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Combination therapy with low dose ruxolitinib and cyclosporine in murine immune bone marrow failure

ABSTRACT: Combination therapy with low dose ruxolitinib and cyclosporine in murine immune bone marrow failure

PROVIDER: PRJNA1005598 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25645300_1.fastq.gz	Fastqsanger.gz
	SRR25645300_2.fastq.gz	Fastqsanger.gz
	SRR25645301_1.fastq.gz	Fastqsanger.gz
	SRR25645301_2.fastq.gz	Fastqsanger.gz
	SRR25645302_1.fastq.gz	Fastqsanger.gz

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Low dose ruxolitinib plus cyclosporine to treat murine immune-mediated bone marrow failure

Project description:Background and methods: Ruxolitinib (RUX), a Jak1/2 inhibitor, has been reported to attenuate murine bone marrow failure recently. Its potential toxocicty of anemia and thrombocytopenia in human remains a concern. To minimize its potential toxoxicity, we tested therapeutic effectsof low dose ruxolitinib plus cyclosporine in murine model of immune-mediated bone marrow failure. Bone marrow CD8 and CD4 T cells were sorted from treated or untreated bone marrow failure mice. RNA-Seq and analysis was performed using SMART-Seq mRNA LP Kit (Takara) and the Illumina Novaseq6000, according to the Institute's protocols. Results: low dose of ruxolitinib plus cyclosporine improved pancytopenia and BM cellularity and decreased BM T cell infiltration in bone marrow failure mice. RNA sequencing demonstrated that low dose of ruxolitinib plus cyclosporine suppressed immune-related pathways in bone marrow infiltrated CD8 T cells and MHC-II expression in CD4 T cells compared with untreated mice. Conclusion: Our results demonstrate that low dose of ruxolitinib plus cyclosporine remains the efficacy in attenuation of disease and extending survival of immune-mediated bone marrow failure mice.

2024-05-08 | GSE240864 | GEO

Low dose ruxolitinib plus cyclosporine to treat murine immune-mediated bone marrow failure

Project description:Low dose ruxolitinib plus cyclosporine to treat murine immune-mediated bone marrow failure

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Ruxolitinib inhibits Cyclosporine-induced proliferation of cutaneous squamous cell carcinoma

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Combination therapy with low dose ruxolitinib and cyclosporine in murine immune bone marrow failure

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-08 | GSE240867 | GEO

Ruxolitinib inhibits Cyclosporine-induced proliferation of cutaneous squamous cell carcinoma

Project description:Organ transplant recipients (OTRs) on Cyclosporine A (CSA) are prone to catastrophic cutaneous squamous cell carcinoma (SCC). Allograft-sparing, cancer-targeting systemic treatments are unavailable. We have shown increased risk for catastrophic SCC in OTRs via CSA-mediated induction of Interleukin-22 (IL-22). Herein, we found CSA drives SCC proliferation and tumor growth through IL-22 and JAK/STAT pathway induction. We in turn inhibited SCC growth with an FDA-approved JAK 1/2 inhibitor, Ruxolitinib. In human SCC cells, greatest proliferative response to IL-22 and CSA treatment occurred in non-metastasizing lines. IL-22 treatment upregulated JAK1 and STAT1/3 in A431 SCC cells. JAK/STAT pathway genes were highly expressed in tumors from a cohort of CSA-exposed OTRs, and in SCC with high risk for metastasis. Compared to immunocompetent SCC, genes associated with innate immunity, response to DNA damage and p53 regulation were differentially expressed in SCC from OTRs. In nude mice engrafted with human A431 cells, IL-22 and CSA treatment increased tumor growth and upregulated IL-22 receptor, JAK1 and STAT 1/3 expression. Ruxolitinib treatment significantly reduced tumor volume and reversed the accelerated tumor growth. CSA and IL-22 exacerbate aggressive behavior in SCC. Targeting the IL-22 axis via selective JAK/STAT inhibition may reduce the progression of aggressive SCC in OTRs, without compromising immunosuppression. In this study, microarray data was used to compare normal skin to immunocompetent SCC, to transplant associated SCC (TSCC)

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Cyclosporine on fibroblast

Project description:To elucidate the gene profile of anti-fibroproliferative effects of cyclosporine, we added TGF-b and/or CsA to MRC5 (fetal human lung fibroblast) cell line. After 24 hours serum starvation, fibroblasts were treated with 3 ng/ml TGF-β1 and were treated with or without 2μg/ml Cyclosporine and effects were examined at 48 hours after treatment. Expression of three genes (IGFBP3, ID1 and PPARG) from this signature was quantified in the same RNA samples by real-time PCR. TGF-β and cyclosporine induced gene expression data was measured in MRC5 (fetal human fibroblast cell line) at 48h after treatments. The dose of TGF-β was 3 ng/ml and cyclosporine was 2 μg/ml. The comparison was done between four groups (control, TGF-β, cyclosporine and TGF-β plus cyclosporine).Three independent experiments were performed at each treatments using different samples for each experiment.

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Inhibition of CDK6 using Palbociclib in combination with Ruxolitinib markedly improves myelofibrosis in murine models

Project description:Myelofibrosis (MF) is a deadly blood neoplasia that presents the worst prognosis among myeloproliferative neoplasms (MPN). Expression of CDK6 is significantly elevated in MPN/MF hematopoietic progenitor cells. In this study, we investigated the efficacy of CDK4/6 inhibitor Palbociclib alone or in combination with Ruxolitinib in Jak2V617F and MPLW515L murine models of MF. Treatment of Palbociclib alone significantly reduced leukocytosis, splenomegaly and inhibited bone marrow fibrosis in Jak2V617F and MPLW515L mouse models of MF. Combined treatment of Palbociclib and Ruxolitinib resulted in normalization of peripheral blood leukocyte counts, marked reduction of spleen size and abrogation of bone marrow fibrosis in murine models of MF. Mechanistically, we show that Palbociclib treatment or depletion of CDK6 inhibits Aurora kinase, NF-κB and TGF-β signaling pathways in Jak2V617F mutant hematopoietic cells. Overall, our data suggest that Palbociclib in combination with Ruxolitinib may have therapeutic potential for treatment of MF.

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RNA-seq of human leukemia cell lines, MHH-CALL-4 and MUTZ-5, treated either with Ruxolitinib, FX1, or their combination.

Project description:CRLF2-rearranged acute lymphoblastic leukemia (ALL) is associated with poor clinical outcomes. Although JAK1/2 is activated in this type of ALL, treatment with JAK1/2 inhibitors is insufficient in inhibiting cell growth and inducing apoptosis. BCL6 upregulation upon JAK inhibition may account for this insufficiency. Therefore, we compared gene expression changes of two CRLF2-rearranged ALL cell lines, MHH-CALL-4 and MUTZ-5, treated with either ruxolitinib(a JAK1/2 inhibitor), FX1(a BCL6 inhibitor), their combination, or control.

2022-07-31 | E-MTAB-10755 | biostudies-arrayexpress

Toxicicty of ruxolitinib in normal mice

Project description:Background and methods: Ruxolitinib (RUX), a Jak1/2 inhibitor, has been reported to attenuate murine bone marrow failure recently. Its potential toxocicty of anemia and thrombocytopenia in human remains a concern. We tested the toxicity of ruxolitinib on hematopoiesis in normal mice by feeding the mice with RUX chow for 3 months. Bone marrow Lin-CD117+ cells were sorted from treated or untreated mice. RNA-Seq and analysis was performed using SMART-Seq mRNA LP Kit (Takara) and the Illumina Novaseq6000, according to the Institute's protocols. Results: Ruxolitinib reduced RBC and lymphocytes, but did not affect NEU and PLT in normal mice. RNA sequencing demonstrated that HSPCs from RUX-treated and untreated mice had overlapped transcriptome distribution in multiple dimentional scalling plot, indicating overall similarity at molecular level. Conclusion: Our results demonstrate that ruxolitinib has minimal toxicity on hematopoiesis in normal mice.

2024-05-08 | GSE240866 | GEO

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