus on the cardioprotective benefit observed under ADR adoption. Histopathological analysis indicated that SMAE could substantially alleviate cardiomyopathy and cell apoptosis caused by ADR. Meanwhile, the two-dimensional electrophoresis (2-DE) oxyblots demonstrated that SMAE treatment could effectively reduce carbonylation of specific proteins associated with oxidative stress response and various metabolic pathways in the presence of ADR. SMAE application also showed protective efficacy against ADR-mediated H9c2 cell death in a dose-dependent manner without causing any cytotoxicity and significantly attenuated the reactive oxygen species production. Particularly, the simultaneous administration of ADR and SMAE could remarkably suppress the growth of breast cancer cells. We also noticed that there was a marked upregulation of detoxifying enzyme system in the presence of SMAE, and its exposure also contributed to an increase in Nrf2 and HO-1 content as well. SMAE also amended the ERK/p53/Bcl-xL/caspase-3 signaling pathways and the mitochondrial dysfunction, which eventually attribute to apoptotic cathepsin B/AIF cascades. Correspondingly, both the ERK1/2 inhibitor (U0126) and pan-caspase inhibitor (Z-VAD-FMK) could at least partially abolish the ADR-associated cytotoxicity in H9c2 cells. Collectively, these results support that ROS apoptosis-inducing molecule release is closely involved in ADR-induced cardiotoxicity while SMAE could prevent or mitigate the causative cardiomyopathy through controlling multiple targets without compromising the efficacy of chemotherapy.

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Protein carbonylation in human bronchial epithelial cells exposed to cigarette smoke extract

Abstract: Affiliations are correct.2. Please check if the captured "Abbreviations" are correct.

Cited by 30 publications

References 76 publications

RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion

RETRACTED: Matrine Protects Cardiomyocytes Against Hyperglycemic Stress by Promoting Mitofusin 2-Induced Mitochondrial Fusion

Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer

Functional Redox Proteomics Reveal That Salvia miltiorrhiza Aqueous Extract Alleviates Adriamycin-Induced Cardiomyopathy via Inhibiting ROS-Dependent Apoptosis

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