Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA94155 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:PI-3K inhibitor (LY294002) was added to quiescent fibroblasts 30 minutes prior growth factor/serum treatments. The role of PI-3K pathway was thus monitored by comparing with untreated samples. Keywords: time course, growth factor response, cell line comparison
2006-04-12 | GSE3902 | GEO
Project description:Response of quiescent human fibroblasts to different growth factors and serum
| PRJNA94153 | ENA
Project description:Quiescent human fibroblasts (2091 and Wi-38) were stimulated with different growth factors and serum. Cells were collected at 6 different time points followed by global transcriptional profiling. Keywords: time course, growth factor response, cell line comparison
2006-04-12 | GSE3901 | GEO
Project description:A balance between angiogenesis inducers and inhibitors in the microenvironment controls the rate of new blood vessel formation. We hypothesized that fibroblasts, an important cellular constituent of the tissue stroma, secrete molecules that contribute to this balance. We further hypothesized that fibroblasts secrete molecules that promote angiogenesis when they are in a proliferative state and molecules that inhibit angiogenesis when they are not actively cycling (quiescent). Microarray analysis revealed that angiogenesis inducers and inhibitors are regulated as fibroblasts transition into a quiescent state and reenter the cell cycle in response to changes in serum. To assess whether changes in transcript levels result in changes in the levels of secreted proteins, we collected conditioned medium from proliferating and quiescent fibroblasts and performed immunoblotting for selected proteins. Secreted protein levels of the angiogenesis inhibitor pigment epithelium derived factor (PEDF) were higher in quiescent than proliferating fibroblasts. Conversely, proliferating fibroblasts secreted increased levels of the angiogenesis inducer vascular endothelial growth factor-C (VEGF-C). For the angiogenesis inhibitor thrombospondin-2, quiescent cells secreted a prominent 160 kDa form in addition to the 200 kDa form secreted by proliferating and restimulated fibroblasts. Using immunohistochemistry we discovered that fibroblasts surround blood vessels and that the angiogenesis inhibitor PEDF is expressed by quiescent fibroblasts in uterine tissue, supporting a role for PEDF in maintaining quiescence of the vasculature. This work takes a new approach to the study of angiogenesis by examining the expression of multiple angiogenesis regulators secreted from a key stromal cell, the fibroblast. mRNAs were analyzed by two color microarray from a human neonatal dermal fibroblasts cell line over a timecourse of serum starvation and serum restimulation.
2012-12-03 | E-GEOD-42681 | biostudies-arrayexpress
Project description:Growth recovery from serum starvation requires the activation of PI3 kinase (PI3K)- PDK1-Akt-mTOR pathways. Claspin plays multiple important roles in regulation of DNA replication as a mediator for the cellular response to replication stress, an integral replication fork factor that facilitates replication fork progression and a factor that promotes initiation by recruiting Cdc7 kinase. Here, we report a novel role of Claspin in growth recovery from serum starvation. In the absence of Claspin, cells do not proceed into S phase and eventually die. Claspin interacts with PI3K and mTOR, and is required for activation of PI3K-PDK1-mTOR and for that of mTOR downstream factors, p70S6K and 4E-BP1, but not for p38 MAPK cascade during the recovery from serum starvation. PDK1 interacts with Claspin, notably with CKBD, in a manner dependent on phosphorylation of the latter protein, and is required for interaction of mTOR with Claspin. p53 and ROS (Reactive Oxygen Species) inhibitors increased survival of Claspin-deficient cells released from serum starvation. Thus, Claspin plays a novel role as a mediator/protein platform for nutrition-induced proliferation/survival signaling by activating the mTOR pathway.
2022-04-15 | GSE200669 | GEO
Project description:A balance between angiogenesis inducers and inhibitors in the microenvironment controls the rate of new blood vessel formation. We hypothesized that fibroblasts, an important cellular constituent of the tissue stroma, secrete molecules that contribute to this balance. We further hypothesized that fibroblasts secrete molecules that promote angiogenesis when they are in a proliferative state and molecules that inhibit angiogenesis when they are not actively cycling (quiescent). Microarray analysis revealed that angiogenesis inducers and inhibitors are regulated as fibroblasts transition into a quiescent state and reenter the cell cycle in response to changes in serum. To assess whether changes in transcript levels result in changes in the levels of secreted proteins, we collected conditioned medium from proliferating and quiescent fibroblasts and performed immunoblotting for selected proteins. Secreted protein levels of the angiogenesis inhibitor pigment epithelium derived factor (PEDF) were higher in quiescent than proliferating fibroblasts. Conversely, proliferating fibroblasts secreted increased levels of the angiogenesis inducer vascular endothelial growth factor-C (VEGF-C). For the angiogenesis inhibitor thrombospondin-2, quiescent cells secreted a prominent 160 kDa form in addition to the 200 kDa form secreted by proliferating and restimulated fibroblasts. Using immunohistochemistry we discovered that fibroblasts surround blood vessels and that the angiogenesis inhibitor PEDF is expressed by quiescent fibroblasts in uterine tissue, supporting a role for PEDF in maintaining quiescence of the vasculature. This work takes a new approach to the study of angiogenesis by examining the expression of multiple angiogenesis regulators secreted from a key stromal cell, the fibroblast.
2012-12-03 | GSE42681 | GEO
Project description:Myopalladin promotes muscle growth through modulation of the serum response factor pathway
| PRJNA513343 | ENA
Project description:Quiescent keratinocytes and fibroblasts: radiation dose response
| PRJNA111465 | ENA
Project description:Response of quiescent human fibroblasts to miR-22 overexpression
| PRJNA183136 | ENA
Project description:ELABELA Is an Endogenous Growth Factor that Sustains hESC Self-Renewal Via the PI3K/AKT Pathway
| PRJNA292549 | ENA