Differential effects of arsenic species on Nrf2 and Bach1 nuclear localization in cultured hepatocytes

Liú, Dan; Xu, Guangyu; Bai, Caijun; Gu, Yuqin; Da, Wang; Li, Bing

doi:10.1016/j.taap.2021.115404

Cited by 7 publications

(4 citation statements)

References 49 publications

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“…Therefore, Bach1 could be a promising target for enhancing periodontal tissue regeneration under periodontitis conditions. It has also been reported that drugs and biomaterials such as hyperoside, gold nanoparticles and sodium arsenite could elicit Bach1 nuclear export and increase the expression of antioxidative enzymes 37–39 . At the genetic level, it has been reported that the elevated expression of ST8SIA1, a periodontitis risk gene, caused by weakening of Bach1's binding to effect T allele of its coinherited variants is a genetic cause of periodontitis 40 .…”

Section: Discussionmentioning

confidence: 99%

“…It has also been reported that drugs and biomaterials such as hyperoside, gold nanoparticles and sodium arsenite could elicit Bach1 nuclear export and increase the expression of antioxidative enzymes. [37][38][39] At the genetic level, it has been reported that the elevated expression of F I G U R E 6 Graphical summary. The increased Bach1 expression in PDLCs under inflammatory conditions directly inhibits antioxidant factors such as HO-1 and GCLM.…”

Section: Discussionmentioning

confidence: 99%

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Knockdown of Bach1 protects periodontal bone regeneration from inflammatory damage

Yuan,

Li,

Zou

et al. 2023

J Cellular Molecular Medi

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Periodontal bone regeneration is a major challenge in the treatment of periodontitis. However, the regenerative vitality of periodontal ligament cells (PDLCs) declines in the environment of periodontitis and accompanying oxidative stress. This study aimed to investigate the functional mechanisms of Bach1, a transcriptional suppressor involved in oxidative stress response, and its regulation of PDLC osteogenesis under inflammatory conditions. We observed a significant elevation in Bach1 expression in periodontal tissues with periodontitis and PDLCs under inflammatory conditions. Knockdown of Bach1 alleviated the inflammation‐induced oxidative stress level and partly offset the inhibitory effect of inflammatory conditions on osteogenesis, as well as the expression of osteogenic genes BMP6, OPG and RUNX2. Similarly, knockdown of Bach1 protects PDLCs from inflammatory damage to periodontal bone regeneration in vivo. Furthermore, we found that Bach1 could bind to the histone methyltransferase EZH2, and the binding increased under inflammatory conditions. Bach1 enhanced the ability of EZH2 to catalyse H3K27me3 on the promoter region of RUNX2 and BMP6, thus repressing the expression of osteoblastic genes. In conclusion, our study revealed that knockdown of Bach1 effectively rescued the osteogenesis and oxidative stress of PDLCs with inflammation. Bach1 could be a promising target for enhancing periodontal tissue regeneration under periodontitis conditions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Knockdown of Bach1 protects periodontal bone regeneration from inflammatory damage

Yuan,

Li,

Zou

et al. 2023

J Cellular Molecular Medi

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“…Arsenic accumulates in organs, particularly in the liver where it may cause liver injury and increase the risk of liver cancer ( Palma-Lara et al, 2020 ). Transcription repressor BACH1 nuclear export increased and the expression of the downstream target genes HO-1, NADPH, and NQO1 increased in inorganic arsenic-induced liver injury samples, whereas BACH1 expression levels showed no change after organic arsenic treatment ( Liu D. et al, 2013 ; Liu D. et al, 2021 ). Despite these findings, the functions of BACH1 in arsenic-induced liver injury warrants further study.…”

Section: Bach Proteins and Benign Diseases Of The Digestive Systemmentioning

confidence: 98%

Pathophysiological role of BACH transcription factors in digestive system diseases

et al. 2023

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BTB and CNC homologous (BACH) proteins, including BACH1 and BACH2, are transcription factors that are widely expressed in human tissues. BACH proteins form heterodimers with small musculoaponeurotic fibrosarcoma (MAF) proteins to suppress the transcription of target genes. Furthermore, BACH1 promotes the transcription of target genes. BACH proteins regulate physiological processes, such as the differentiation of B cells and T cells, mitochondrial function, and heme homeostasis as well as pathogenesis related to inflammation, oxidative-stress damage caused by drugs, toxicants, or infections; autoimmunity disorders; and cancer angiogenesis, epithelial-mesenchymal transition, chemotherapy resistance, progression, and metabolism. In this review, we discuss the function of BACH proteins in the digestive system, including the liver, gallbladder, esophagus, stomach, small and large intestines, and pancreas. BACH proteins directly target genes or indirectly regulate downstream molecules to promote or inhibit biological phenomena such as inflammation, tumor angiogenesis, and epithelial-mesenchymal transition. BACH proteins are also regulated by proteins, miRNAs, LncRNAs, labile iron, and positive and negative feedback. Additionally, we summarize a list of regulators targeting these proteins. Our review provides a reference for future studies on targeted drugs in digestive diseases.

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“…A number of studies have reported HO-1 induction by arsenic exposure [ 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 ]. The liver is the most extensively studied organ in this regard.…”

Section: Introductionmentioning

confidence: 99%

Differential Effects of Arsenic in Drinking Water on Mouse Hepatic and Intestinal Heme Oxygenase-1 Expression

Fan

et al. 2022

Antioxidants

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Arsenic exposure has been associated with the risks of various diseases, including cancers and metabolic diseases. The aim of this study was to examine the effects of arsenic exposure via drinking water on the expression of heme oxygenase-1 (HO-1), a major responsive gene to arsenic-induced oxidative stress, in mouse intestinal epithelial cells which is the first site of exposure for ingested arsenic, and the liver, a known target of arsenic toxicity. The expression of HO-1 was determined at mRNA, protein, or enzymic activity levels in mice exposed to sodium arsenite through drinking water, at various doses (0, 2.5, 10, 25, 100 ppm), and for various time periods (1, 3, 7, or 28 days). HO-1 was significantly induced in the intestine, but not liver, at arsenic doses of 25 ppm or lower. The intestinal HO-1 induction was seen in both males and females, plateaued within 1–3 days of exposure, and was accompanied by increases in microsomal HO activity. In mice exposed to 25-ppm of arsenite for 7 days, total arsenic and As(III) levels in intestinal epithelial cells were significantly higher than in the liver. These findings identify intestinal epithelial cells as likely preferential targets for arsenic toxicity and support further studies on the functional consequences of intestinal HO-1 induction.

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Differential effects of arsenic species on Nrf2 and Bach1 nuclear localization in cultured hepatocytes

Cited by 7 publications

References 49 publications

Knockdown of Bach1 protects periodontal bone regeneration from inflammatory damage

Knockdown of Bach1 protects periodontal bone regeneration from inflammatory damage

Pathophysiological role of BACH transcription factors in digestive system diseases

Differential Effects of Arsenic in Drinking Water on Mouse Hepatic and Intestinal Heme Oxygenase-1 Expression

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