Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq analysis of arterial smooth muscle cells (ASMCs) isolated from the lung, heart, aorta, stomach, intestine, kidney and bladder

ABSTRACT: None of the currently available Cre recombinase-expressing mouse lines allows exclusive and specific manipulation of arterial smooth muscle cells (ASMCs). To enable targeted manipulation of ASMCs, we generated two knock-in mouse lines: one carrying a Dre recombinase cassette inserted into the Cspg4 locus (Cspg4-Dre) and another carrying a Rox-Stop-Rox-CreER cassette inserted into the Acta2 locus (Acta2-Rox-CreER). These two lines (hereafter referred to as ASMC-effector mice) were crossed with R26-LoxP-GFP reporter animals, and the offspring were treated with three doses of tamoxifen to induce recombination. This strategy resulted in robust and specific labeling of ASMCs in virtually all arteries examined.To further enhance specificity, we generated an additional line in which a tamoxifen-inducible DreERT cassette was inserted into the Cspg4 locus. This Cspg4-DreERT line also enabled specific labeling of ASMCs in distinct organs.

ORGANISM(S): Mus musculus

PROVIDER: GSE301477 | GEO | 2026/04/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq analysis of non-vascular smooth muscle cells (NVSMCs) isolated from the lung, intestine and bladder

Project description:None of the currently available Cre recombinase-expressing mouse lines allows for exclusive and specific manipulation of non-vascular smooth muscle cells (NVSMCs). To address this, we focused on the Chrm2 gene, which encodes the M2 muscarinic acetylcholine receptor (M2R), a G protein-coupled receptor (GPCR) previously reported to be expressed selectively in NVSMCs and also in CD45-positive immune cells. In contrast, Acta2 is broadly and strongly expressed in all smooth muscle cells (SMCs), including both vascular and non-vascular populations. To achieve specific labeling of NVSMCs, we generated NVSMC-effector mice by combining Chrm2-Dre with Acta2-Rox-CreER and R26-LoxP-GFP alleles. Following tamoxifen administration, we observed robust GFP fluorescence specifically in NVSMCs of the lung, stomach, and intestine. Notably, GFP labeling was virtually absent in vascular SMCs across multiple organs, confirming the specificity of this genetic strategy.

2026-04-11 | GSE301480 | GEO

RNA-seq analysis of pulmonary arterial smooth muscle cells (PASMCs) and bronchial smooth muscle cells (BSMCs) after pulmonary arterial hypertension (PAH) treatment

Project description:Previous studies to determine transcriptional changes in PASMCs during PAH were affected by the inevitable contamination with BSMCs and venous SMCs. To specific target ASMCs, we generated an ASMC-effector mouse line by combining Cspg4/Acta2 intersectional genetics, enabling specific targeting of vascular SMCs, including PASMCs. To target non-vascular SMCs, including BSMCs, we generated the NVSMC-effector mouse line using Chrm2/Acta2 intersectional genetics. The development of ASMC-effector mice, excluding venous and BSMCs, enabled us to avoid such problems and determine PASMC-specific reactions after induction of PAH.

2026-04-11 | GSE301479 | GEO

RNA-seq analysis of lung smooth muscle cells

Project description:Lung smooth muscle cells are including bronchiolar and vascular smooth muscle cells. In order to get adult lung smooth muscle cells, we use transgenic mouse line with smooth muscle actin creERT2, which is a transgenic cre recombinase in Acta2 (contractile smooth muscle cell gene). This mouse line also contains a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the ROSA26 locus. This mouse line express robust tdTomato fluorescence following cre-mediated recombination after Tamoxifen injection.

2020-05-01 | GSE148008 | GEO

Guiding T lymphopoiesis from pluripotent stem cells by defined transcription factors [iR_iHEC]

Project description:We inserted the inducible expression cassette of Runx1 into the Rosa26 locus of embryonic stem cells. Based on a modified protocol for HEC induction from PSC, we successfully generated iHEC Under the haematopoietic induction process (iR-HEC).

2020-07-31 | GSE129444 | GEO

RNA sequencing on stem cell-derived endothelial cells

Project description:We generated a stable H9 stem cell line with an FRT cassette in the AAVS1 safe harbour locus, which allows recombinase-mediated cassette exchange. We used this system to overexpress ETV2, a master regulator of endothelial fating. This study contains gene expression characterisation of endothelial cells derived through overexpression of ETV2, at day 10 of differentiation. These endothelial cells are referred to as ETV2-ECs.

2021-01-14 | GSE156009 | GEO

An approach to intersectionally target mature enteroendocrine cells in the small intestine of mice

Project description:Enteroendocrine cells (EECs) constitute only a small proportion of Villin-1 (Vil1)-expressing intestinal epithelial cells (IECs) of the gastrointestinal tract; yet, in sum, they build the largest endocrine organ of the body, with each of them storing and releasing a distinct set of peptides for the control of feeding behavior, glucose metabolism, and gastrointestinal motility. Like all IEC types, EECs are continuously renewed from intestinal stem cells in the crypt base and terminally differentiate into mature subtypes while moving up the crypt-villus axis. Interestingly, EECs adjust their hormonal secretion according to their migration statues as EECs receive altering differentiation signals along the crypt-villus axis and thus undergo functional readaptation. Cell-specific targeting of mature EEC subtypes by specific promoters is challenging because the expression of EEC-derived peptides and their precursors are not limited to EECs but are also found in other organs, such as the brain (e.g. Cck and Sst) as well as in the pancreas (e.g. Sst and Gcg). Here, we describe an intersectional genetic approach that enables cell type-specific targeting of functionally distinct EEC subtypes by combining a newly-generated Dre-recombinase expressing mouse line (Vil1-2A-DD-Dre) with multiple existing Cre-recombinase mice, and mouse strains with rox and loxP sites flanked stop cassettes for transgene expression. We found that transgene expression in triple-transgenic mice is highly specific in I, but not D and L cells in the apical villi of the small intestine. The targeting of EECs only in villi is likely caused by the intrinsic Vil1 expression, limiting our Vil1-2A-DD-Dre mouse line and the intersectional genetic approach described here for the investigation of mature EECs.

2024-01-15 | GSE250433 | GEO

Estrogen Receptor beta cistrome in mouse endometriotic tissue.

Project description:Estrogen Receptor beta (ERβ) has an essential role in endometriosis progression. However, the role of genomic ERβ in the pathogenesis of endometriosis is not elucidated, yet. To get ERβ cistrome, we employed endometrium specific ERβ overexpression (ERBOE) mouse model by crossing mouse having pCAG promoter-loxPSTOPloxP-ERβ cassette with PRCre knockin mice that Cre recombinase cDNA was inserted into exon 1 of PR gene. Using ERBOE mouse model, we determine ERβ-cistrome in endometriotic lesions and eutopic endometrium of mice with endometriosis.

2019-09-12 | GSE114047 | GEO

Transcription profiling by array of mouse wild type and Nkx2.2 knock-out embryos

Project description:The goal: Investigate the genes differentlly expressed during pancreas development. The model: The Nkx2.2 null allele was generated using standard homologous recombination in ES cells. The Pgk:NeoR cassette was inserted into a 4.4 Kb deletion of the Nkx2.2 genomic locus, effectively deleting both coding exons. The mice are maintained on a Swiss Black strain background.

2011-08-27 | E-MTAB-356 | biostudies-arrayexpress

Jak2V617F Reversible Activation Shows an Essential Requirement for Jak2V617F in Myeloproliferative Neoplasms

Project description:Janus kinases (JAKs) mediate cytokine signaling, cell growth and hematopoietic differentiation. Gain-of-function mutations activating JAK2 signaling are seen in the majority of myeloproliferative neoplasm (MPN) patients, most commonly due to the JAK2V617F driver allele. While clinically-approved JAK inhibitors improve symptoms and outcomes in MPNs, remissions are rare, and mutant allele burden does not substantively change with chronic JAK inhibitor therapy in most patients. This has been postulated to be due to incomplete dependence on constitutive JAK/STAT signaling, alternative signaling pathways, and/or the presence of cooperating disease alleles; however we hypothesize this is due to the inability of current JAK inhibitors to potently and specifically abrogate mutant JAK2 signaling. We therefore developed a conditionally inducible mouse model allowing for sequential activation, and then inactivation, of Jak2V617F from its endogenous locus using a Dre-rox/Cre-lox dual orthogonal recombinase system. Deletion of oncogenic Jak2V617F abrogates the MPN disease phenotype, induces mutant-specific cell loss including in hematopoietic stem/progenitor cells, and extends overall survival to an extent not observed with pharmacologic JAK inhibition. Furthermore, reversal of Jak2V617F in MPN cells with antecedent loss of Tet2 abrogates the MPN phenotype and inhibits mutant stem cell persistence suggesting cooperating epigenetic-modifying alleles do not alter dependence on mutant JAK/STAT signaling. Our results suggest that mutant-specific inhibition of JAK2V617F represents the best therapeutic approach for JAK2V617F-mutant MPN and demonstrate the therapeutic relevance of a dual-recombinase system to assess mutant-specific oncogenic dependencies in vivo.

2022-05-25 | GSE203464 | GEO

miR-99a let7c cluster

Project description:To investigate the function of miR99a/let-7c miRNAs during cardiomyogenesis, we decided to perturb their expression using transgenic mES cell lines the corresponding precursors (pre-miRNA) of the two miRNAs. We used the ROSA-TET system (EB3 tet off), in which the transgene is inserted in Rosa26 locus by Cre recombinase. We generated three different clones both miRNAs let-7c/miR-99a and those only one miRNA, namely the let-7cdeletedmiR-99a and the miR-99adeletedlet-7c.

2013-07-01 | E-MEXP-3748 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data