Nrf1 and Nrf2 Regulate Rat Glutamate-Cysteine Ligase Catalytic Subunit Transcription Indirectly via NF-κB and AP-1

Heping Yang; Nathaniel Magilnick; Candy Lee; Denise Kalmaz; Xiaopeng Ou; Jefferson Y. Chan; Shelly C. Lu

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Nrf1 and Nrf2 Regulate Rat Glutamate-Cysteine Ligase Catalytic Subunit Transcription Indirectly via NF-κB and AP-1

机译：Nrf1和Nrf2通过NF-κB和AP-1间接调节大鼠谷氨酸半胱氨酸连接酶催化亚基的转录

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Glutamate-cysteine ligase catalytic subunit (GCLC) is regulated transcriptionally by Nrf1 and Nrf2. tert-Butylhydroquinone (TBH) induces human GCLC via Nrf2-mediated trans activation of the antioxidant-responsive element (ARE). Interestingly, TBH also induces rat GCLC, but the rat GCLC promoter lacks ARE. This study examined the role of Nrf1 and Nrf2 in the transcriptional regulation of rat GCLC. The baseline and TBH-mediated increase in GCLC mRNA levels and rat GCLC promoter activity were lower in Nrf1 and Nrf2 null (F1 and F2) fibroblasts than in wild-type cells. The basal protein and mRNA levels and nuclear binding activities of c-Jun, c-Fos, p50, and p65 were lower in F1 and F2 cells and exhibited a blunted response to TBH. Lower c-Jun and p65 expression also occurs in Nrf2 null livers. Levels of other AP-1 and NF-κB family members were either unaffected (i.e., JunB) or increased (i.e., Fra-1). Overexpression of Nrf1 and Nrf2 in respective cells restored the rat GCLC promoter activity and response to TBH but not if the AP-1 and NF-κB binding sites were mutated. Fra-1 overexpression lowered endogenous GCLC expression and rat GCLC promoter activity, while Fra-1 antisense had the opposite effects. In conclusion, Nrf1 and Nrf2 regulate rat GCLC promoter by modulating the expression of key AP-1 and NF-κB family members.

机译：谷氨酸-半胱氨酸连接酶催化亚基（GCLC）由Nrf1和Nrf2转录调控。叔-丁基氢醌（TBH）通过Nrf2介导的抗氧化剂响应元件（ARE）的 trans 激活诱导人GCLC。有趣的是，TBH也诱导大鼠GCLC，但大鼠GCLC启动子缺乏ARE。这项研究检查了Nrf1和Nrf2在大鼠GCLC转录调控中的作用。 Nrf1和Nrf2无效（F1和F2）成纤维细胞中，基线和TBH介导的GCLC mRNA水平增加和大鼠GCLC启动子活性低于野生型细胞。 F1和F2细胞中c-Jun，c-Fos，p50和p65的基础蛋白和mRNA水平以及核结合活性较低，并且对TBH的反应迟钝。较低的c-Jun和p65表达也发生在Nrf2无效的肝脏中。其他AP-1和NF-κB家族成员的水平未受影响（即JunB）或升高（即Fra-1）。 Nrf1和Nrf2在各自细胞中的过表达恢复了大鼠GCLC启动子的活性和对TBH的反应，但如果AP-1和NF-κB结合位点发生突变则无法恢复。 Fra-1过表达降低了内源性GCLC表达和大鼠GCLC启动子活性，而Fra-1反义具有相反的作用。总之，Nrf1和Nrf2通过调节关键AP-1和NF-κB家族成员的表达来调节大鼠GCLC启动子。 展开▼

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《Molecular and Cellular Biology》 |2005年第14期|共14页

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Heping Yang; Nathaniel Magilnick; Candy Lee; Denise Kalmaz; Xiaopeng Ou; Jefferson Y. Chan; Shelly C. Lu;
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中图分类细胞生物学;

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1. Nrf1 and Nrf2 Regulate Rat Glutamate-Cysteine Ligase Catalytic Subunit Transcription Indirectly via NF-κB and AP-1 [J] . Heping Yang, Nathaniel Magilnick, Candy Lee, Molecular and Cellular Biology . 2005,第14期

机译：Nrf1和Nrf2通过NF-κB和AP-1间接调节大鼠谷氨酸半胱氨酸连接酶催化亚基的转录

2. Hydrogen sulfide upregulates glutamate-cysteine ligase catalytic subunit, glutamate-cysteine ligase modifier subunit, and glutathione and inhibits interleukin-1β secretion in monocytes exposed to high glucose levels [J] . JainS.K., HuningL., MicinskiD. Metabolic syndrome and related disorders . 2014,第5期

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3. Distinct Nrf1/2-independent mechanisms mediate As 3+-induced glutamate-cysteine ligase subunit gene expression in murine hepatocytes. [J] . Thompson JA, White CC, Cox DP, Free Radical Biology and Medicine: The Official Journal of the Oxygen Society . 2009,第12期

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6. Nrf1 and Nrf2 Regulate Rat Glutamate-Cysteine Ligase Catalytic Subunit Transcription Indirectly via NF-κB and AP-1 [O] . Heping Yang, Nathaniel Magilnick, Candy Lee, 2005

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7. Nrf1 and Nrf2 Regulate Rat Glutamate-Cysteine Ligase Catalytic Subunit Transcription Indirectly via NF-κB and AP-1 [O] . Yang, Heping, Magilnick, Nathaniel, Lee, Candy, 2005

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Nrf1 and Nrf2 Regulate Rat Glutamate-Cysteine Ligase Catalytic Subunit Transcription Indirectly via NF-κB and AP-1

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