Endothelial cells (ECs) express two members of the cadherin family, VE- and N-cadherin. While VE-cadherin induces EC homotypic adhesion, N-cadherin function in ECs remains largely unknown. EC-specific inactivation of either VE- or N-cadherin leads to early foetal lethality suggesting that these cadherins play a non-redundant role in vascular development.
Overlapping and divergent signaling pathways of N-cadherin and VE-cadherin in endothelial cells.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.
Specimen part, Disease, Disease stage
View SamplesOlsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.
Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.
Specimen part, Disease, Disease stage
View SamplesOlsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.
Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.
Specimen part, Disease, Disease stage
View SamplesThe Epidermal Growth Factor Receptor 2 (ERBB2 or HER2) is amplified and overexpressed in approximately 20% of invasive breast cancers and is associated with metastasis and poor prognosis. Here we describe the role of a constitutively active splice variant of HER2 (Delta-HER2) in human mammary epithelial cells. Overexpression of Delta-HER2 in human mammary cells decreased apoptosis and increased proliferation and expression of epithelial-to-mesenchymal markers. It also induced invasion in three-dimensional cultures and promoted tumorigenicity and metastasis in vivo. In contrast, similar overexpression of wild-type HER2 failed to evoke the same effects. Unbiased protein-tyrosine phosphorylation profiling revealed a significant increase in phosphorylation of several key signaling proteins upon Delta-HER2 expression, some of which not previously shown to belong to the HER2 pathway. In addition, microarray analysis revealed the expression of a set of genes specifically associated with Delta-HER2 expression. We found those genes to be highly expressed in ER-negative, high grade and metastatic primary breast tumors. Altogether, these results provide new insights into the function of a tumorigenic splice variant of HER2 and the signaling cascade deriving from its activity
Mammary tumor formation and metastasis evoked by a HER2 splice variant.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Age, Specimen part
View SamplesThe mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart.
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Age, Specimen part
View SamplesThe mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions, 4 biological replicates per condition
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
No sample metadata fields
View SamplesThe mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart.
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Specimen part
View SamplesThe mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions, 3 biological replicates per condition
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Age, Specimen part, Cell line, Subject
View Samples