Transcriptome analysis of C1q treated lung fibroblasts
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA764675 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15971103.fastq.gz | Fastqsanger.gz | |||
| SRR15971104.fastq.gz | Fastqsanger.gz | |||
| SRR15971105.fastq.gz | Fastqsanger.gz | |||
| SRR15971106.fastq.gz | Fastqsanger.gz | |||
| SRR15971107.fastq.gz | Fastqsanger.gz |
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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.
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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)
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