Hyphthalamic mRNA expression of leptin receptor-expressing cell-specific Slug knockout mice
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ABSTRACT:
PROVIDER: PRJNA900258 | ENA |
REPOSITORIES: ENA
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Project description:Leptin resistance is a driving force for obesity and metabolic syndrome. Slug (Snai2 or Snail2) is an epignetic factor that may play a critical role in the development of leptin resistance in obesity. We conducted a microarray to detect molecular targets of Slug in the hypothalamus.
2022-11-15 | GSE217748 | GEO
Project description:Studies of the zinc finger transcription factors Slug and Snail have largely focused on their important role in modulating epithelial-mesenchymal transition during embryonic development and tumor progression. However, these transcription factors also appear to regulate local inflammation. In previous studies, we showed that Slug knockout mice were resistant to sunburn, an acute cutaneous inflammatory response, compared to wild type mice. In the present studies, we used Slug knockout, chimeric Slug knockout/wild type, conditional Slug knockout, and Slug transgenic mice to study the role of Slug in ultraviolet radiation (UVR)-induced cutaneous inflammation. We demonstrated, using immunohistochemistry, in vivo imaging, and neutrophil migration studies, that it was Slug expression in the epidermis rather than in neutrophils that modulated the UVR response. Microarray analysis indicated that this modulation was effected by the production of epidermal cytokines, including CCL3, CCL4, oncostatin, and interleukin-1β, that recruited neutrophils to UVR-exposed skin. The pattern of pro-inflammatory gene regulation by Slug suggested a central role for NF-κB in mediating gene induction. Immunohistochemical analysis of UVR-induced NF-κB activation demonstrated reduced activation in Slug knockout and enhanced activation in Slug transgenic epidermis. Slug thus appears to modulate NF-κB activation in response to UVR.
2016-08-27 | GSE86107 | GEO
Project description:Liver steatosis is a driving force for nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease, insulin resistance, and type 2 diabetes. Slug (also called Snai2 or Snail2) is a transcriptional regulator that may play a critical role in the regulation of liver function. To prove that, we used microarrays to detail the hepatic Slug regulated gene expression underlying liver steatosis and identified distinct pathways controlled by Slug during this process.
2020-02-18 | GSE145404 | GEO
Project description:This experiment intended to look for the transcriptome changes that happen in neuronal cells from the preoptic area of the hypothalamus expressing leptin receptors during heat acclimation conditions. 3 groups of animals were used; long-term heat-acclimated animals constantly exposed to 36˚C for 28-35 days, short-term heat-acclimated animals constantly exposed to 36˚C for 5 days, and non-habituated (non-acclimated) animals which were not exposed to heat. The animal line used was LepRCreHTB.
2024-05-06 | E-MTAB-14029 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in hepatocellular carcinoma cell line hepG2 in regular culture, hepG2-slug in regular culture and hepG2-slug on Matrigel. Whole genome gene expression level changes have been compared in hepatocellular carcinoma cell line hepG2 in regular culture, hepG2-slug in regular culture and hepG2-slug on Matrigel.
2012-09-21 | GSE41026 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE41026: Expression analysis of HepG2, HepG2-slug and HepG2-slug on Matrigel GSE41027: Chip-chip from HepG2 cells and HepG2 cells with slug overexpression Refer to individual Series
2012-09-21 | E-GEOD-41028 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in hepatocellular carcinoma cell line hepG2 in regular culture, hepG2-slug in regular culture and hepG2-slug on Matrigel. Whole genome gene expression level changes have been compared in hepatocellular carcinoma cell line hepG2 in regular culture, hepG2-slug in regular culture and hepG2-slug on Matrigel. Roche NimbleGen micro-array analysis was employed to assess global genome expression in HepG2 in regular culture, HepG2-slug in regular culture and HepG2-slug on Matrigel. The results demonstrated that the up-regulated genes and the down-regulated genes increased significantly when HepG2-slug cells with VM forming ablity were cultured on Matrigel and formed VM.
2012-09-21 | E-GEOD-41026 | biostudies-arrayexpress
Project description:To establish the role of Slug in CRC, we created a genetic CRC model for Slug expression. As parental cells, we selected HT-29 cells that display a pronounced epithelial phe-notype. HT-29 cells were transfected with Slug, and two stable Slug-expressing clones. (Slug1, Slug2) were isolated. As transfection control, we used HT-29 cells transfected with empty vector (control). To characterize the influence of Slug on gene ex-pression, transcriptome analysis was performed for the four HT-29 cell lines as well as for the corresponding tumor xenografts. Global expression profiling showed that Slug-overexpressing cells and tumors were clustered together while the parental and control cells and tumors formed a separate cluster. Next, a two-step analysis was carried out. First, a subtractive analysis was carried out comparing the gene profiles of Slug-expressing cells and tumors with the corresponding parental/control samples. Genes were considered to be significantly upregulated by Slug if the fold change (FC) was greater than +2 and downregulated if the fold change was less than −2 with p-values (false dis-covery rates) less than 0.01
2022-06-11 | E-MTAB-11812 | biostudies-arrayexpress
Project description:The relationship between loss of hypothalamic function and onset of diabetes mellitus remains elusive. Therefore, we generated a targeted oxidative-stress murine model utilizing conditional knockout of selenocysteine-tRNA (Trsp) using rat insulin promoter-driven-Cre (RIP-Cre). These Trsp-knockout (TrspRIPKO) mice exhibit deletion of Trsp in both hypothalamic cells and pancreatic β-cells leading to increased hypothalamic oxidative stress and severe insulin resistance. Leptin signals were suppressed and numbers of proopiomelanocortin-positive neurons in the hypothalamus were decreased. In contrast, a Trsp-knockout mouse (TrspIns1KO) expressing Cre specifically in pancreatic β-cells, but not in the hypothalamus, did not display insulin and leptin resistance, demonstrating a critical role of the hypothalamus in the onset of diabetes mellitus. Nrf2 (NF-E2-related-factor-2) regulates antioxidant gene expression. Gene-driven increase in Nrf2 signaling suppressed hypothalamic oxidative stress and improved insulin and leptin resistance in TrspRIPKO mice. Thus, Nrf2 harbors the potential to prevent the onset of diabetic mellitus by reducing hypothalamic oxidative damage.
2017-02-06 | GSE92235 | GEO
Project description:The relationship between loss of hypothalamic function and onset of diabetes mellitus remains elusive. Therefore, we generated a targeted oxidative-stress murine model utilizing conditional knockout of selenocysteine-tRNA (Trsp) using rat insulin promoter-driven-Cre (RIP-Cre). These Trsp-knockout (TrspRIPKO) mice exhibit deletion of Trsp in both hypothalamic cells and pancreatic β-cells leading to increased hypothalamic oxidative stress and severe insulin resistance. Leptin signals were suppressed and numbers of proopiomelanocortin-positive neurons in the hypothalamus were decreased. In contrast, a Trsp-knockout mouse (TrspIns1KO) expressing Cre specifically in pancreatic β-cells, but not in the hypothalamus, did not display insulin and leptin resistance, demonstrating a critical role of the hypothalamus in the onset of diabetes mellitus. Nrf2 (NF-E2-related-factor-2) regulates antioxidant gene expression. Gene-driven increase in Nrf2 signaling suppressed hypothalamic oxidative stress and improved insulin and leptin resistance in TrspRIPKO mice. Thus, Nrf2 harbors the potential to prevent the onset of diabetic mellitus by reducing hypothalamic oxidative damage.
2017-02-06 | GSE92234 | GEO