Inhibition of Mertk Receptor Signaling Enhances Bone Regeneration After Tooth Extraction
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ABSTRACT:
PROVIDER: PRJNA928354 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23241807_1.fastq.gz | Fastqsanger.gz | |||
| SRR23241807_2.fastq.gz | Fastqsanger.gz | |||
| SRR23241808_1.fastq.gz | Fastqsanger.gz | |||
| SRR23241808_2.fastq.gz | Fastqsanger.gz | |||
| SRR23241809_1.fastq.gz | Fastqsanger.gz |
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Project description:Regeneration of alveolar bone is an essential step in restoring healthy function following tooth extraction. Growth of new bone in the healing extraction socket can be variable and often unpredictable when systemic comorbidities are present, leading to the need for additional therapeutic targets to accelerate the regenerative process. This study examined the effect of signaling through the TAM (Tyro3, Axl, Mertk) family of receptors on alveolar bone regeneration. We performed RNA sequencing on human alveolar bone stem cells treated with a pan-TAM inhibitor in vitro. We also performed RNA sequencing on tissue isolated from the extraction socket of WT and Mertk-\- mice.
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Project description:Tolerogenic dendritic cells (tol-DCs) offer a promising therapeutic potential for autoimmune diseases. Tol-DCs have been reported to inhibit immunogenic responses, yet little is known about the mechanisms controlling their tolerogenic status, as well as associated specific markers. Here we show that the anti-inflammatory TAM receptor tyrosine kinase MERTK, is highly expressed on clinical grade dexamethasone-induced human tol-DCs and mediates their tolerogenic effect. Neutralization of MERTK in allogenic mixed lymphocyte reactions as well as autologous DC-T cell cultures leads to increased T cell proliferation and IFN-g production. Additionally, we identify a previously unrecognized non-cell autonomous regulatory function of MERTK expressed on DCs. Recombinant Mer-Fc protein, used to mimic MERTK on DCs, suppresses naïve and antigen-specific memory T cell activation. This mechanism is mediated by the neutralization of the MERTK agonist Protein S (PROS1) expressed by T cells. We find that MERTK and PROS1 are expressed in human T cells upon TCR activation and drive an autocrine pro-proliferative mechanism. Collectively, these results suggest that MERTK on tol-DCs directly inhibits T cell activation through the competition for PROS1 interaction with MERTK in the T cells. Targeting MERTK may provide an interesting approach to effectively increase or suppress tolerance for the purpose of immunotherapy. The complete database comprised the expression measurements of 54,675 genes for: immature (n=9), mature (n=7) and tolerogenic (n=8). Influence of treatment with dexamethasone (n=3) and LPS (n=2) are included.
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Project description:Tolerogenic dendritic cells (tol-DCs) offer a promising therapeutic potential for autoimmune diseases. Tol-DCs have been reported to inhibit immunogenic responses, yet little is known about the mechanisms controlling their tolerogenic status, as well as associated specific markers. Here we show that the anti-inflammatory TAM receptor tyrosine kinase MERTK, is highly expressed on clinical grade dexamethasone-induced human tol-DCs and mediates their tolerogenic effect. Neutralization of MERTK in allogenic mixed lymphocyte reactions as well as autologous DC-T cell cultures leads to increased T cell proliferation and IFN-g production. Additionally, we identify a previously unrecognized non-cell autonomous regulatory function of MERTK expressed on DCs. Recombinant Mer-Fc protein, used to mimic MERTK on DCs, suppresses naïve and antigen-specific memory T cell activation. This mechanism is mediated by the neutralization of the MERTK agonist Protein S (PROS1) expressed by T cells. We find that MERTK and PROS1 are expressed in human T cells upon TCR activation and drive an autocrine pro-proliferative mechanism. Collectively, these results suggest that MERTK on tol-DCs directly inhibits T cell activation through the competition for PROS1 interaction with MERTK in the T cells. Targeting MERTK may provide an interesting approach to effectively increase or suppress tolerance for the purpose of immunotherapy.
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Project description:Whole transcriptome RNA-seq analysis to measure group-wise RNA expression level of the MERTK gene in 3 healthy controls (known to be homozygous non-risk haplotype at MERTK gene locus) and to compare this to the group-wise RNA expression level of the MERTK gene in 5 Multiple Sclerosis-affected (MS-affected) individuals (known to be homozygous for the MS risk haplotype at the MERTK gene locus). We sequenced the whole transcriptome of 3 healthy control samples which were all homozygous for the MS non-risk haplotype at the MERTK gene. We also did the same RNA-seq protocol on 5 MS-affected subjects that were all homozygous for the Risk haplotype at the MERTK gene. All 8 samples were sequenced evenly across 3 lanes of an Illumina HiSeq NGS machine to remove any batch-type effects that could be caused by sequencing e.g. all cases in one lane and all controls in another lane.
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