α-Tocopherol induces calnexin in renal tubular cells: Another protective mechanism against free radical-induced cellular damage

Lee, Wen-Hua; Akatsuka, Shinya; Shirase, Tomoyuki; Dutta, Khokon Kumar; Jiang, Li; Liu, Yuting; Onuki, Janice; Yamada, Yoshihiro; Okawa, Katsuya; Wada, Youichiro; Watanabe, Akira; Kohro, Takahide; Noguchi, Noriko; Toyokuni, Shinya

doi:10.1016/j.abb.2006.07.002

Cited by 5 publications

(4 citation statements)

References 56 publications

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“…Total RNA was isolated with Isogen (Nippon Gene Co. Ltd., Tokyo, Japan), and the degree of gene expression was then evaluated with GeneChip analysis (Focus array; Affymetrix) as previously described. 23 Network analysis was performed using Ingenuity Pathways Analysis (Ingenuity Systems, Redwood City, CA).…”

Section: Gene Expression Microarraymentioning

confidence: 99%

“…The glyceraldehyde 3-phosphate dehydrogenase gene was used as an internal control as previously described. 23 PCR reactions for each target and control genes were performed in triplicate. Primer sequences used were as follows: ptprz1 based on NM_013080: forward, 5Ј-cccagctggtggttatgattcc-3Ј, and reverse, 5Ј-cgtgactttgaagctctctcgcaa-3Ј (104-bp product); cyclinD1 based on NM_171992: forward, 5Ј-tgtgccatccatgcggaaa-3Ј, and reverse, 5Ј-gacaagaaacggtccaggtagt-3Ј (114-bp product); c-myc based on NM_012603: forward, 5Ј-tgtctatttggggacagtgttc-3Ј, and reverse, 5Ј-ctgttagcgaagctcacgtt-3Ј (149-bp product); c-jun based on NM_021835: forward, 5Ј-gtgaaatgacagctgagtgtctg-3Ј, and reverse, 5Ј-gtcaacagtctggacttgtgg-3Ј (141-bp product); fra-1 based on NM_012953: forward, 5Ј-ctgctaagtgcagaaaccga-3Ј, and reverse, 5Ј-caaggcgttccttctgctt-3Ј (129-bp product); and CD44 based on NM_012924: forward, 5Ј-tttggtggcacacagcttg-3Ј, and reverse, 5Ј-atggaatacacctgcgtaacgg-3Ј (104-bp product).…”

Section: Rt-pcrmentioning

confidence: 99%

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Chronic Oxidative Stress Causes Amplification and Overexpression of ptprz1 Protein Tyrosine Phosphatase to Activate β-Catenin Pathway

Liu

Shang

Akatsuka

et al. 2007

The American Journal of Pathology

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Ferric nitrilotriacetate induces oxidative renal tubular damage via Fenton-reaction, which subsequently leads to renal cell carcinoma (RCC) in rodents. Here, we used gene expression microarray and array-based comparative genomic hybridization analyses to find target oncogenes in this model. At the common chromosomal region of amplification (4q22) in rat RCCs, we found ptprz1, a tyrosine phosphatase (also known as protein tyrosine phosphatase zeta or receptor tyrosine phosphatase beta) highly expressed in the RCCs. Analyses revealed genomic amplification up to eightfold. Despite scarcity in the control kidney, the amounts of PTPRZ1 were increased in the kidney after 3 weeks of oxidative stress, and mRNA levels were increased 16 approximately 552-fold in the RCCs. Network analysis of the expression revealed the involvement of the beta-catenin pathway in the RCCs. In the RCCs, dephosphorylated beta-catenin was translocated to nuclei, resulting in the expression of its target genes cyclin D1, c-myc, c-jun, fra-1, and CD44. Furthermore, knockdown of ptprz1 with small interfering RNA (siRNA), in FRCC-001 and FRCC-562 cell lines established from the induced RCCs, decreased the amounts of nuclear beta-catenin and suppressed cellular proliferation concomitant with a decrease in the expression of target genes. These results demonstrate that chronic oxidative stress can induce genomic amplification of ptprz1, activating beta-catenin pathways without the involvement of Wnt signaling for carcinogenesis. Thus, iron-mediated persistent oxidative stress confers an environment for gene amplification.

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Section: Gene Expression Microarraymentioning

confidence: 99%

Section: Rt-pcrmentioning

confidence: 99%

Chronic Oxidative Stress Causes Amplification and Overexpression of ptprz1 Protein Tyrosine Phosphatase to Activate β-Catenin Pathway

Liu

Shang

Akatsuka

et al. 2007

The American Journal of Pathology

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“…There is a possibility that α‐tocopheryl phosphate is a more efficient biomolecule 125 . We recently observed that one of the anti‐oxidant mechanisms of vitamin E is via inducing chaperone proteins associated with glycoproteins 126 …”

Section: Redox Regulation and Signal Cascades Under Oxidative Stressmentioning

confidence: 99%

“…125 We recently observed that one of the antioxidant mechanisms of vitamin E is via inducing chaperone proteins associated with glycoproteins. 126…”

Section: Redox Regulation and Signal Cascades Under Oxidative Stressmentioning

confidence: 99%

Pathological investigation of oxidative stress in the post‐genomic era

Toyokuni

Akatsuka

2007

Pathology International

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Aerobes, including humans, are consistently exposed to oxidative stress by consuming oxygen. The biological significance of oxidative stress via reactive oxygen and nitrogen species consists of two stages: reversible redox regulation and irreversible oxidative molecular damage, which are sometimes intermingled. During the past decade, many signaling cascades associated with oxidative stress have been discovered. An interaction between Keap1 and the Nrf2 transcription factor is among the most fundamental mechanisms of the defense system against oxidative or similar stress. Furthermore, it became apparent that reactive oxygen species are actively produced through enzymes such as xanthine oxidoreductase and nicotinamide adenine dinucleotide phosphate, reduced (NADPH) oxidases in nonphagocytic cells as well. The role of a-tocopherol solely as an anti-oxidant was also questioned. Now there is a long list of pathological states implicating oxidative stress. At the same time, genome projects on various species have been completed. These efforts convincingly led to a new era of oxidative stress investigation, contributing powerful strategies to select candidate genes or biomolecules. Herein are reviewed recent advances and novel concepts in this field, including oxygenomics. These fruitful results may lead to more accurate and useful pathological diagnosis and more efficient prophylaxis and therapeutic interventions on human diseases.

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Lectins in Quality Control: Calnexin and Calreticulin

Gupta

2012

Animal Lectins: Form, Function and Clinical Applications

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α-Tocopherol induces calnexin in renal tubular cells: Another protective mechanism against free radical-induced cellular damage

Cited by 5 publications

References 56 publications

Chronic Oxidative Stress Causes Amplification and Overexpression of ptprz1 Protein Tyrosine Phosphatase to Activate β-Catenin Pathway

Chronic Oxidative Stress Causes Amplification and Overexpression of ptprz1 Protein Tyrosine Phosphatase to Activate β-Catenin Pathway

Pathological investigation of oxidative stress in the post‐genomic era

Lectins in Quality Control: Calnexin and Calreticulin

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