Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Epithelia and fibroblasts gene profile in 4NQO induced tongue carcinogenesis

ABSTRACT: Nine groups of rat tongue epithelia and submucosal fibroblasts RNA samples respectively, including three from normal control, three from dysplasia, and three from carcinoma (3 rats per group) were collected for gene microarray hybridization. Significant fold changes among genes were determined by taking the ratio of the expression between dysplasia group and carcinoma group versus normal group in epithelia and fibroblasts cells

ORGANISM(S): Rattus norvegicus

SUBMITTER: Tong Wu

PROVIDER: E-GEOD-42780 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Modulation of IL-1β reprogrammes the tumor microenvironment to interrupt oral carcinogenesis.

Wu Tong T Hong Yun Y Jia Lihua L Wu Jie J Xia Juan J Wang Juan J Hu Qinchao Q Cheng Bin B

Scientific reports 20160201

Head and neck squamous cell carcinoma (HNSCC) development is a multistage process includes the normal, dysplasia and squamous cell carcinoma (SCC) stages. Recently, increasing evidence has suggested that the tumor microenvironment (TME) is an integral part of malignant transformation. Exploring certain key node genes in TME for future intervention in dysplasia to interrupt oral carcinogenesis was the primary goal of this research. To achieve this goal, systems biology approaches were first appli ...[more]

PMID: 26831400

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Project description:Left heart disease (LHD) frequently causes lung vascular remodelling and pulmonary hypertension (PH). Yet, pharmacological treatment for PH in LHD is lacking and its pathophysiological basis remains obscure. We aimed to identify candidate mechanisms of PH in LHD and to test their relevance and therapeutic potential. In rats, LHD was induced by supracoronary aortic banding. Whole genome microarray analyses were performed, candidate genes were confirmed by RT-PCR and Western blots and functional relevance was tested in vivo by genetic and pharmacological strategies. In lungs of LHD rats, mast cell activation was the most prominently upregulated gene ontology cluster. Mast cell gene upregulation was confirmed at RNA and protein levels and remodelled vessels showed perivascular mast cell accumulations. In LHD rats treated with the mast cell stabiliser ketotifen, or in mast cell deficient Ws/Ws rats, PH and vascular remodelling were largely attenuated. Both strategies also reduced PH and vascular remodelling in monocrotaline-induced pulmonary arterial hypertension, suggesting that the role of mast cells extends to noncardiogenic PH. In PH of different aetiologies, mast cells accumulate around pulmonary blood vessels and contribute to vascular remodelling and PH. Mast cells and mast cell-derived mediators may present promising targets for the treatment of PH. Whole rat genome microarray analyses were performed in lung homogenates of three rats with established PH following supracoronary aortic banding and in three sham-operated controls. Out of a total of 28,000 analysed genes, differential expression defined as 2-fold change with p<0.05 was evident for 120 genes. Of these, 76 were upregulated and 44 downregulated in aortic banding compared with control lungs gene. Enrichment analysis revealed regulation of mast cell specific genes - 13 out of 20 genes were significantly upregulated in aortic banding compared with control lungs. To test for a putative functional role of mast cells in lung vascular remodelling and PH in LHD, we applied a pharmacological approach by treatment of aortic banding rats with the mast cell stabiliser ketotifen. Microarray analysis then compared rats that were treated with untreated. In brief, congestive heart failure (CHF) was induced in juvenile rats by supracoronary aortic banding and rats were analyzed 9 weeks thereafter when they had established left heart failure with preserved ejection fraction and secondary pulmonary hypertension. Three heart failure rats were untreated, and 3 received the mast cell stabilizer ketotifen (1 mg/kg-1 bodyweight/day-1) with the drinking water. Sham rats underwent the same surgical procedure but without placement of a clip on the supracoronary aorta. Microarray analyses: Lungs from banded and control rats were excised and total RNA was extracted (Stratagene Absolutely RNA Miniprep Kit; Stratagene, La Jolla, USA). Three Âµg total RNA from three control and three banded rats each were processed according to the One-Cycle Target Labeling protocol (GeneChip Expression Analysis, Affymetrix, Santa Clara, USA). Before and after amplifications, the total RNA/complementary RNA concentrations were checked with NanoDrop ND-1000 (Thermo Scientific, Wilmington, USA) and quality was controlled (Experion electrophoresis station, BioRad; Hercules, USA). Samples were hybridized to GeneChipÂ® Rat Genome 230 2.0 arrays (Affymetrix; Santa Clara, USA) containing 31,000 probe sets covering 28,000 rat genes.

Project description:The study aimed to investigate the mechanisms of Jianxin (JX) granules, a Traditional Chinese Medicine formulation, in the treatment of heart failure (HF) using metabolomic profiling. The HF model was established by ligation of left coronary artery. The successfully modeled rats were randomly divided into three groups: the model group, the JX granules group, and Sacubitril/Valsartan (S/V) group. Four weeks after treatment, LV tissue samples were collected. Proteomics was used to identify the differentially expressed proteins and potential pathways. The differential expressed proteins (DEPs) were obtained with Tandem Mass Tags approach. As compared to the control group, 150 DEPs were identified in model rats, comprising 112 up-regulated and 38 down-regulated proteins. Notably, in the JX granules group, 25 DEPs were identified compared to the model rats, encompassing 18 up-regulated and 7 down-regulated proteins. In comparison with the control group, 228 DEPs in the JX granules group were obtained, which comprised of 128 up-regulated and 100 down-regulated proteins. As compared with the control group, BP in the model group was mainly enriched in humoral immune response, positive regulation of apoptotic cell clearance, and the response to metal ions; Meanwhile, CC was mainly related to contractile and stress fibers, actin filaments, and extracellular space; MF was mainly enriched in the serine-type peptidase activity, actin binding, and peptidase activity. Furthermore, DEPs indicated by KEGG analysis were primarily linked to pathways such as the complement and coagulation cascades, regulation of the actin cytoskeleton, and adrenergic signaling. In contrast to the model group, BP in JX granules group was primarily associated with processes involving nucleosome organization, chromatin assembly or disassembly, DNA conformation change and small molecule catabolic processes; CC was primarily related to the protein-DNA complex, mitochondrion, intracellular, nucleosome, cytoplasm; MF displayed significant enrichment in protein dimerization and homodimerization activity, catalase activity, chromatin and nucleosomal DNA binding. Considering KEGG enrichment information, DEPs in the JX granules group were mainly enriched in metabolic pathways and ribosome pathway. The key differential genes, such as triosephosphate isomerase 1 (TPI1), lactate dehydrogenase B (LDHB), pyruvate kinase M (PKM), protein kinase B (Akt), and lactate dehydrogenase A (LDHA) were identified. The vital pathways including carbon metabolism, the PI3K-Akt signaling pathway, pyruvate metabolism, and HIF-1α signaling pathway were obtained.

Project description:Background: Sepsis-associated encephalopathy (SAE) is a common and severe complication of sepsis. While several studies have reported the proteomic alteration in plasma, urine, heart, etc. of sepsis, few research focused on the brain tissue. This study aims at discovering the differentially abundant proteins in the brains of septic rats to identify biomarkers of SAE. Methods: The Prague-Dawley rats were randomly divided into sepsis (n = 6) or sham (n = 6) groups, and then the whole brain tissue was dissected at 24 h after surgery for further protein identification by TMT-LC–MS/MS-based proteomics. Ingenuity pathway analysis, Gene ontology knowledgebase, and STRING database are used to explore the biological significance of proteins with altered concentration. Results: Among the total of 3163 proteins identified in the brain tissue, 57 were increased while 38 were decreased in the sepsis group compared to the sham group. Bioinformatic analyses suggest that the differentially abundant proteins are highly related to cellular microtubule metabolism, energy production, nucleic acid metabolism, neurological disease, etc. Additionally, acute phase response signaling was possibly activated and PI3K/AKT signaling was suppressed during sepsis. An interaction network established by IPA revealed that Akt1, Gc-globulin, and ApoA1 were the core proteins. The increase of Gc-globulin and the decrease of Akt1 were confirmed by Western blot. Conclusions: Based on the multifunction of these proteins in several brain diseases, we first propose that Gc-globulin, ApoA1, PI3K/AKT pathway, and acute phase response proteins (hemopexin and cluster of alpha-2-macroglobulin) can potentially be diagnosis biomarkers, therapeutic targets, and prognosis indicators of SAE. These results may provide new insights into the pathologic mechanism of SAE, yet further research is required to explore the functional implications and clinical applications of the differentially abundant proteins in the brains of sepsis group.

Dataset Information

Epithelia and fibroblasts gene profile in 4NQO induced tongue carcinogenesis

Publications

Modulation of IL-1β reprogrammes the tumor microenvironment to interrupt oral carcinogenesis.

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