Protein carbonylation in human endothelial cells exposed to cigarette smoke extract

Gornati, Rosalba; Colombo, Graziano; Clerici, Marigrazia; Rossi, Federica; Gagliano, Nicoletta; Riva, Consuelo; Colombo, Roberto; Dalle‐Donne, Isabella; Bernardini, Giovanni; Milzani, Aldo

doi:10.1016/j.toxlet.2013.01.023

Cited by 27 publications

(32 citation statements)

References 46 publications

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“…On the other hand, a marked effect was reached with CSC at 4 mg/ml with a maximal relative increase in ROS generation of 113%. Similar to our results, CSE solubilized in PBS and CSC in DMSO were found to induce oxidative stress by generating ROS in cells (Asano et al, 2012;Gornati et al, 2013;Vaid and Katiyar, 2014;Wu et al, 2014). In addition, Gornati et al (2013) noted that 48 and 72 h of exposure to CSE and CSC increased intracellular ROS generation.…”

Section: Ros Generation Induced By Cse and Cscsupporting

confidence: 90%

Oxidative Stress Induced by Cigarette Smoke Extracts in Human Brain Cells (T98G) and Human Brain Microvascular Endothelial Cells (HBMEC) in Mono- and Co-Culture

Kim

Cho

Choi

et al. 2015

Journal of Toxicology and Environmental Health, Part A

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The objective of the current study was to examine oxidative stress induced by cigarette smoke extract (CSE) or cigarette smoke condensate (CSC) in human brain cells (T98G) and human brain microvascular endothelial cells (HBMEC) in mono- and co-culture systems. Cell viability of T98G cells exposed to CSC (0.05-4 mg/ml) was significantly decreased compared to CSE (0.025-20%). There were no marked differences between quantities of reactive oxygen species (ROS) generation by either CSE (2, 4, and 10%) or CSC (0.2, 0.4, and 0.8 mg/ml) treatment compared to control. However, a significant effect was noted in ROS generation following CSC incubation at 4mg/ml. Cellular integrity of HBMEC decreased to 74 and 64% within 120 h of exposure at the IC50 value of CSE and CSC, respectively. This study suggests that chronic exposure to cigarette smoking might initiate damage to the blood-brain barrier.

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Section: Ros Generation Induced By Cse and Cscsupporting

confidence: 90%

Oxidative Stress Induced by Cigarette Smoke Extracts in Human Brain Cells (T98G) and Human Brain Microvascular Endothelial Cells (HBMEC) in Mono- and Co-Culture

Kim

Cho

Choi

et al. 2015

Journal of Toxicology and Environmental Health, Part A

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“…Reactive carbonyl species can be derived from exposure to CSE and the oxidation of lipids (acrolein, 4-hydroxynonenal, malondialdehyde) and sugars (glyoxal, methylglyoxal) (Suzuki et al, 2010). Although it was not determined in this study, an increase in actin carbonylation by CSE was reported in our previous work (Lin et al, 2009) and in a recent report by Gornati et al (2013). In the present study, CSE-induced actin disorganization and cellular shrinkage were effectively prevented by various antioxidants, including N-acetyl cysteine, glutathione, lipoic acid, vitamin C, vitamin E, and aminoguanidine ( Figs.…”

Section: Discussionmentioning

confidence: 47%

IP3 and calcium signaling involved in the reorganization of the actin cytoskeleton and cell rounding induced by cigarette smoke extract in human endothelial cells

Lin

Tsai

Lii

et al. 2015

Environmental Toxicology

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Smoking increases the risk of cardiovascular disorders and leads to damage caused by inflammation and oxidative stress. The actin cytoskeleton is a key player in the response to inflammatory stimuli and is an early target of cellular oxidative stress. The purpose of this study was to investigate the changes in actin cytoskeleton dynamics in human endothelial EA.hy926 cells exposed to cigarette smoke extract (CSE). Immunostaining revealed that CSE exposure resulted in modification of the actin cytoskeleton and led to cell rounding in a dose- and time-dependent manner. In addition, the intracellular calcium concentration was increased by treatment with CSE. Pretreatment with antioxidants (lipoic acid, glutathione, N-acetyl cysteine, aminoguanidine, α-tocopherol, and vitamin C) significantly attenuated the CSE-induced actin cytoskeleton reorganization and cell rounding. Calcium ion chelators (EGTA, BAPTA-AM AM) and a potent store-operated calcium channel inhibitor (MRS 1845) also reduced CSE-induced intracellular calcium changes and attenuated actin cytoskeleton reorganization and cell morphology change. Moreover, the CSE-induced intracellular calcium increase was suppressed by pretreatment with the inositol trisphosphate receptor (IP3R) inhibitor xestospongin C, the phospholipase C (PLC) inhibitor U-73122, and the protein kinase C (PKC) inhibitor GF109203X. These results suggest that reactive oxygen species production and intracellular calcium increase play an essential role in CSE-induced actin disorganization and cell rounding through a PLC-IP3-PKC signaling pathway. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1293-1306, 2016.

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“…Oxidative stress including cigarette smoke is known to induce protein carbonylation, which are distributed throughout the cell including the ER[31]. These damaged proteins can be sensed, resulting in the UPR, which is an early and downstream cytoprotective response elicited by the ER.…”

Section: Resultsmentioning

confidence: 99%

Oxidative stress induces mitochondrial dysfunction and a protective unfolded protein response in RPE cells

Cano

Wang

Wan

et al. 2014

Free Radical Biology and Medicine

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How cells degenerate from oxidative stress in aging-related disease is incompletely understood. The study’s intent was to identify key cytoprotective pathways activated by oxidative stress, and determine the extent of their protection. Using an unbiased strategy with microarray analysis, retinal pigmented epithelial (RPE) cells treated with cigarette smoke extract (CSE) had over-represented genes involved in the antioxidant and unfolded protein response (UPR). Differentially expressed antioxidant genes were predominantly located in the cytoplasm, with no induction of genes that neutralize superoxide and H2O2 in the mitochondria, resulting in accumulation of superoxide and decreased ATP production. Simultaneously, CSE induced the UPR sensors IRE1α, p-PERK, and ATP6, including CHOP, which was cytoprotective because CHOP knockdown decreased cell viability. In mice given intravitreal CSE, the RPE had increased IRE1α and decreased ATP, and developed epithelial-mesenchymal transition, as suggested by decreased LRAT abundance, altered ZO1 immunolabeling, and dysmorphic cell shape. Mildly degenerated RPE from early AMD samples had prominent IRE1α, but minimal mitochondrial TOM20 immunolabeling. While oxidative stress is thought to induce an antioxidant response with cooperation between the mitochondria and ER, herein, we show that mitochondria become impaired sufficiently to induce epithelial-mesenchymal transition despite a protective UPR. With similar responses in early AMD samples, these results suggest that mitochondria are vulnerable to oxidative stress despite a protective UPR during early phases of aging-related disease.

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Protein carbonylation in human endothelial cells exposed to cigarette smoke extract

Cited by 27 publications

References 46 publications

Oxidative Stress Induced by Cigarette Smoke Extracts in Human Brain Cells (T98G) and Human Brain Microvascular Endothelial Cells (HBMEC) in Mono- and Co-Culture

Oxidative Stress Induced by Cigarette Smoke Extracts in Human Brain Cells (T98G) and Human Brain Microvascular Endothelial Cells (HBMEC) in Mono- and Co-Culture

IP3 and calcium signaling involved in the reorganization of the actin cytoskeleton and cell rounding induced by cigarette smoke extract in human endothelial cells

Oxidative stress induces mitochondrial dysfunction and a protective unfolded protein response in RPE cells

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