Pseudomonas aeruginosa use quorum-sensing molecules, including N-(3-oxododecanoyl)-homoserine lactone (C12), for intercellular communication. C12 activated apoptosis in mouse embryo fibroblasts (MEF) from both wild type (WT) and Bax/Bak double knock-out mice (WT MEF and DKO MEF that were responsive to C12, DKOR MEF): nuclei fragmented; mitochondrial membrane potential (??mito) depolarized; Ca2+ was released from the endoplasmic reticulum (ER), increasing cytosolic [Ca2+] (Cacyto); caspase 3/7 was activated. DKOR MEF had been isolated from a nonclonal pool of DKO MEF that were non-responsive to C12 (DKONR MEF). RNAseq analysis, qPCR and western blots showed that WT and DKOR MEF both expressed genes associated with cancer, including paraoxonase 2 (PON2), while DKONR MEF expressed little PON2. Adenovirus-mediated expression of human PON2 in DKONR MEF rendered them responsive to C12: ??mito depolarized, Cacyto increased and caspase 3/7 activated. Human embryonic kidney 293T (HEK293T) cells expressed low levels of endogenous PON2, and these cells were also less responsive to C12. Overexpression of PON2, but not PON2-H114Q (no lactonase activity) in HEK293T cells caused them to become sensitive to C12. Because [C12] may reach high levels in biofilms in lungs of cystic fibrosis (CF) patients, PON2 lactonase activity may control ??mito, Ca2+ release from the ER and apoptosis in CF airway epithelia. Coupled with previous data, these results also indicate that PON2 uses its lactonase activity to prevent Bax- and Bak-dependent apoptosis in response to common proapoptotic drugs like doxorubicin, staurosporine but activates Bax- and Bak-independent apoptosis in response to C12. Overall design: Gene expression profiling of mouse embryo fibroblasts from WT and Bax/Bak double knock-out mice (C12 responsive and non-reponsive cell lines).
Paraoxonase 2 serves a proapopotic function in mouse and human cells in response to the Pseudomonas aeruginosa quorum-sensing molecule N-(3-Oxododecanoyl)-homoserine lactone.
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Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with polybrominated diphenyl ether 47 (PBDE47), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.0485, 0.485, 4.85, 48.5 or 485 mg/kg PBDE47, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with 1,3,5,7,9,11-hexabromocyclododecane (HBCD), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.06, 0.641, 6.41, 64.1 or 641 mg/kg HBCD, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with bis(2-ethylhexyl) tetrabromophthalate (TBPH), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.07, 0.71, 7.06, 70.6 or 706 mg/kg TBPH, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-DBPE), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.1, 0.94, 9.4, 94.3 or 943 mg/kg TBBPA.DBPE, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with hexachlorocyclopentadienyl-dibromocyclooctane (HCDBCO), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.05, 0.54, 5.41, 54.1 or 541 mg/kg HCDBCO, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with decabromodiphenyl oxide (decaBDE), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.1, 0.959, 9.59, 95.9 or 959 mg/kg decaBDE, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with decabromodiphenylethane (DBDPE), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.1, 0.97, 9.71, 97.1 or 970 mg/kg DBDPE, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View SamplesTo identify liver transcripts differentially expressed due to treatment with 2-ethylhexyl-2,3,4,5-tetrabromobenzoate (TBB), we collected RNA from male Harlan Sprague Dawley rats exposed to 0, 0.05, 0.55, 5.50, 55 or 550 mg/kg TBB, 5 days after exposure for animals 7 weeks of age. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array.
Transcriptomic data from the rat liver after five days of exposure to legacy or emerging brominated flame retardants.
Sex, Specimen part, Treatment
View Samples