Analysis of rice leaves (V2 stage) in response to a short treatment with very high CO2 concentration in the dark, using standard atmosphere as control.
High CO2 concentration as an inductor agent to drive production of recombinant phytotoxic antimicrobial peptides in plant biofactories.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Downregulation of Sfrp5 promotes beta cell proliferation during obesity in the rat.
Specimen part
View SamplesObesity is associated with an increase in -cell mass in response tothe rising demand for insulin. -cell plasticity is essential to maintaining glucose homeostasis, however,the cellular and molecular mechanisms by which -cell mass is regulated remain poorly understood.Recently, we described the existence of a crosstalk between the peripancreatic adipose tissue and -cells as a novel mechanism that participates in the regulation of -cell plasticity. Here, we identify the secreted frizzled-related protein (Sfrp) 5 as down-regulated in the pancreatic islets of obese rats as well as in the pancreatic islets of human obese patients. Our results demonstrate that the silencing of Sfrp5 induces an increase in -cell proliferation, which we correlate with the activation of Wnt signaling and of the MAPK and PI3 kinase pathways. Together, these findings expand our understanding of the mechanisms underlying -cell proliferation under conditions of obesity. Furthermore, this study opens new insights into the specific targeting of Sfrp5 as a novel therapeutic strategy for balancing -cell mass.
Downregulation of Sfrp5 promotes beta cell proliferation during obesity in the rat.
Specimen part
View SamplesObesity is associated with an increase in -cell mass in response tothe rising demand for insulin. -cell plasticity is essential to maintaining glucose homeostasis, however,the cellular and molecular mechanisms by which -cell mass is regulated remain poorly understood.Recently, we described the existence of a crosstalk between the peripancreatic adipose tissue and -cells as a novel mechanism that participates in the regulation of -cell plasticity. Here, we identify the secreted frizzled-related protein (Sfrp) 5 as down-regulated in the pancreatic islets of obese rats as well as in the pancreatic islets of human obese patients. Our results demonstrate that the silencing of Sfrp5 induces an increase in -cell proliferation, which we correlate with the activation of Wnt signaling and of the MAPK and PI3 kinase pathways. Together, these findings expand our understanding of the mechanisms underlying -cell proliferation under conditions of obesity. Furthermore, this study opens new insights into the specific targeting of Sfrp5 as a novel therapeutic strategy for balancing -cell mass.
Downregulation of Sfrp5 promotes beta cell proliferation during obesity in the rat.
Specimen part
View SamplesChanges in the secretion profile of visceral-pancreatic white adipose tissue (pWAT) due to diet-induced obesity are partially responsible for increased beta cell replication, suggesting that a crosstalk between pWAT and beta cells may play a role in regulating beta cell plasticity. The molecular mechanisms underlying this cross-talk are still not fully understood.
Downregulation of Sfrp5 promotes beta cell proliferation during obesity in the rat.
Specimen part
View SamplesBackground and Aims: It is well demonstrated that in the beta cell population of the pancreas there is a dynamic turnover, which results from the net balance of several processes; beta cell replication, apoptosis and neogenesis. These processes have been studied in partial pancreatectomy and glucagon-like peptide 1 treated animals, where an increase in pancreas regeneration has been observed. Similarly, sodium tungstate, which decreases hyperglycemia in several animal models of diabetes, promotes a rise in the beta cell mass of nSTZ and STZ animals. However, the molecular mechanisms underlying this pancreas regeneration remain unknown. Therefore the objective of this study is to identify which genes are up or down regulated in the increase of the beta cell population of STZ rats treated with sodium tungstate.
Molecular mechanisms of tungstate-induced pancreatic plasticity: a transcriptomics approach.
No sample metadata fields
View SamplesBisphenol-A is a widespread endocrine disruptor chemical. In utero or perinatal exposure to bisphenol-A (BPA), leads to impaired glucose metabolism during adulthood. To investigate the consequences of the exposure to bisphenol-A during development in pancreatic beta-cell growth
Maternal Exposure to Bisphenol-A During Pregnancy Increases Pancreatic β-Cell Growth During Early Life in Male Mice Offspring.
Sex, Specimen part
View SamplesWe performed RNA sequencing to assess changes in gene expression in lung cancer cell lines with MET genetic alterations with or without co-occurrence of JAK2 inactivating mutations. Different treatments have been administrated to activate or inhibit selected pathways in order to define MET signature and IFNg (or JAK/STAT) signature. Overall design: Differential expression analysis of RNA sequencing of 4 different lung cancer cell lines with MET genetic alterations treated with different treatements to activate or inhibit selected pathways
<i>MET</i>-Oncogenic and <i>JAK2</i>-Inactivating Alterations Are Independent Factors That Affect Regulation of PD-L1 Expression in Lung Cancer.
Disease, Disease stage, Cell line, Treatment, Subject
View SamplesTranscriptome analysis of a population of control animals vs cisplatin-treated, in duplicate Overall design: A mixed population of worms representing all stages and growing under control conditions was exposed to 60 µg/ml of cisplatin for 24 hours at 20ºC. Treated and control samples weer collected in biological replicates.
Genetic and cellular sensitivity of <i>Caenorhabditis elegans</i> to the chemotherapeutic agent cisplatin.
Cell line, Treatment, Subject
View SamplesBrain metastasis is one of the most feared complications of cancer and the most common intracranial malignancy in adults. Its underlying mechanisms remain unknown. From breast cancer patients with metastatic disease we isolated cell populations that aggressively colonize the brain. Transcriptomic analysis of these cells yielded overlapping gene sets whose expression is selectively associated with brain metastasis. The expression of seventeen of these genes in primary breast tumors is associated with brain relapse in breast cancer patients. Some of these genes are also associated with metastasis to lung but not to liver, bone or lymph nodes, providing a molecular basis for the long-observed link between brain and lung metastasis. Among the functionally validated brain metastasis genes, the cyclooxigenase COX-2, the EGFR ligand HB-EGF, and the brain-specific 2-6 sialyltransferase ST6GALNAC5 mediate cancer cell passage through the blood-brain barrier. Other brain metastasis genes encode inflammatory factors and brain-specific proteolytic regulators, suggesting a multifaceted program for breast cancer colonization of the brain.
Genes that mediate breast cancer metastasis to the brain.
No sample metadata fields
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