Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA176924 | ENA |
REPOSITORIES: ENA
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Project description:Investigation of the transcription profile of cells transformed by Cr6+ in vivo was undertaken. The objective was to elucidate genomic changes underlying the mechanism of action of the carcinogenic dose of Cr6+and their prevention using metabolic antioxidant Lipoic acid (LA). Cr6+ was administered intraperitoneally to LPS+TPA challenged Swiss albino mice in host mediated cell transformation assay using peritoneal macrophages in vivo. The cell transforming potential of Cr6+ test doses was validated by gain of anchorage independent growth potential in soft agar and loss of Fc receptor on target cells. LA was administered in equimolar doses. Compared to non-transformed cells, the gene expression profile of transformed cells was found to be dysregulated substantially and in dose dependent manner. Genes showing down regulation were found to be involved in tumour suppression; apoptosis, DNA repair, and cell-cycle. A similar response was noted in the genes pertaining to immune system, morphogenesis, cell-communication, energy-metabolism, and biosynthesis. The co-administration of lipoic acid prevented the transcription dysregulation and cell transformation by Cr6+ in vivo. The influenced pathways seem to be crucial for progression as well as mitigation of Cr toxicity; and their response to LA indicated their critical role in mechanism of anti-carcinogenic action of LA. Results are of importance to mitigate Cr6+ induced occupational cancer hazard. Agilent one-color experiment, Organism: Mus musculus, Agilent-Whole Genome Mouse 4x44k (AMADID: 14868), Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
2013-05-01 | E-GEOD-41419 | biostudies-arrayexpress
Project description:Investigation of the transcription profile of cells transformed by Cr6+ in vivo was undertaken. The objective was to elucidate genomic changes underlying the mechanism of action of the carcinogenic dose of Cr6+and their prevention using metabolic antioxidant Lipoic acid (LA). Cr6+ was administered intraperitoneally to LPS+TPA challenged Swiss albino mice in host mediated cell transformation assay using peritoneal macrophages in vivo. The cell transforming potential of Cr6+ test doses was validated by gain of anchorage independent growth potential in soft agar and loss of Fc receptor on target cells. LA was administered in equimolar doses. Compared to non-transformed cells, the gene expression profile of transformed cells was found to be dysregulated substantially and in dose dependent manner. Genes showing down regulation were found to be involved in tumour suppression; apoptosis, DNA repair, and cell-cycle. A similar response was noted in the genes pertaining to immune system, morphogenesis, cell-communication, energy-metabolism, and biosynthesis. The co-administration of lipoic acid prevented the transcription dysregulation and cell transformation by Cr6+ in vivo. The influenced pathways seem to be crucial for progression as well as mitigation of Cr toxicity; and their response to LA indicated their critical role in mechanism of anti-carcinogenic action of LA. Results are of importance to mitigate Cr6+ induced occupational cancer hazard.
2013-05-01 | GSE41419 | GEO
Project description:The molecular mechanism of Cr6+ carcinogenicity is not well understood. Studies advocate a key involvement of the altered cytogenomics and dysregulated pathways in Cr6+ toxicity. However, the dissimilarity in expression of genes and pathways in cells transformed by Cr6+ has led us to supplement more data on the subject. We report here genomics of cells transformed after acute exposure to submicromolar (0.01or1µM) test doses of Cr6+; the non-cytotoxic submicromolar test concentrations transformed the mammalian cells; the characteristic gain of anchorage independent growth potential was demonstrable in soft agar assay. C3H10T1/2 and BALB/c 3T3 cell transformation assay has been used which is established in literature as the in vitro carcinogenesis test system. Gene expression profile of the transformed cells was found to be dysregulated at both the toxicant doses. PARP1 gene was significantly up regulated and SFN, MTIF2, IRGQ, RAVER2, SLC2A6, MLLT3, EPB4.1L3, JAK1, RALGPS1, EXTL3, PRMT6, PREB, SERPINE1, MORC4 genes were significantly down regulated commonly at two test concentrations. These genes were found to be involved in tumour suppression, DNA repair, cell cycle control, energy metabolism and biosynthesis.Cr6+ also induced MAPK signalling via ERK phosphorylation. Activation of ERK signalling, dysregulation of gene expressions, and cell transformation was prevented by alpha lipoic acid (LA) in equimolar concentrations. The acute exposure to submicromolar concentrations of Cr6+ can induce cell transformation and gene dysregulations in mammalian cell. The influenced genes are crucial for progression of Cr6+ toxicity and their mitigation by LA shows critical role of redox reactions in Cr6+ toxicity.
2015-12-31 | GSE43156 | GEO
Project description:The molecular mechanism of Cr6+ carcinogenicity is not well understood. Studies advocate a key involvement of the altered cytogenomics and dysregulated pathways in Cr6+ toxicity. However, the dissimilarity in expression of genes and pathways in cells transformed by Cr6+ has led us to supplement more data on the subject. We report here genomics of cells transformed after acute exposure to submicromolar (0.01or1µM) test doses of Cr6+; the non-cytotoxic submicromolar test concentrations transformed the mammalian cells; the characteristic gain of anchorage independent growth potential was demonstrable in soft agar assay. C3H10T1/2 and BALB/c 3T3 cell transformation assay has been used which is established in literature as the in vitro carcinogenesis test system. Gene expression profile of the transformed cells was found to be dysregulated at both the toxicant doses. PARP1 gene was significantly up regulated and SFN, MTIF2, IRGQ, RAVER2, SLC2A6, MLLT3, EPB4.1L3, JAK1, RALGPS1, EXTL3, PRMT6, PREB, SERPINE1, MORC4 genes were significantly down regulated commonly at two test concentrations. These genes were found to be involved in tumour suppression, DNA repair, cell cycle control, energy metabolism and biosynthesis.Cr6+ also induced MAPK signalling via ERK phosphorylation. Activation of ERK signalling, dysregulation of gene expressions, and cell transformation was prevented by alpha lipoic acid (LA) in equimolar concentrations. The acute exposure to submicromolar concentrations of Cr6+ can induce cell transformation and gene dysregulations in mammalian cell. The influenced genes are crucial for progression of Cr6+ toxicity and their mitigation by LA shows critical role of redox reactions in Cr6+ toxicity. Agilent one-color experiment,Organism: Mus musculus ,Agilent-Whole Genome Mouse 4x44k (AMADID: 14868) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) C3H10T1/2 cells treated with 1uM or 0.01uM Cr(V1)
2015-12-31 | E-GEOD-43156 | biostudies-arrayexpress
Project description:ERK activation, gene dysregulations and cell transformation at submicromolar doses of Cr6+ in C3H10T1/2 and BALB/c 3T3 cells: interaction with Lipoic acid
| PRJNA184732 | ENA
Project description:Study gene expression during apoptotic process α Lipoic acid-induced.
2019-12-01 | GSE59164 | GEO
Project description:Aging and age-related pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using small molecule inhibitors would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of alpha lipoic acid (ALA), a naturally existing antioxidant, in targeting senescent cells via induction of programmed cell death. This study demonstrates the impact of alpha-lipoic acid as a medicinal compound on the expression profile of senescent cells and provides a strong rationale for its future use in geriatric medicine.
2022-12-31 | GSE156184 | GEO
Project description:Using RNA-seq, 39 cerebral cortex RNA samples were sequenced. The study design was as follows: Ad libitum fed rats at 6 months (n=3, 6 individuals pooled), 12 months (n=3, 6 individuals pooled) and 28 months (n=3, 6 individuals pooled). Calorie restricted rats at 6 months (n=3, 6 individuals pooled), 12 months (n=3, 6 individuals pooled) and 28 months (n=3, 6 individuals pooled). Rats fed alpha lipoic acid as a supplement to ad libitum at 12 months (n=3, 6 individuals pooled) and 28 months (n=3, 6 individuals pooled). Diet switching groups, where diet was changes at 12 months; 28 month ad libitum switched to calorie restriction (n=3, 6 individuals pooled), 28 month calorie restriction switched to ad libitum (n=3, 6 individuals pooled), 28 month ad libitum plus lipoic acid switched to calorie restriction (n=3, 6 individuals pooled), 28 month calorie restriction switched to ad libitum plus lipoic acid (n=3, 6 individuals pooled). Transcriptional profiling of the ageing cerebral cortex at 6, 12 and 28 months and the effect of diet on age and longevity, using carlorie restriction and alpha lipoic acid supplementation
2015-11-22 | E-GEOD-57110 | biostudies-arrayexpress
Project description:We found that BAP1 (BRCA1 Associated Protein-1) shows loss of heterozygosity in over 25% of pancreatic cancer patients and functions as tumor suppressor. Conditional deletion of Bap1 in murine pancreas led to genomic instability, accumulation of DNA damage, and an inflammatory response that evolved to pancreatitis with full penetrance. Concomitant expression of oncogenic KrasG12D led to malignant transformation and development of invasive and metastatic pancreatic cancer. At the molecular level, BAP1 maintains the integrity of the exocrine pancreas by regulating genomic stability and its loss confers sensitivity to radio- and platinum-based therapies.
2020-04-14 | GSE121709 | GEO
Project description:Alpha lipoic acid is reported to inhibit neutrophil lineage determination by targeting transcription factor ELK1 in granulocyte-monocyte progenitors. Here, we provide new evidence of alpha lipoic acid in promoting erythroid differentiation by targeting transcription factor ELK1 in CD34+CD371– hematopoietic stem progenitor cells. Over expression of both L-ELK1 and S-ELK1 greatly inhibit erythroid cell differentiation, but not knocking down of ELK1. Thus, RNAseq of CD34+CD123+CD38+CD371– HSPCs is performed to dissect the molecular mechanism of ELK1 in blocking erythrocyte differentiation.
2023-06-01 | GSE217887 | GEO