A role for Bach1 and HO-2 in suppression of basal and UVA-induced HO-1 expression in human keratinocytes

Zhong, Julia Li; Raval, Chintan M; Edwards, Gavin P.; Tyrrell, Rex M.

doi:10.1016/j.freeradbiomed.2009.10.037

Cited by 32 publications

(59 citation statements)

References 57 publications

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“…The upregulation of HO-1 by ultraviolet A (UVA; 320-380 nm) irradiation of human skin cells protects the cells against oxidative stress. In addition, UVA irradiation of cultured human skin fibroblasts enhances the accumulation of Bach1 mRNA and proteins, which may function as a compensatory mechanism for controlling HO-1 overexpression (Zhong et al 2010). While HO-1 is induced during keratinocyte differentiation, the HO-1 induction does not involve any changes in the expression of Bach1, suggesting that HO-1 induction upon keratinocyte differentiation is independent of the actions of Bach1 (Okada et al 2010).…”

Section: Bach1 As a Potential Therapeutic Target In Oxidative Stressrmentioning

confidence: 99%

Wearing Red for Signaling: The Heme-Bach Axis in Heme Metabolism, Oxidative Stress Response and Iron Immunology

Igarashi

Watanabe-Matsui

2014

Tohoku J. Exp. Med.

100

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The connection between gene regulation and metabolism is an old issue that warrants revisiting in order to understand both normal as well as pathogenic processes in higher eukaryotes. Metabolites affect the gene expression by either binding to transcription factors or serving as donors for post-translational modification, such as that involving acetylation and methylation. The focus of this review is heme, a prosthetic group of proteins that includes hemoglobin and cytochromes. Heme has been shown to bind to several transcription factors, including Bach1 and Bach2, in higher eukaryotes. Heme inhibits the transcriptional repressor activity of Bach1, resulting in the derepression of its target genes, such as globin in erythroid cells and heme oxygenase-1 in diverse cell types. Since Bach2 is important for class switch recombination and somatic hypermutation of immunoglobulin genes as well as regulatory and effector T cell differentiation and the macrophage function, the heme-Bach2 axis may regulate the immune response as a signaling cascade. We discuss future issues regarding the topic of the iron/heme-gene regulation network based on current understanding of the heme-Bach axis, including the concept of "iron immunology" as the synthesis of the iron metabolism and the immune response.

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Section: Bach1 As a Potential Therapeutic Target In Oxidative Stressrmentioning

confidence: 99%

Wearing Red for Signaling: The Heme-Bach Axis in Heme Metabolism, Oxidative Stress Response and Iron Immunology

Igarashi

Watanabe-Matsui

2014

Tohoku J. Exp. Med.

100

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“…Human immortalized skin keratinocytes (HaCaT cells) (14) were maintained in Dulbecco's Modified Eagle's Medium (DMEM) supplemented with 10% heat-inactivated fetal calf serum (FCS). Antibodies against Nrf2 (H300, sc-13032), and β-actin (sc-9104) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA).…”

Section: Cell Culture and Antibodiesmentioning

confidence: 99%

“…Anti-vinculin was purchased from Upstate Biotechnology (Waltham, MA, USA). Antimouse and anti-rabbit IgG secondary antibodies were from Sigma-Aldrich China (Shanghai, China) (10,14). A lactate dehydrogenase (LDH) cytotoxicity assay kit was obtained from Roche Diagnostics (Mannheim, Germany).…”

Section: Cell Culture and Antibodiesmentioning

confidence: 99%

“…Prior to UVA irradiation, the growth medium was removed from the cells and retained; each dish was washed twice with phosphate-buffered saline (PBS) and cells were irradiated in PBS. In order to maintain a consistent temperature of 25°C, irradiation of cells with UVA was performed in an air-conditioned room as previously described (10,14). Non-irradiated cells were covered with foil to prevent exposure and used as a background control (sham = 0 kJ•m…”

Section: Irradiation Of Cells With Uvamentioning

confidence: 99%

“…Nrf2 knockout mice have a prolonged inflammatory response after skin injury (8). Previously, a significant increase in Nrf2 was not detected in human HaCaT skin keratinocytes following a low to moderate dose (50-250 kJ•m −2 ) of UVA irradiation (14,15). However, down-regulation of Nrf2 expression may suppress cellular functions, such as antioxidant response, so cells may be more susceptible to oxidative damage, including UVA irradiation (5,7,8).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Nrf2-mediated protection against UVA radiation in human skin keratinocytes

Tian

Zhang

Lai

et al. 2011

BST

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m6A‐activated BACH1 exacerbates ferroptosis by epigenetic suppression HSPB1 in severe acute pancreatitis

Zhou,

Li,

Liu

et al. 2024

Drug Development Research

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Severe acute pancreatitis (SAP) is characterized by acute inflammation of the pancreas. The transcription factor BTB and CNC homology 1 (BACH1) has been implicated in various biological processes, including oxidative stress, apoptosis, and cell cycle regulation. However, its involvement in the pathogenesis of SAP remains relatively understudied. In the present work, our data demonstrated that BACH1 level was significantly increased in SAP patients, cellular, and animal models, while heat shock protein B1 (HSPB1) expression was weakened. Mechanistic assays validated that BACH1 acted as a transcriptional inhibitor of HSPB1. Moreover, HPDE6‐C7 cells were stimulated with cerulein (Cer) and LPS to mimic the pathological stages of SAP in vitro. Depletion of BACH1 remarkably improved cell survival and alleviated the oxidative stress, ferroptosis, and inflammatory responses in SAP cell models. However, these changes were dramatically reversed upon co‐inhibition of HSPB1. Animal findings confirmed that loss of BACH1 decreased pancreatic injury, inflammatory responses, and ferroptosis, but these effects were weakened by HSPB1 silence. Overall, these findings elucidate that the overexpression of BACH1 favors the ferroptosis and inflammation by transcriptionally inhibiting HSBP1, thereby exacerbating SAP progression.

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A role for Bach1 and HO-2 in suppression of basal and UVA-induced HO-1 expression in human keratinocytes

Cited by 32 publications

References 57 publications

Wearing Red for Signaling: The Heme-Bach Axis in Heme Metabolism, Oxidative Stress Response and Iron Immunology

Wearing Red for Signaling: The Heme-Bach Axis in Heme Metabolism, Oxidative Stress Response and Iron Immunology

Nrf2-mediated protection against UVA radiation in human skin keratinocytes

m6A‐activated BACH1 exacerbates ferroptosis by epigenetic suppression HSPB1 in severe acute pancreatitis

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