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Links from GEO DataSets

Items: 8

1.

AngII-regulated genes sensitive to CsA in Vascular Smooth muscle cells.

(Submitter supplied) We have employed whole genome microarray expression profiling as a platform to identify AngII -regulated genes sensitive to CsA. VSMC were treated with AngII with or without CsA ( as an inhibitor of the CN/NFAT pathway).
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
8 Samples
Download data: TXT
Series
Accession:
GSE31321
ID:
200031321
2.

Regulation of Angiotensin II Actions by Enhancers and Super-enhancers in Vascular Smooth Muscle Cells

(Submitter supplied) We have profiled Ang II regulated enhancer and super-enhancers in Rat Vascular smooth muscle cells using genomewide analysis of enhancer marks H3K27ac, H3K4me1 and super-enhancer mark BRD4.
Organism:
Rattus norvegicus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18694
14 Samples
Download data: TDF
Series
Accession:
GSE95067
ID:
200095067
3.

Expression data from PDGF-BB-treated rat aortic smooth muscle cells

(Submitter supplied) Unlike other terminally differentiated cell types, vascular SMCs display remarkable phenotypic plasticity. The adult, differentiated state is traditionally defined by expression of well-characterized SMC contractile genes. Extracellular cues, however, can induce contractile SMCs to remodel toward a synthetic state characterized by a spectrum of proliferative, migratory, and inflammatory phenotypes. We used whole-genome expression arrays to to identify genes associated with SMC phenotypic modulation.
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL1355
4 Samples
Download data: CEL
Series
Accession:
GSE19106
ID:
200019106
4.

Identification of MCIP1 as an ATF6-inducible ER Stress Response Gene in the Heart by Gene Expression Profiling

(Submitter supplied) We recently found that the endoplasmic reticulum (ER) stress response (ERSR) is activated in surviving cardiac myocytes in a mouse model of in vivo myocardial infarction. ATF6 is an ER stress-activated transcription factor that induces ERSR genes, some of which encode proteins that may protect against ischemic damage. However, few ERSR genes have been identified in the heart, and there have been no gene expression profiling studies of ATF6-inducible genes, in vivo. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3667
Platform:
GPL1261
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE8322
ID:
200008322
5.
Full record GDS3667

Transgenic model of selective ATF6 activation: heart

Analysis of heart left ventricle from ATF6-MER transgenic (TG) males, treated with tamoxifen to confer activation to ATF6-MER. Activating ATF6 protects the heart of TG animals from endoplasmic reticulum stress. Results provide insight into molecular mechanisms underlying this protective effect.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 agent, 2 genotype/variation sets
Platform:
GPL1261
Series:
GSE8322
12 Samples
Download data: CEL, CHP
6.

EP4-Tg aortic VSMCs: Control vs PGE2

(Submitter supplied) Microarray data of EP4-Tg VSMCs with or without 24 h of PGE2 (1 µmol/L)
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL21810
4 Samples
Download data: CSV, TXT
Series
Accession:
GSE146758
ID:
200146758
7.

Cerulein induced acute pancreatitis in C57Bl/6J

(Submitter supplied) There still is a lack of specific, early markers for acute pancreatitis. We used the gene expression profiling Affimetrix mouse gene 1.0 ST arrays (Affymetrix , Inc. Santa Clara, CA), to cmpare the gene expression between control mice and mice with induced experimental acute pancreatitis, in order to identify new potential biomarkers of acute pancreatitis.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
11 Samples
Download data: CEL
Series
Accession:
GSE109227
ID:
200109227
8.

TWEAK/Fn14 axis is a therapeutic target for post-angioplasty restenosis

(Submitter supplied) Aim: Next generation sequencing-based methods were performed to identify genes and pathways regulated by TWEAK in VSMCs Methods: Using a gene-set enrichment method, we found a functional module involved in cell proliferation defined as the minimal network connecting top TWEAK up-regulated genes. Results: TWEAK increased the number of VSMCs in S phase and the total number of proliferative cells. Conclusions: Our data define a major role of TWEAK/Fn14 in the control of VSMCs proliferation and migration during neointimal hyperplasia after wire injury in mice, and identify TWEAK/Fn14 as a potential target for treating restenosis after angioplasty. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: XLSX
Series
Accession:
GSE114166
ID:
200114166
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