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MRNA-seq to test effect of PYK2 inhibitor (defactinib) on LPS induced gene expression in WT and IRF5-/- BMDMs

ABSTRACT: mRNA-seq to test effect of PYK2 inhibitor (defactinib) on LPS induced gene expression in WT and IRF5-/- BMDMs

PROVIDER: PRJNA591950 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10540078_1.fastq.gz	Fastqsanger.gz
	SRR10540078_2.fastq.gz	Fastqsanger.gz
	SRR10540079_1.fastq.gz	Fastqsanger.gz
	SRR10540079_2.fastq.gz	Fastqsanger.gz
	SRR10540080_1.fastq.gz	Fastqsanger.gz

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mRNA-seq to test effect of PYK2 inhibitor (defactinib) on LPS induced gene expression in WT and IRF5-/- BMDMs

Project description:To investigate the specificity of Defactinib on IRF5 target genes we compare LPS-induced transcriptomes in WT and IRF5 KO BMDMs treated with either Defactinib or vehicle. Macrophage transcriptomic signature under PYK2 inhibition phenocopied IRF5 deficiency

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Bone Marrow Derived Macrophages(BMDMs) transcriptome analysis of control, LPS and LPS plus BHB group

Project description:Purpose: The purpose of this study was to compare the BMDMs transcriptome in the control LPS and LPS plus BHB group in order to identify the critical pathway that contributed to the inhibiton of BHB on M1 polarization. Methods: 1× 106 BMDMs were pre-treated with PBS or BHB for 1 hours before LPS administration. Four hours later, BMDMs were harvested for RNA preparation. Results: Among 16650 mapped genes, 7325 differentially expressed genes were identified, including 244 LPS inducible BHB down regulated named class A and 537 LPS repressed BHB up regulated genes named class B. The genes in class A were mainly TLR4 and TNF signaling pathway, while genes in class B were associated with negative regulation of transcription and NF-KB signaling. The GSEA showed that BHB have the similar profiles chnage on BMDMs with TSA. Conclusions: Our study revealed that BHB down regulated TLR4 and NF-KB pathway related genes to inhibited M1 polarization, and BHB have a similar effect on BMDMs with TSA through comparing the genetic changes of two substance caused in cells.

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Kinetics of LPS induction in wt and Cop1-ko BMDMs

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LPS time-course in WT and Stk40 KO BMDMs

Project description:Bone marrow was harvested from Rosa26CreER; Stk40+/+ (WT; n = 3) and Rosa26CreER; Stk40loxp/loxp (Stk40 KO; n = 3) mice and differentiated for 6 days in the presence of 100 nM 4-OHT to generate WT and Stk40 KO bone-marrow derived macrophages (BMDMs). 2. On day 7 following differentiation BMDMs were treated with 100 ng x ml-1 LPS and harvested at 0 hrs, 6 hrs, 16 hrs, and 32 hrs following LPS exposure. 3. The cells were snap-frozen at the time of harvest. RNA was extracted using the Qiagen RNeasy mini kit as per manufacturer’s protocol including the on-column DNase digestion. Groups: There are cells from 3 mice x 2 genotypes x 4 time points G1: WT 0 hr LPS G2: WT 6 hr LPS G3: WT 16 hr LPS G4: WT 32 hr LPS G5: Stk40 KO 0 hr LPS G6: Stk40 KO 6 hr LPS G7: Stk40 KO 16 hr LPS G8: Stk40 KO 32 hr LPS

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Project description:Interferon regulatory factor 5 (IRF5) plays a distinct role in the regulation of immune responses in health and disease and is a genetic risk factor several autoimmune conditions, including systemic lupus erythematosus, diabetes, arthritis and inflammatory bowel disease. IRF5 function as a transcription factor requires post-translational modifications of the protein such as phosphorylation. Though several upstream signalling regulators of IRF5 have been identified, there is as yet little understanding of how they control IRF5 activity or whether other unknown kinases are involved. In this study, we systematically searched for IRF5 kinases using a reporter-based method for screening a library of 365 inhibitors of protein kinases. Based on the pool of the identified IRF5-inhibiting compounds we have compiled a list of putative IRF5 kinases, which we tested in subsequent in vitro assays. Protein-tyrosine kinase 2-beta (Ptk2b or PYK2) was one of the top hits, capable of binding to and phosphorylating mouse IRF5 at tyrosine (Y) 171. We have shown that IRF5 recruitment to target genes and IRF5-dependent transcription was impaired in cells treated with highly selective PYK2 inhibitors or in PYK2-deficient cells. Moreover, expression of pro-inflammatory cytokines was blocked in the supernatants of human biopsies from inflamed colon of patients with ulcerative colitis and treated ex vivo with a PYK2 inhibitor. Thus, we have identified a major role for PYK2 in regulating the inflammatory response and mapped its activity to the IRF5 innate sensing pathways.

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