Effect of crotonaldehyde on the induction of HO-1 expression in A549 cells

Lee, Seung Eun; Park, Hye Rim; Yun, Hong Duck; Kim, Hyemi; Jin, Yongfeng; Park, Cheung-Seog; Ahn, Hyun-Jong; Cho, Jeong-Je; Park, Yong Seek

doi:10.1007/s13273-017-0024-7

Cited by 4 publications

(2 citation statements)

References 40 publications

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“…We used here human lung tissue-derived epithelial cell line and type II pneumocyte lung tumor all in one by Giard et al (1973) . In previous studies, A549 cell line has been used in in vitro cell systems and toxicology studies because of characteristic features of AT II cells including production of surfactant proteins, synthesis of phospholipids, cytoplasmic lamellar bodies, and apical microvilli ( Lee S. et al, 2017 ; Kim et al, 2018 ). However, they have important limitation to characterize other in vitro lung cell biology because of distinct difference including the architecture, barrier properties, lipid content and transition to ATI-like phenotype from those of primary AT II cells ( Lieber et al, 1976 ; Mason and Williams, 1980 ; Salmona et al, 1992 ; Godfrey, 1997 ).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of RAGE Attenuates Cigarette Smoke-Induced Lung Epithelial Cell Damage via RAGE-Mediated Nrf2/DAMP Signaling

Lee

Hong

et al. 2018

Front. Pharmacol.

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The oxidative stress and cellular apoptosis by environmental factor including cigarette smoke induces alveolar airway remodeling leading to chronic obstructive pulmonary disease (COPD). Recently, the receptor for advanced glycan end products (RAGE) which is highly expressed in alveolar epithelium is emerging as a biomarker for COPD susceptibility or progression. However, it still remains unknown how RAGE plays a role in cigarette smoke extract (CSE)-exposed human alveolar type II epithelial cell line. Therefore, we determined the efficacy of RAGE-specific antagonist FPS-ZM1 in response to CSE-induced lung epithelial cells. CSE induced the elevated generation of RONS and release of pro-inflammatory cytokines, and impaired the cellular antioxidant defense system. Further, CSE induced the alteration of RAGE distribution via the activation of redox-sensitive DAMP (Damage-associated molecular patterns) signaling through Nrf2 in cells. Although pre-treatment with SB202190 (p38 inhibitor) or SP600125 (JNK inhibitor) failed to recover the alteration of RAGE distribution, treatment of FPS-ZM1 significantly exhibited anti-inflammatory and anti-oxidative/nitrosative effects, also inhibited the activation of redox-sensitive DAMP signaling through Nrf2 (nuclear factor erythroid 2-related factor 2) migration in the presence of CSE. Taken together, our data demonstrate that RAGE and Nrf2 play a pivotal role in maintenance of alveolar epithelial integrity.

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Section: Discussionmentioning

confidence: 99%

Inhibition of RAGE Attenuates Cigarette Smoke-Induced Lung Epithelial Cell Damage via RAGE-Mediated Nrf2/DAMP Signaling

Lee

Hong

et al. 2018

Front. Pharmacol.

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“…The epithelial cells were fixed in 4% paraformaldehyde for 20 min. After fixation, the cells were stained with H&E solution [ 35 ]. The outgrowth of H&E-stained cells was scanned by microscope (Olympus, Tokyo, Japan) and measured using ImageJ freeware at 12 d and 24 d, respectively.…”

Section: Methodsmentioning

confidence: 99%

Ferulic Acid Induces Keratin 6α via Inhibition of Nuclear β-Catenin Accumulation and Activation of Nrf2 in Wound-Induced Inflammation

et al. 2021

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Injured tissue triggers complex interactions through biological process associated with keratins. Rapid recovery is most important for protection against secondary infection and inflammatory pain. For rapid wound healing with minimal pain and side effects, shilajit has been used as an ayurvedic medicine. However, the mechanisms of rapid wound closure are unknown. Here, we found that shilajit induced wound closure in an acute wound model and induced migration in skin explant cultures through evaluation of transcriptomics via microarray testing. In addition, ferulic acid (FA), as a bioactive compound, induced migration via modulation of keratin 6α (K6α) and inhibition of β-catenin in primary keratinocytes of skin explant culture and injured full-thickness skin, because accumulation of β-catenin into the nucleus acts as a negative regulator and disturbs migration in human epidermal keratinocytes. Furthermore, FA alleviated wound-induced inflammation via activation of nuclear factor erythroid-2-related factor 2 (Nrf2) at the wound edge. These findings show that FA is a novel therapeutic agent for wound healing that acts via inhibition of β-catenin in keratinocytes and by activation of Nrf2 in wound-induced inflammation.

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MicroRNA Expression Analysis of Human Pulmonary Fibroblasts Treated with Acrolein

et al. 2018

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Effect of crotonaldehyde on the induction of HO-1 expression in A549 cells

Cited by 4 publications

References 40 publications

Inhibition of RAGE Attenuates Cigarette Smoke-Induced Lung Epithelial Cell Damage via RAGE-Mediated Nrf2/DAMP Signaling

Inhibition of RAGE Attenuates Cigarette Smoke-Induced Lung Epithelial Cell Damage via RAGE-Mediated Nrf2/DAMP Signaling

Ferulic Acid Induces Keratin 6α via Inhibition of Nuclear β-Catenin Accumulation and Activation of Nrf2 in Wound-Induced Inflammation

MicroRNA Expression Analysis of Human Pulmonary Fibroblasts Treated with Acrolein

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