An Antisense Oligonucleotide to 1-cys Peroxiredoxin Causes Lipid Peroxidation and Apoptosis in Lung Epithelial Cells

Pak, Jhang Ho; Manevich, Yefim; Kim, Han Suk; Feinstein, Sheldon I.; Fisher, Aron B.

doi:10.1074/jbc.m204222200

Cited by 108 publications

(96 citation statements)

References 39 publications

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“…The adenoviral constructs with the 1-cysPrx (AdPrx), LacZ gene (AdLacZ), or empty vector (AdNull) were kindly provided by the Institute of Human Gene Therapy, University of Pennsylvania (2). The assembly and production of recombinant adenovirus were performed with the Adeno-X Expression System (Clontech, Palo Alto, CA) as described previously (20). Briefly, a shuttle vector containing a cytomegalovirus immediateearly promoter-driven expression cassette with full-length cDNAs for rat 1-cysPrx or LacZ genes was cotransfected with a plasmid that contains first-generation replication-incompetent human type 5 adenovirus genome into competent TOP10F' Escherichia coli cells (Invitrogen, Carlsbad, CA).…”

Section: Methodsmentioning

confidence: 99%

“…X-galactosidase (X-gal) staining was used as described previously to provide a qualitative measurement of gene transfer (1,16,20,22). The X-gal solution (pH 7.9) (Roche Diagnostics, Indianapolis, IN) was used to detect the activity of E. coli ␤-galactosidase (␤-gal).…”

Section: Methodsmentioning

confidence: 99%

“…Protein samples (10 g) were subjected to a 12% SDS-PAGE gel on a XCell electrophoresis apparatus (Invitrogen, Carlsbad, CA) and then were transferred to a polyvinylidene fluoride membrane (Millipore, Bedford, MA). Membranes were incubated in blocking solution (0.1% Tween 20-TBS buffer containing 10% nonfat dry milk; Bio-Rad, Richmond, CA) for 1 h and then were probed with a polyclonal antibody (1:2,000 dilution) to a 1-cysPrx peptide (1: 2,000 dilution) followed by peroxidase-conjugated secondary antibody as described previously (17,20). The reaction was detected by enhanced chemiluminescence (ECL; NEN Life Science, Bos- ton, MA) and quantitated by densitometric scanning of X-ray film using the FluorS multi-imager (Bio-Rad).…”

Section: Methodsmentioning

confidence: 99%

“…Previous studies have demonstrated that overexpression of 1-cysPrx in NIH 3T3 cells enhances their ability to reduce H 2 O 2 and protects their glutamine synthetase against H 2 O 2 -mediated inactivation (12). Our laboratory has shown that 1-cysPrx can reduce peroxidized membrane phospholipids in H441 cells, a lung epithelial cell line (17), whereas an antisense-mediated decrease in expression of 1-cysPrx in L2 cells, another lung epithelial cell line, resulted in apoptotic cell death (20). Recently, gene-targeted mice with absent 1-cysPrx have been shown to be more sensitive to paraquat-induced oxidative injury (23).…”

mentioning

confidence: 88%

“…DISCUSSION 1-cysPrx is a recently described antioxidant enzyme member of the Prx family that is expressed at relatively high levels in the lung (14). In lung epithelial cell lines, overexpression of 1-cysPrx protein was shown to increase the ability of these cells to degrade H 2 O 2 and to protect them against oxidantinduced plasma membrane damage (17), whereas treatment with an antisense oligonucleotide to 1-cysPrx resulted in lipid peroxidation and apoptosis (20). 1-cysPrx knockout mice showed increased sensitivity to paraquat-induced oxidative lung injury compared with wild-type mice (23).…”

Section: Lung Distribution Of Gene Transfermentioning

confidence: 99%

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Adenovirus-mediated transfer of the 1-cys peroxiredoxin gene to mouse lung protects against hyperoxic injury

Wang

Manevich

Feinstein

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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1-Cys peroxiredoxin (1-cysPrx) is a novel antioxidant enzyme that has been shown to reduce a broad spectrum of peroxides including phospholipid hydroperoxides. We tested the hypothesis that adenovirus-mediated transfer of the 1-cysPrx gene can protect lungs of mice from oxidant injury. Mice infected with AdLacZ/AdNull were used as a control (AdCon). X-galactosidase staining revealed widespread expression of the LacZ gene in airways and lung alveoli. Compared with AdCon, 1-cysPrx expression was increased about twofold at 3 days after adenovirus infection. Mice with increased Prx expression showed less loss of body weight and longer survival during exposure to 100% O2 or to 85% O2 for 4 days followed by 100% O2. At 72 h of 100% O2 exposure, AdPrx infection protected mouse lungs from injury as indicated by less pleural effusion, lower lung wet/dry weight, less protein and fewer nucleated cells in bronchoalveolar lavage fluid, and lower content of thiobarbituric acid-reactive substances and protein carbonyls in lung homogenate. These findings show that increased expression of 1-cysPrx through adenovirus-mediated gene transfer protects mouse lungs from hyperoxic injury and delays death.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 88%

Section: Lung Distribution Of Gene Transfermentioning

confidence: 99%

See 3 more Smart Citations

Adenovirus-mediated transfer of the 1-cys peroxiredoxin gene to mouse lung protects against hyperoxic injury

Wang

Manevich

Feinstein

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Lipid Peroxidation and Nitration

Davies¹,

Guo²

2013

Molecular Basis of Oxidative Stress

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Comparative proteomic analysis identifies protein disulfide isomerase and peroxiredoxin 1 as new players involved in embryonic interdigital cell death

Shan

Tang

Cai³

et al. 2005

Developmental Dynamics

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In this study, we used comparative proteomics to identify proteins that were involved in the regulation of interdigital cell death. The protein profiles of embryonic day (E) 12.5 and 13.5 mouse hindlimb interdigital tissues were compared to identify proteins that were differentially expressed. The interdigital cells are irreversibly committed to programmed cell death (PCD) at E13.5, whereas they are developmentally plastic at E12.5. We established that protein disulfide isomerase (PDI) expression was up-regulated at E13.5, while peroxiredoxin 1 (Prdx1) expression was down-regulated at this time point. Semiquantitative reverse transcriptase-polymerase chain reaction and Western blot analyses confirmed the data obtained from the two-dimensional electrophoresis gels. Furthermore, we were able to up-regulate PDI expression by manipulating the E12.5 interdigital tissues to die during culture, although this up-regulation was not possible when cell survival was promoted. In addition, we could inhibit interdigital cell death and expression of proapoptotic genes (Bmp-4 and Bambi) by treating interdigital tissues with PDI antibodies and bacitracin (a PDI enzyme inhibitor). These findings suggested that PDI was involved in the activation and maintenance of interdigital cell death. Conversely, we determined that Prdx1 expression was maintained when interdigital cultures were manipulated to survive but down-regulated when the cultures were permitted to die. The result suggested that Prdx1 was involved in maintaining interdigital cell survival. However, we were unable to induce interdigital cell death by means of RNA interference-mediated silencing of Prdx1 expression, indicating that Prdx1 down-regulation is not sufficient for PCD to occur. Proteomic analysis of the Prdx1 knock-down cells revealed that the level of NF-kappaB inhibitor epsilon (IB) was dramatically reduced. Furthermore, we found an increase in NFB activation and reactive oxygen species (ROS) levels in the cytoplasm as a result of Prdx1 knockdown. We also found that silencing Prdx1 made the interdigital cells more susceptible to ROS-induced cell death. Taken together, our study identifies two new players in interdigital cell death and highlights that PCD is regulated by a delicate balance of proapoptotic and survival-promoting activities. Developmental Dynamics 233:266 -281, 2005.

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An Antisense Oligonucleotide to 1-cys Peroxiredoxin Causes Lipid Peroxidation and Apoptosis in Lung Epithelial Cells

Cited by 108 publications

References 39 publications

Adenovirus-mediated transfer of the 1-cys peroxiredoxin gene to mouse lung protects against hyperoxic injury

Adenovirus-mediated transfer of the 1-cys peroxiredoxin gene to mouse lung protects against hyperoxic injury

Lipid Peroxidation and Nitration

Comparative proteomic analysis identifies protein disulfide isomerase and peroxiredoxin 1 as new players involved in embryonic interdigital cell death

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