Effect of dmPGE2 radioprotection on hematopoietic stem cell (HSC) gene expression 1 h and 24 h after lethal irradiation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE151799 | GEO | 2020/07/15
REPOSITORIES: GEO
Similar Datasets
Project description:Effect of dmPGE2 radioprotection on hematopoietic stem cell (HSC) gene expression 1 h and 24 h after lethal irradiation
| PRJNA637300 | ENA
Project description:To further investigate the potential molecular basis of the protective effects of HSC on irradiation (6.5Gy) damage, gene expression analysis was conducted on rats liver tissues using microarrays.Pre-treatment with HSC prevented differential expression of 66% (1,398 genes) of 2,126 genes differentially expressed in response to radiation. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 32 pathways, such as olfactory transduction, uroactive ligand-receptor interaction, pathways in cancer, calcium signaling pathway, vascular smooth muscle contraction, cytokine-cytokine receptor interaction, mitogen-activated protein kinase (MAPK) signaling pathway, peroxisomal proliferator-activated receptor (PPAR）signaling pathway, gonadotropin-releasing hormone (GnRH) signaling pathway, Wnt signaling pathway, janus kinase-signal transducers and activators of transcription (Jak-STAT) signaling pathway, Notch signaling pathway.Our analysis indicated that the pretreatment of rats with HSC attenuated radiation-induced these pathways, such as multiple MAPK pathways, suggesting that the protective effect of HSC acts mainly through the attenuation of these pathways. The rats were randomly assigned to one of the three following treatment groups (10-12 animals per group): normal control, radiation and HSC dose (10g/kg body weight/day) + radiation. HSC dissolved in double distilled water were administered intragastrically to the male animals for 3 consecutive days before irradiation. Radiation induced gene expression in rat liver was measured at 24 hours after 6.5 Gy exposure.
2014-05-15 | E-GEOD-57692 | biostudies-arrayexpress
Project description:To further investigate the potential molecular basis of the protective effects of HSC on irradiation (6.5Gy) damage, gene expression analysis was conducted on rats liver tissues using microarrays.Pre-treatment with HSC prevented differential expression of 66% (1,398 genes) of 2,126 genes differentially expressed in response to radiation. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 32 pathways, such as olfactory transduction, uroactive ligand-receptor interaction, pathways in cancer, calcium signaling pathway, vascular smooth muscle contraction, cytokine-cytokine receptor interaction, mitogen-activated protein kinase (MAPK) signaling pathway, peroxisomal proliferator-activated receptor (PPAR）signaling pathway, gonadotropin-releasing hormone (GnRH) signaling pathway, Wnt signaling pathway, janus kinase-signal transducers and activators of transcription (Jak-STAT) signaling pathway, Notch signaling pathway.Our analysis indicated that the pretreatment of rats with HSC attenuated radiation-induced these pathways, such as multiple MAPK pathways, suggesting that the protective effect of HSC acts mainly through the attenuation of these pathways.
2014-05-15 | GSE57692 | GEO
Project description:Matrine is an alkaloid extracted from Sophora flavescens Ait and has many biological activities, such as anti-inflammatory, antitumor, anti-fibrosis, and immunosuppressive properties. In our previous studies, the matrine derivative MASM was synthesized and exhibited potent inhibitory activity against liver fibrosis. In this study, we mainly investigated its protection against lethal total-body irradiation (TBI) in rats. Administration of MASM reduced the radiation sickness characteristics and increased the 30-day survival of rats before or after lethal TBI. Ultrastructural observation illustrated that pretreatment of rats with MASM significantly attenuated the TBI-induced morphological changes in the different organs of irradiated rats. Gene expression profiles revealed that pretreatment with MASM had a dramatic effect on gene expression changes caused by TBI. Pretreatment with MASM prevented differential expression of 53% (765 genes) of 1445 differentially expressed genes induced by TBI. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 21 pathways, such as metabolic pathways, pathways in cancer, and mitogen-activated protein kinase (MAPK) pathways. Our data indicated that pretreatment of rats with MASM modulated these pathways induced by TBI, suggesting that the pretreatment with MASM might provide the protective effects on lethal TBI mainly or partially through the modulation of these pathways, such as multiple MAPK pathways. Therefore, MASM has the potential to be used as an effective therapeutic or radioprotective agent to minimize irradiation damages and in combination with radiotherapy to improve the efficacy of cancer therapy.
| S-EPMC6273364 | biostudies-literature
Project description:We report transcriptional analyses of individual and combined EP receptor stimulation in radioprotective administration of dmPGE2 and other EP receptor agonists with varying radioprotective capacities. We find that in both hematopoietic stem cells, and in BM stromal (non-hematopoietic) cells, dmPGE2 radioprotection is primarily mediated through EP4 stimulation, but full activity likely requires interactive stimulation of both EP4 and EP3.
2023-05-19 | GSE218443 | GEO
Project description:To further investigate the potential molecular basis of the protective effects of MASM on irradiation (6.5Gy) damage, gene expression analysis was conducted on rats liver tissues using microarrays. Pre-treatment with MASM prevented differential expression of 53% (766 genes) of 1445 genes differentially expressed in response to radiation. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 21 pathways, such as metabolic pathways, pathways in cancer, and MAPK signaling pathway. The rats were randomly assigned to one of the three following treatment groups (10-12 animals per group): normal control, radiation and MASM dose (30 mg/kg body weight/day) + radiation. MASM dissolved in double distilled water were administered intragastrically to the male animals for 3 consecutive days before irradiation. Radiation induced gene expression in rat liver was measured at 24 hours after 6.5 Gy exposure.
2014-03-28 | E-GEOD-56263 | biostudies-arrayexpress
Project description:We analyzed the combination of ionizing radiation (IR, 2.0 Gy) along with microRNA-mediated targeting of genes involved in DSB repair to sensitize human non-small cell lung cancer (NSCLC) cells.
2018-11-13 | GSE112375 | GEO
Project description:DNA damage response (DDR) is a complex process, essential for cell survival. Especially deleterious type of DNA damage are DNA double-strand breaks (DSB), which can lead to genomic instability and malignant transformation if not repaired correctly. The central player in DSB detection and repair is the ATM kinase which orchestrates the action of several downstream factors. Despite substantial knowledge of DNA repair processes, still several aspects of DNA damage detection and signaling are not fully understood. Recent studies have suggested that long non-coding RNAs (lncRNAs) are involved in DDR. Here, we aimed to identify lncRNAs induced upon DNA damage in an ATM-dependent manner. 7 mRNAs and 10 lncRNAs were significantly induced 1h after ionizing radiation (IR) in healthy donors, whereas none in AT patients. 447 mRNAs and 149 lncRNAs were induced 8h after IR in the control group, while only 100 mRNAs and 3 lncRNAs in AT patients. Among IR-induced mRNAs, we found several genes with well-known functions in DDR. Gene Set Enrichment Analysis and Gene Ontology revealed delayed induction of key DDR pathways in AT patients compared to controls. The induction and dynamics of selected 9 lncRNAs were confirmed by RT-qPCR at several time-points after IR on a larger cohort. Moreover, inhibition of ATM with a specific inhibitor (KU-60019) proved that those lncRNAs are dependent on ATM. Some of the detected lncRNAs are localized next to protein-coding genes involved in DDR. We observed that induction of lncRNAs after IR preceded changes in expression of adjacent genes. This indicates that IR-induced lncRNAs may regulate the transcription of nearby genes. Subcellular fractionation into chromatin, nuclear, and cytoplasmic fractions revealed that the majority of studied lncRNAs are localized in chromatin, which further suggests their role in regulation of gene expression. In summary, our study revealed several lncRNAs induced by IR in an ATM-dependent manner. Their co-localization and co-expression with genes involved in DDR suggest that those lncRNAs may be important players in cellular response to DNA damage.
2024-02-16 | GSE243468 | GEO
Project description:To further investigate the potential molecular basis of the protective effects of MASM on irradiation (6.5Gy) damage, gene expression analysis was conducted on rats liver tissues using microarrays. Pre-treatment with MASM prevented differential expression of 53% (766 genes) of 1445 genes differentially expressed in response to radiation. Pathway enrichment analysis indicated that these genes were mainly involved in a total of 21 pathways, such as metabolic pathways, pathways in cancer, and MAPK signaling pathway.
2014-03-28 | GSE56263 | GEO
Project description:Childhood exposure to carcinogens renders a higher risk of breast cancer. The molecular mechanisms underlying cancer development after such exposure are not, however, well understood. Here we examined how the mechanism of cancer development relates to the age at exposure to ionizing radiation (IR) or the carcinogen 1-methyl-1-nitrosourea (MNU). Pre- and postpubertal (3- and 7-week-old, respectively) female Sprague-Dawley rats were whole-body gamma-irradiated (2 Gy), injected intraperitoneally with MNU (20 mg/kg) or left untreated and were autopsied at 50 weeks of age. Mammary carcinomas were examined for estrogen receptor (ER) alpha, progesterone receptor (PR) and ErbB ligand expression and for expression microarrays. Early histological changes of the ovaries were also evaluated. The incidence of mammary cancer was higher after postpubertal, rather than prepubertal, IR exposure; the inverse was true for MNU. Most cancers were positive for both ER alpha and PR except for the prepubertal IR group. Interestingly, cancers of the prepubertal IR group expressed a different set of ErbB ligands from those of the other groups and did not overexpress Areg, which encodes an estrogen-regulated ErbB ligand, or other developmentally related genes including those for hormonally regulated mammary gland development. Prepubertal IR exposure resulted in ovarian dysfunction as revealed by a reduced follicular pool. Evidence thus suggests that mammary carcinogenesis induced by prepubertal IR exposure is independent of ovarian hormones but requires certain ErbB ligands; induction by postpubertal exposure depends on ovarian hormones and different ErbB ligands. In contrast, MNU-induced carcinogenesis was less influenced by the age at exposure.
2011-01-19 | GSE22770 | GEO