Mouse kidney arteriolar smooth muscle cells derived from the renin cell lineage: control vs. forskolin treatment to induce renin expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE31780 | GEO | 2012/02/25
SECONDARY ACCESSION(S): PRJNA145289
REPOSITORIES: GEO
Similar Datasets
Project description:miRNA profiling of mouse kidney arteriolar smooth muscle cells (aSMCs) of the renin lineage comparing control untreated cells with cells treated with forskolin to induce renin expression. Two condition experiment: control untreated aSMCs vs forskolin treated aSMCs; Biological replicates: control 3, treated 3; independently grown and harvested. One replicate per array.
2012-02-25 | E-GEOD-31780 | biostudies-arrayexpress
Project description:Normally functioning brains depend on neurovascular coupling (NVC) and its dysfunction underlies many neuropathologies. Although cell-type specificity has been implicated in NVC, how active neural information is specifically conveyed to the targeted arterioles in the brain remains poorly understood. Here, using two-photon focal optogenetics in the mouse cerebral cortex, we demonstrated that single glutamatergic axons dilate their innervating arterioles via synaptic-like transmission between neural-arteriolar smooth muscle cells junction (NsMJ). The presynaptic parental-daughter bouton makes dual innervations on postsynaptic dendrites and on arteriolar smooth muscles cells (aSMCs), which expressed many types of neuromediator receptors, including glutamate NMDA receptor subunit 1 (Grin1). Disruption of NsMJ transmission, by aSMC specific knockout of GluN1, diminished the optogenetic and whisker stimulation-caused functional hyperemia. Notably, the absence of GluN1 subunit in aSMCs protected the brain atrophy from cerebral ischemia by preventing Ca2+ overload in aSMCs during arteriolar constriction caused by the ischemia-induced spreading depolarization. Our findings reveal that NsMJ transmission drives neurovascular coupling and also open up a new avenue for studying stroke.
2023-10-05 | GSE213026 | GEO
Project description:Libraries were made to compare the transcriptome of renin lineage cells (RLCs) from wild-type versus ren knockout zebrafish kidneys. RLCs were FAC sorted from pooled kidneys of ren+/+ or ren-/- zebrafish, which carried ren:RFP and acta2:EGFP reporter genes, allowing the isolation of renin-expressing cells and smooth muscle cells.
2022-06-10 | E-MTAB-11079 | biostudies-arrayexpress
Project description:Mouse kidney arteriolar smooth muscle cells derived from the renin cell lineage: control vs. forskolin treatment to induce renin expression
| PRJNA145289 | ENA
Project description:Arterial smooth muscle cells (ASMCs) undergo phenotypic changes during development and pathological processes in vivo and during cell culture in vitro. Our previous studies demonstrated that retrovirally-mediated expression of the versican V3 splice variant (V3) that lacks glycosaminoglycan chains by ASMCs retards cell proliferation and migration in vitro and reduces neointimal thickening, macrophage and lipid accumulation in animal models of vascular injury and atherosclerosis. However, the molecular pathways induced by V3 expression that are responsible for these changes are not yet clear. In the present study, we employed a microarray approach to examine how expression of V3 induced changes in gene expression and the molecular pathways in ASMCs. We found that forced expression of V3 by ASMCs affected expression of 521 genes by more than 1.5 fold. Gene ontology (GO) analysis shows that components of extracellular matrix were the most significantly affected by V3 expression, indicating that V3 expression elicits profound remodeling of extracellular matrix. In addition, genes regulating the formation of the cytoskeleton which also serve as markers of contractile smooth muscle cells were significantly upregulated. On the other hand, components of the complement system, chemokines, chemokine receptors, and transcription factors crucial for regulating inflammatory processes were among the genes most downregulated. Consistently, we found that the level of myocardin, a key transcription factor promoting contractile ASMC phenotype, was greatly increased while proinflammatory transcription factors NFkappaB1 and C/EBPβ were significantly attenuated in V3-expressing SMCs. Such results indicate that V3 expression reprograms ASMC into differentiated and anti-inflammatory phenotypes. Overall, these findings demonstrate that expression of V3 reprograms ASMCs promoting anti-inflammatory and differentiated smooth muscle cell phenotypes potentially by altering cell-ECM interaction and focal adhesion signaling pathways. Fischer rat ASMCs were transduced with either a retroviral vector expressing the Versican V3 splice variant (LV3SN) or an empty control vector (LXSN) in three independent experiments. In the first experiment, V3 and control transductions were performed with four technical replicates. In the subsequent two experiments, individual transductions were done for the V3 or control treatments. For data analysis, the technical replicates from the first experiment were averaged, and then data from the three experiments was evaluated in a paired manner.
2015-07-07 | E-GEOD-66624 | biostudies-arrayexpress
Project description:We generated genome-wide methylation data from primary cultured airway smooth muscle cells (ASMCs) exposed to IL-13, IL-17, IL-13+IL-17, and vehicle. This data was generated in combination with genome-wide expression data from the same individuals.
2020-03-30 | GSE146376 | GEO
Project description:We generated genome-wide expression data from primary cultured airway smooth muscle cells (ASMCs) exposed to IL-13, IL-17, IL-13+IL-17, and vehicle. This data was generated in combination with genome-wide methylation data from the same individuals.
2020-03-30 | GSE146374 | GEO
Project description:Arterial smooth muscle cells (ASMCs) undergo phenotypic changes during development and pathological processes in vivo and during cell culture in vitro. Our previous studies demonstrated that retrovirally-mediated expression of the versican V3 splice variant (V3) that lacks glycosaminoglycan chains by ASMCs retards cell proliferation and migration in vitro and reduces neointimal thickening, macrophage and lipid accumulation in animal models of vascular injury and atherosclerosis. However, the molecular pathways induced by V3 expression that are responsible for these changes are not yet clear. In the present study, we employed a microarray approach to examine how expression of V3 induced changes in gene expression and the molecular pathways in ASMCs. We found that forced expression of V3 by ASMCs affected expression of 521 genes by more than 1.5 fold. Gene ontology (GO) analysis shows that components of extracellular matrix were the most significantly affected by V3 expression, indicating that V3 expression elicits profound remodeling of extracellular matrix. In addition, genes regulating the formation of the cytoskeleton which also serve as markers of contractile smooth muscle cells were significantly upregulated. On the other hand, components of the complement system, chemokines, chemokine receptors, and transcription factors crucial for regulating inflammatory processes were among the genes most downregulated. Consistently, we found that the level of myocardin, a key transcription factor promoting contractile ASMC phenotype, was greatly increased while proinflammatory transcription factors NFkappaB1 and C/EBPβ were significantly attenuated in V3-expressing SMCs. Such results indicate that V3 expression reprograms ASMC into differentiated and anti-inflammatory phenotypes. Overall, these findings demonstrate that expression of V3 reprograms ASMCs promoting anti-inflammatory and differentiated smooth muscle cell phenotypes potentially by altering cell-ECM interaction and focal adhesion signaling pathways.
2015-07-07 | GSE66624 | GEO
Project description:The long term objective is to create an encyclopedia of the expression levels of all genes in multiple components of the developing kidney. The central thesis is straightforward. The combination of fluorescent activated cell sorting (FACS) plus microarray analysis offers a powerful, efficient and effective method for the creation of a global gene expression atlas of the developing kidney. Microarrays with essentially complete genome coverage can be used to quantitate expression levels of every gene in FACS isolated components of the developing kidney. The ensuing rapid read-out provides an expression atlas that is more sensitive, more economical and more complete than would be possible by in situ hybridizations alone Renin-GFP transgenic mice were utilized to isolate renin producing cells from the kidneys of either P0 neonatal pups or Adult mice. Renin producing cells were isolated from the kidney by fluorescent activated cell sorting (FACS). RNA was isolated from FACS sorted cells and the gene expression profiles were determined by microarrays.
2010-07-16 | E-GEOD-17138 | biostudies-arrayexpress
Project description:Renin cells are essential for survival. They control the morphogenesis of the kidney arterioles, and the composition and volume of our extracellular fluid, arterial blood pressure, tissue perfusion, and oxygen delivery. Renin cells and associated arteriolar cells descend from FoxD1+ progenitor cells. The chromatin states and transcription factors that determine the differentiation of these cells into those that compose the kidney vasculature are unknown. To answer these questions, we isolated progenitors and their descendants at different embryonic and postnatal stages, and using integrated scRNA-seq and scATAC-seq established the developmental trajectory that leads to the mosaic of cells that compose the kidney arterioles. We constructed a single-cell atlas of chromatin accessibility and gene expression profiles-including the critical transcription factors that determine the identity and fate of the mosaic of cells that occur during kidney vascular development. Furthermore, we identified the factors that determine the elusive, myo-endocrine adult renin-secreting juxtaglomerular cell.
2023-07-06 | GSE218569 | GEO