Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Time-series single-cell RNA sequencing analysis of C1q-administrated murine lungs

ABSTRACT: Pulmonary fibrosis (PF) is a progressive fibrotic disease with a poor prognosis and suboptimal therapeutic options. The complement molecule C1q, which plays an important role in the phagocytic capacity of macrophages, has recently been reported to exacerbate several fibrosis-related diseases. On the other hand, there are still no reports in PF. Here, we analyzed detailed gene expression changes of each cell population in C1q-administrated murine lungs.

ORGANISM(S): Mus musculus

PROVIDER: GSE186269 | GEO | 2024/03/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis of C1q-administrated murine lungs

Project description:Pulmonary fibrosis (PF) is a progressive fibrotic disease with a poor prognosis and suboptimal therapeutic options. The complement molecule C1q, which plays an important role in the phagocytic capacity of macrophages, has recently been reported to exacerbate several fibrosis-related diseases. On the other hand, there are still no reports in PF. Here, we analyzed gene expression changes of C1q-administrated murine lungs.

2024-03-31 | GSE184445 | GEO

Transcriptome analysis of C1q treated lung fibroblasts

2024-03-31 | GSE184438 | GEO

Time-series single-cell RNA sequencing analysis of WT or CCR2-/- murine lungs in silica-induced pulmonary fibrosis model.

Project description:Pulmonary fibrosis (PF) is a progressive fibrotic disease with a poor prognosis and suboptimal therapeutic options. Macrophages have been implicated in PF; however, the roles of macrophage subsets, particularly interstitial macrophages (IM), remain unknown. To address this issue, we performed time-series single-cell RNA sequencing (scRNA-seq) analysis in silica-induced PF model mice and clarify the characteristics of IM. In addition, to elucidate the origin of IM, we used CCR2-/- mice which supressed classical monocyte infiltration.

2022-02-15 | GSE184854 | GEO

C1q elicited macrophage gene expression

Project description:We have data from a previous microarray experiment which shows that C1q elicits macrophages to express genes important for clearance of dead (apoptotic) cells. In this experiment we want to determine the signaling mechanism by which C1q is turning on macrophage gene expression. For our control (sample 1-3) we heated C1q to denature it so it is inactive. We also want to know which portion of C1q is responsible for activation the macrophage so we generated C1qtails (samples 4-5). We also have macrophages treated with the whole C1q molecule (7-9). And finally we have a cell line (J774) treated with C1q but does not activate the cells (samples 10-12). Bone marrow derived macrophages or J774 cells were adhered to heat inactivated C1q, C1q tails or C1q for 18 hours. Cells were harvested and RNA was isolated and converted to double stranded cDNA and subsequently labeled and hybridized onto NimbleGen mouse gene expression array [100718_MM9_EXP] using Nimblegen Hybridization system 4 according to manufacturerM-bM-^@M-^Ys instructions (Roche)

2014-07-10 | E-GEOD-48619 | biostudies-arrayexpress

C1q elicited macrophage gene expression

2014-07-10 | GSE48619 | GEO

Regulation of neuronal gene and miRNA expression by the complement protein C1q associated with neuroprotection

Project description:Identification of transcriptional profiles stimulated by the complement protein C1q in rat immature neurons associated with the C1q-dependent neuroprotection observed in vitro. Use of the unbiased whole genome microarray approach to identify genes regulated by C1q. Immature neurons grown in vitro for 3 days were stimulated with 10 nM C1q for 3h.

2011-03-07 | E-GEOD-18860 | biostudies-arrayexpress

Modulation of gene expression by complement protein C1q in amyloid-beta injured neurons

Project description:Complement protein C1q is induced after injury in the brain and during Alzheimer's disease and has been shown to protect against amyloid-beta induced neuronal death. In this study, we used microarray approach to identify the pathways modulated by C1q that are associated with neuroprotection. Immature rat cortical primary neurons are treated with fibrillar amyloid-beta peptides and/or C1q for 3h before RNA extraction and hybridization on rat Affymetrix microarrays. Supplementary file: Processed/normalized, probe-level signal intensities from neurons treated with amyloid-beta or C1q. Median signal intensity used as global normalization method, done with JMP genomics (v5.0) software.

2012-12-21 | E-GEOD-28886 | biostudies-arrayexpress

Regulation of neuronal gene and miRNA expression by the complement protein C1q associated with neuroprotection

2011-03-07 | GSE18860 | GEO

Complement factor C1q mediates sleep spindle disruption and epileptic spikes after mild brain injury

Project description:While traumatic brain injury (TBI) acutely disrupts the cortex, most TBI-related disabilities reflect secondary injuries that accrue over time. The thalamus is a likely site of secondary damage because of its reciprocal connections with the cortex. Using a mouse model of mild cortical injury that does not directly damage subcortical structures (mTBI), we found a chronic increase in C1q expression specifically in the corticothalamic circuit. Increased C1q expression co-localized with neuron loss and chronic inflammation, and correlated with disruption in sleep spindles and emergence of epileptic activities. Blocking C1q counteracted these outcomes, suggesting that C1q is a disease modifier in mTBI. Single-nucleus RNA sequencing demonstrated that microglia are the source of thalamic C1q. Since the corticothalamic circuit is important for cognition and sleep, which can be impaired by TBI, this circuit could thus be a new target for treating TBI-related disabilities.

2021-09-14 | GSE179541 | GEO

Modulation of gene expression by complement protein C1q in amyloid-beta injured neurons

2012-12-21 | GSE28886 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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