Evidence map›Paper›PMID 25148934›Full record

ArticleMolecular neurobiology2015

CO Induces Nrf2-Dependent Heme Oxygenase-1 Transcription by Cooperating with Sp1 and c-Jun in Rat Brain Astrocytes.

Pei-Ling Chi, Chih-Chung Lin, Yu-Wen Chen, Li-Der Hsiao, Chuen-Mao Yang

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Nrf2 signaling pathway: focus on oxidative stress in osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
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  12. Induction of Heme Oxygenase-1 by 15d-Prostaglandin JAntioxidants (Basel, Switzerland) · 2022
    Article
  13. Article
  14. 5,8-Dihydroxy-4 ', 7-dimethoxyflavone Attenuates TNF-Oxidative medicine and cellular longevity · 2022
    Article
  15. Article
  16. Article
  17. Towards "CO in a pill": Pharmacokinetic studies of carbon monoxide prodrugs in mice.Journal of controlled release : official journal of the Controlled Release Society · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Pei-Ling ChiDepartment of Physiology and Pharmacology and Health Ageing Research Center, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-Shan, 33302, Tao-Yuan, Taiwan.
Chih-Chung Lin
Yu-Wen Chen
Li-Der Hsiao
Chuen-Mao Yang
Chang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upregulation of heme oxygenase 1 (HO-1) by carbon monoxide (CO) delivered by CO-releasing molecules (CORMs) may be utilized as a therapeutic intervention for neurodegenerative diseases. This study was to delineate the two putative anti-oxidant response elements (AREs) in modulating HO-1 gene by participating with its promoter elements in rat brain astrocytes (RBA-1). CORM-2-induced HO-1 expression was mediated through superoxide, p38 mitogen-activated protein kinase(MAPK), extracellular signal-regulated protein kinases 1 and 2 (Erk1/2), protein tyrosine kinase 2 (Pyk2), platelet-derived growth factor receptor (PDGFR), and phosphatidylinositol 3'-kinase (PI3K/Akt), revealed by the pharmacological inhibitors or knockdown of these signaling molecules. CORM-2-enhanced HO-1 promoter activity was inhibited by co-transfection with small interfering RNA (siRNA) of c-Jun, specificity protein 1 (Sp1), or nuclear factor-erythroid 2-related factor 2 (Nrf2). Immunoprecipitation assay showed that CORM-2 increased the association of nuclear Nrf2 with Sp1 and c-Jun. Furthermore, chromatin immunoprecipitation (ChIP) assay confirmed that Nrf2, Sp1, and c-Jun are associated with the proximal ARE binding site on HO-1 promoter, suggesting that Nrf2/Sp1/c-Jun cooperations are key transcription factors modulating HO-1 expression. Mechanistically, CORM-2-induced ARE promoter activity was reduced by the inhibitors of reactive oxygen species (ROS), p38 MAPK, Pyk2, MAPK/ERK kinases 1 and 2 (MEK1/2), PDGFR, and PI3K/Akt or the siRNAs of c-Jun, SP1, and Nrf2. These findings suggested that CORM-2 increases formation of c-Jun, Sp1, and Nrf2 complex and binding with ARE1 binding site, which is mediated through both ROS/p38 MAPK and Pyk2-dependent PDGFR/PI3K/Akt/Erk1/2 pathways, resulting in HO-1 expression in RBA-1 cells.

Indexed as

AnimalsAntioxidantsAstrocytesBrainCarbon MonoxideExtracellular Signal-Regulated MAP KinasesFocal Adhesion Kinase 2Heme Oxygenase-1MitochondriaNADPH OxidasesNF-E2-Related Factor 2Organometallic Compoundsp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProtein BindingProto-Oncogene Proteins c-junAntioxidantsCarbon MonoxideExtracellular Signal-Regulated MAP KinasesFocal Adhesion Kinase 2Heme Oxygenase-1NADPH OxidasesNF-E2-Related Factor 2Organometallic Compoundsp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-junReactive Oxygen SpeciesReceptors, Platelet-Derived Growth FactorSp1 Transcription FactorSuperoxidestricarbonyldichlororuthenium (II) dimer

Identifiers

PMID25148934
OpenAlexW2041810204

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.