Maternal smoking-induced lung injuries in dams and offspring via inflammatory cytokines

Ji, Xiaotong; Yue, Huifeng; Li, Guangke; Sang, Nan

doi:10.1016/j.envint.2021.106618

Cited by 12 publications

(5 citation statements)

References 43 publications

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“…A [ 3 H]-nicotine binding assay demonstrated that nicotine binds to complex I and inhibits its NADH-ubiquinone reductase activity and results in inhibition of electrons flowing from NADH to complex I ( Cormier et al, 2001 ), which is linked to a detectable decrease in oxygen consumption by mitochondria ( Malińska et al, 2019 ). Even, maternal smoking has been identified as a risk factor for poor postnatal health, including increased OS and pro-inflammatory cytokines, mitochondrial dysfunction ( Chan et al, 2016 ; Lei et al, 2018 ; Ji et al, 2021 ), reduced antioxidative enzymes as well as glutathione content ( Lei et al, 2018 ) which may result in several cerebrovascular dysfunction and neurodegenerative diseases ( Sivandzade et al, 2019a ) in neonates.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have demonstrated that chronic exposure to several exogenous factors, including TS and nicotine, can hamper the activation of the NRF2-ARE signaling pathway and related downstream effectors leading to OS and inflammation ( Sivandzade et al, 2019b ). In fact, several studies have reported that in utero exposure to TS resulted in postnatal inflammation, OS and disrupted neuroimmune and mitochondrial functions ( Bruin et al, 2010 ; Primo et al, 2013 ; Banderali et al, 2015 ; Chahal et al, 2017 ; Cheemarla et al, 2019 ; Janbazacyabar et al, 2021 ; Ji et al, 2021 ; Huang et al, 2022 ). Interestingly, e-cig exposure has also been identified as a contributor to ROS generation, OS, and neuroinflammation ( Chatterjee et al, 2019 ; Ma et al, 2021 ; Sun et al, 2021 ; Emma et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

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Impact of in-utero electronic cigarette exposure on neonatal neuroinflammation, oxidative stress and mitochondrial function

Archie,

Sifat,

Mara

et al. 2023

Front. Pharmacol.

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Introduction: Despite the prevalence of the perception that electronic cigarettes (e-cig) are a safer alternative to tobacco smoke, growing concern about their potential toxic impact warrants adequate investigation focusing on special populations like maternal and pediatric groups. This study evaluated the consequences of maternal e-cig use on neonatal neuroinflammation, oxidative stress, and mitochondrial function in primary cultured neurons and postnatal day (PD) 7 and 90 brain.Methodology: Pregnant CD1 mice were exposed to e‐cig vapor (2.4% nicotine) from gestational day 5 (E5) till PD7, and the primary neurons were isolated from pups at E16/17. Cellular total reactive oxygen species (ROS) and mitochondrial superoxide were measured in primary neurons using CM-H2DCFDA and Mitosox red, respectively. Mitochondrial function was assessed by Seahorse XF Cell Mitostress analysis. The level of pro-inflammatory cytokines was measured in primary neurons and PD7 and PD90 brains by RT-PCR and immunobead assay. Western blot analysis evaluated the expression of antioxidative markers (SOD-2, HO-1, NRF2, NQO1) and that of the proinflammatory modulator NF-κB.Results: Significantly higher level of total cellular ROS (p < 0.05) and mitochondrial superoxide (p < 0.01) was observed in prenatally e-cig-exposed primary neurons. We also observed significantly reduced antioxidative marker expression and increased proinflammatory modulator and cytokines expression in primary neurons and PD7 (p < 0.05) but not in PD90 postnatal brain.Conclusion: Our findings suggest that prenatal e-cig exposure induces postnatal neuroinflammation by promoting oxidative stress (OS), increasing cytokines’ levels, and disrupting mitochondrial function. These damaging events can alter the fetal brain’s immune functions, making such offspring more vulnerable to brain insults.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Impact of in-utero electronic cigarette exposure on neonatal neuroinflammation, oxidative stress and mitochondrial function

Archie,

Sifat,

Mara

et al. 2023

Front. Pharmacol.

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“…When conducting the DEGs analysis, we firstly conversed the ID from the GEO database based on the platform information corresponding to the chip, and then the limma package was used for correction ( Ji et al, 2021 ). The data were grouped into two categories (normal vs tumor), and the DEGs were further identified with the standard of —Fold Change—>2, P <0.05.…”

Section: Methodsmentioning

confidence: 99%

MFAP2 enhances cisplatin resistance in gastric cancer cells by regulating autophagy

Meng

Zhang

2023

PeerJ

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Background Cisplatin (CDDP) is of importance in cancer treatment and widely used in advanced gastric cancer (GC). However, its clinical usage is limited due to its resistance, and the regulatory mechanism of CDDP resistance in GC has not yet been fully elucidated. In this study, we first conducted a comprehensive study to investigate the role of MFAP2 through bioinformatics analysis. Methods The Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases were applied to downloadgene expression data and clinicopathologic data, and the differentially expressed genes (DEGs) were further analyzed. Then, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis and survival analysis were conducted. Furthermore, according to the clinicopathological characteristics of TCGA, clinical correlation analysis was conducted, and a receiver operating characteristic curve (ROC) was plotted. Results We revealed that FAP, INHBA and MFAP2 were good diagnostic factors of GC. However, the mechanism of MFAP2 in GC remains elusive, especially in the aspect of chemotherapy resistance. We developed the CDDP-resistant cell line, and found that MFAP2 was upregulated in CDDP-resistant cells, and MFAP2-knockdown improved CDDP sensitivity. Finally, we found that MFAP2 enhanced CDDP resistance by inducing autophagy in drug-resistant cell lines. Conclusions The above results suggested that MFAP2 could affect the chemotherapy resistance by altering the level of autophagy in GC patients as a potential therapeutic target.

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“…Each dataset underwent quality control measures to minimize the false detection rate following the procedures outlined in the original study. The expression matrix was normalized using the normalizeBetweenArrays function from the limma package (version: 3.42.2) [ 55 ]. The normalized data were then subjected to analysis using the limma package to identify genes that showed differential expression between samples exposed to ZEN and those treated with the control vehicle, as well as between IBD samples and their corresponding control samples.…”

Section: Methodsmentioning

confidence: 99%

Zearalenone Exposure Disrupts STAT-ISG15 in Rat Colon: A Potential Linkage between Zearalenone and Inflammatory Bowel Disease

Ruan

Zhang

et al. 2023

Toxins

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Zearalenone (ZEN), a prevalent mycotoxin contaminating food and known for its intestinal toxicity, has been suggested as a potential risk factor for inflammatory bowel disease (IBD), although the exact relationship between ZEN exposure and IBD remains unclear. In this study, we established a rat model of colon toxicity induced by ZEN exposure to investigate the key targets of ZEN-induced colon toxicity and explore the underlying connection between ZEN exposure and IBD. Histological staining of the rat colon revealed significant pathological changes resulting from ZEN exposure (p < 0.01). Furthermore, the proteomic analysis demonstrated a notable upregulation of protein expression levels, specifically STAT2 (0.12 ± 0.0186), STAT6 (0.36 ± 0.0475) and ISG15 (0.43 ± 0.0226) in the rat colon (p < 0.05). Utilizing bioinformatics analysis, we combined ZEN exposure and IBD clinical sample databases to reveal that ZEN exposure may increase the risk of IBD through activation of the STAT-ISG15 pathway. This study identified novel targets for ZEN-induced intestinal toxicity, providing the basis for further study of ZEN exposure to IBD.

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Maternal smoking-induced lung injuries in dams and offspring via inflammatory cytokines

Cited by 12 publications

References 43 publications

Impact of in-utero electronic cigarette exposure on neonatal neuroinflammation, oxidative stress and mitochondrial function

Impact of in-utero electronic cigarette exposure on neonatal neuroinflammation, oxidative stress and mitochondrial function

MFAP2 enhances cisplatin resistance in gastric cancer cells by regulating autophagy

Zearalenone Exposure Disrupts STAT-ISG15 in Rat Colon: A Potential Linkage between Zearalenone and Inflammatory Bowel Disease

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