During neonatal development, skeletal muscle grows dramatically by myonuclei accretion to existing fibers and hypertophic growth of fibers with protein synthesis.
An NF-κB--EphrinA5-Dependent Communication between NG2(+) Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates.
Specimen part
View SamplesDuring neonatal development, skeletal muscle grows dramatically by myonuclei accretion to existing fibers and hypertophic growth of fibers with protein synthesis. Overall design: To understand molecular mechanism underlying neonatal muscle growth, we used RNAseq to profile the global program of gene expressions especially involved in myoblast fusion, migration, and muscle fiber growth by itself. We used two biological replicates for each time point.
An NF-κB--EphrinA5-Dependent Communication between NG2(+) Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates.
Specimen part, Subject
View SamplesWe show that numerous miRNAs are transcriptionally up-regulated in papillary thyroid carcinoma (PTC) tumors compared with unaffected thyroid tissue. Among the predicted target genes of the three most upregulated miRNAs (miRs 221, 222 and 146b), only less than 15% showed significant downexpression in transcript level between tumor and unaffected tissue. The KIT gene which is known to be downregulated by miRNAs 221 and 222 displayed dramatic loss of transcript and protein in those tumors that had abundant mir-221, mir-222, and mir-146b transcript.
The role of microRNA genes in papillary thyroid carcinoma.
Specimen part
View SamplesPapillary thyroid cancers (PTC) that invade into local structures are associated with a poor prognosis, but the mechanisms for PTC invasion are incompletely defined limiting the development of new therapies. To characterize biological processes involved in PTC invasion, we analyzed the gene expression profiles of microscopically dissected intratumoral samples from central and invasive regions of seven widely invasive PTCs and normal thyroid tissue by oligonucleotide microarray and performed confirmatory expression and functional studies. In comparison to the central regions of primary PTCs, the invasive fronts overexpressed TGFbeta, NFkappaB and integrin pathway members, and regulators of small G-proteins and CDC42. Moreover, reduced levels of mRNAs encoding proteins involved in cell-cell adhesion and communication were identified, consistent with epithelial-to-mesenchymal transition (EMT). To confirm that aggressive PTCs were characterized by EMT, 35 additional PTCs were examined for expression of vimentin, a hallmark of EMT. Overexpression of vimentin was associated with PTC invasion and nodal metastasis. Functional, in vitro studies demonstrated that vimentin was required for the development and maintenance of both a mesenchymal morphology and invasiveness in thyroid cancer cells. We conclude that EMT is a common mechanism of PTC invasion and that vimentin regulates thyroid cancer EMT in vitro.
Gene expression and functional evidence of epithelial-to-mesenchymal transition in papillary thyroid carcinoma invasion.
Specimen part
View SamplesWe hypothesized that tissue genome-wide gene expression analysis, coupled with gene network analyses of differentially expressed genes, would provide novel insights into the pathogenesis of pulmonary sarcoidosis.
Gene expression profiling identifies MMP-12 and ADAMDEC1 as potential pathogenic mediators of pulmonary sarcoidosis.
Specimen part, Disease, Disease stage
View SamplesThe majority of NK cells (~90%) are phenotypically characterized as CD56dimCD16+, while the remaining are CD56brightCD16-. The cytotoxic CD56dimCD16+ NK subset expresses higher levels of chemokine receptors, and therefore is preferentially recruited to sites of inflammation. Encounters between CD56dimCD16+ NK cells with target cells and locally secreted inflammatory cytokines synergize to induce activation of this subset, leading to dramatically increased cytotoxic activity against target cells and abundant pro-inflammatory cytokine production often equivalent to that of the CD56brightCD16- population. The early recruitment of activation of CD56dimCD16+ NK cells to sites of inflammation raises many important questions regarding the potential immune functions of these cells that extend beyond their cytotoxic capabilities. This study has sought to elucidate the genetic profile of activated CD56dimCD16+ NK cells via a series of laboratory-based approaches coupled with a bioinformatics persective.
Gene expression profiling of the human natural killer cell response to Fc receptor activation: unique enhancement in the presence of interleukin-12.
Specimen part, Subject
View SamplesAbstract
Breast cancer-associated fibroblasts confer AKT1-mediated epigenetic silencing of Cystatin M in epithelial cells.
No sample metadata fields
View SamplesMENX is a rat multiple endocrine neoplasia syndrome caused by a homozygous mutation of the Cdkn1b gene, encoding p27Kip1. Affected rats develop adrenomedullary hyperplasia which progresses to pheochromocytoma with time (incidence 100%), and to extra-adrenal pheochromocytoma (paraganglioma) (68%).
Pheochromocytoma in rats with multiple endocrine neoplasia (MENX) shares gene expression patterns with human pheochromocytoma.
Sex, Age
View SamplesUnlike ovarian cancer, normal ovarian epithelium response to TGFb1 induced growth inhibition. This time course study tried to idenify genes that showed changes after additionof TGFb1 in immortalized ovarian surface epithelial cells (IOSE) which is derived from normal ovarian epithelial cells
An integrative ChIP-chip and gene expression profiling to model SMAD regulatory modules.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
NF-κB inhibition rescues cardiac function by remodeling calcium genes in a Duchenne muscular dystrophy model.
Age
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