Case story. A patient with massive infiltration of the visceral adipose tissue depot by BAT in a patient with a catecholamine secreting paraganglioma. BAT tissue was identified by protein expression of UCP1 (western blotting and immunostaining)
Chronic adrenergic stimulation induces brown adipose tissue differentiation in visceral adipose tissue.
Specimen part
View SamplesThe endocytic receptor megalin constitutes the main pathway for clearance of plasma proteins from the glomerular filtrate in the proximal tubules. However, little is know about the mechanisms that control receptor activity. A widely discussed hypothesis states that the intracellular domain (ICD) of megalin, released upon ligand binding, acts as a transcription regulator to suppress receptor expression - a mechanism proposed to safeguard the proximal tubules from protein overload. Here, we have put this hypothesis to the test by generating a mouse model co-expressing the soluble ICD and the full-length receptor. Despite pronounced expression in the proximal tubules, the ICD failed to exert any effects on renal proximal tubular function such as megalin expression, protein retrieval, or renal gene transcription. Thus, our data argue that the ICD does not play a role in regulation of megalin activity in vivo in the proximal tubules.
The soluble intracellular domain of megalin does not affect renal proximal tubular function in vivo.
Sex, Age, Specimen part
View SamplesThe ts-p53 E285K protein is a rare p53 mutant with temperature-sensitive (ts) loss of function characteristics. In cancer cells, which express ts-p53 E285K intriniscally, endogenous wild type p53 activity is reconstituted by appropriate cultivation temperature (permissive condition). At non-appropriate cultivation temperature (restrictive condition) this p53 mutant is inactive. The present study took advantage of this mechanism and employed IPH-926 lobular breast cancer cells and BT-474 ductal breast cancer cells, which both harbor endogenous ts-p53 E285K, for the transcriptional profiling of p53-responsive genes. This new approach eliminated the need for genetic modification or cytotoxic stimulation to achive a p53 response in the cells being investigated .
IPH-926 lobular breast cancer cells harbor a p53 mutant with temperature-sensitive functional activity and allow for profiling of p53-responsive genes.
Specimen part, Cell line, Treatment
View SamplesHuman solid tumors contain rare cancer side population (SP) cells, which expel the fluorescencent dye H33342 and display cancer stem cell characteristics. Transcriptional profiling of cancer SP cells isolated by H33342 fluorescence analysis is a newly emerging approach to discover cancer stem cell markers and aberrant differentiation pathways. Using Affymetrix expression microarrays this study investigated differential gene expression between SP and non-SP (NSP) cells isolated from the CAL-51 human mammary carcinoma cell line.
Down-regulation of the fetal stem cell factor SOX17 by H33342: a mechanism responsible for differential gene expression in breast cancer side population cells.
Specimen part
View SamplesGene expression in mice skin stimulated with 3 different cytokines
Thymic stromal lymphopoietin is up-regulated in the skin of patients with systemic sclerosis and induces profibrotic genes and intracellular signaling that overlap with those induced by interleukin-13 and transforming growth factor β.
Specimen part
View SamplesEach total RNA sample is hybridized to two different arrays: Affymetrix U133A (GPL96) and U133B (GPL97).
Previously unidentified changes in renal cell carcinoma gene expression identified by parametric analysis of microarray data.
No sample metadata fields
View SamplesPharmacogenomic identification of targets for adjuvant therapy with the topoisomerase poison camptothecin.
Pharmacogenomic identification of targets for adjuvant therapy with the topoisomerase poison camptothecin.
No sample metadata fields
View SamplesIn the present in vitro study, interactions between P. aeruginosa (sessile biofilms as well as planktonic cells) and PMNs were analyzed by means of DNA microarray based transcriptomics. We found that the P. aeruginosa wild type biofilms, in contrast to planktonic cultures and quorum sensing (QS) deficient strains, respond to PMN exposure in a rather aggressive manner. The response does not involve protective mechanisms such as those involved in oxidative stress. Rather it is dominated by QS controlled virulence determinants such as those encoded by pqs, phz, rhlAB, all of which are designed to cripple Eukaryotic cells including PMNs and macrophages. Our comparative analysis supports the view that QS plays a major role in mechanisms by which P. aeruginosa evades host defense systems.
Pseudomonas aeruginosa recognizes and responds aggressively to the presence of polymorphonuclear leukocytes.
No sample metadata fields
View SamplesBackground: Maize plants developed typical gray leaf spot disease (GLS) symptoms initiating at the lower leaves and progressing to upper leaves through the season. Leaf material was collected at 77 days after planting, at which stage there were a large number of GLS disease necrotic lesions on lower leaves (8% surface area on average determined by digital image analysis), but very few lesions and only at chlorotic stage on leaves above the ear (average of 0.2% lesion surface area). Method:To collect material that reflected a difference between C.zeina infected B73 leaves and control B73 leaf material, samples were collected from two lower GLS infected leaves (second and third leaf internode below ear) , and two upper leaves with minimal GLS symptoms (second and third internode above ear), respectively. The two lower leaves from each plant were pooled prior to RNA extraction, and the two upper leaves from each plant were pooled prior to RNA extraction. Upper and lower leaf samples from three maize B73 plants were subjected to RNA sequencing individually. The three maize plants were selected randomly as one plant per row from three rows of ten B73 plants each. Result: A systems genetics strategy revealed regions on the maize genome underlying co-expression of genes in susceptible and resistance responses, including a set of 100 genes common to the susceptible response of sub-tropical and temperate maize. Overall design: To collect material that reflected a difference between C.zeina infected B73 leaves and control B73 leaf material, samples were collected from two lower GLS infected leaves (second and third leaf internode below ear) , and two upper leaves with minimal GLS symptoms (second and third internode above ear), respectively. The two lower leaves from each plant were pooled prior to RNA extraction, and the two upper leaves from each plant were pooled prior to RNA extraction. Upper and lower leaf samples from three maize B73 plants were subjected to RNA sequencing individually. The three maize plants were selected randomly as one plant per row from three rows of ten B73 plants each.
Systems genetics reveals a transcriptional network associated with susceptibility in the maize-grey leaf spot pathosystem.
Subject
View SamplesOBJECTIVE: Systemic sclerosis (SSc)-related interstitial lung disease (ILD) is one of the leading causes of mortality. We undertook this study to analyze the gene expression of lung tissue in a prospective cohort of patients with SSc-related ILD and to compare it with that in control lungs and with 2 prospective clinical parameters in order to understand the molecular pathways implicated in progressive lung disease. METHODS: Lung tissue was obtained by open lung biopsy in 28 consecutive patients with SSc-related ILD and in 4 controls. High-resolution computed tomography (HRCT) and pulmonary function testing (PFT) were performed at baseline and 2-3 years after treatment based on lung histologic classification. Microarray analysis was performed, and the results were correlated with changes in the HRCT score (FibMax) and PFT values. Quantitative polymerase chain reaction (qPCR) and immunohistochemistry were used to confirm differential levels of messenger RNA and protein. RESULTS: Lung microarray data distinguished patients with SSc-related ILD from healthy controls. In the lungs of patients with SSc-related ILD who had nonspecific interstitial pneumonia (NSIP), expressed genes included macrophage markers, chemokines, collagen, and transforming growth factor (TGF)- and interferon (IFN)-regulated genes. Expression of these genes correlated with progressive lung fibrosis defined by the change in FibMax. Immunohistochemistry confirmed increased markers of collagen (COL1A1), IFN (OAS1 and IFI44), and macrophages (CCL18 and CD163), and the positive correlation with the change in FibMax was confirmed by qPCR in a larger group of SSc patients with NSIP. Several genes correlated with both the change in FibMax (r > 0.4) and the change in % predicted forced vital capacity (r < -0.1), including IFN and macrophage markers, chemokines, and heat-shock proteins. CONCLUSION: These results highlight major pathogenic pathways relevant to progressive pulmonary fibrosis in SSc-related ILD: macrophage emigration and activation, and up-regulated expression of TGF- and IFN-regulated genes
Association of Interferon- and transforming growth factor β-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis.
Specimen part, Disease, Disease stage, Subject
View Samples