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Improved Efficacy of MSCs stably expressing CXCR4 and IL-10 in a xenogeneic Graft versus Host Disease Mouse Model

ABSTRACT: Improved Efficacy of MSCs stably expressing CXCR4 and IL-10 in a xenogeneic Graft versus Host Disease Mouse Model

PROVIDER: PRJNA925908 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23168574_1.fastq.gz	Fastqsanger.gz
	SRR23168574_2.fastq.gz	Fastqsanger.gz
	SRR23168575_1.fastq.gz	Fastqsanger.gz
	SRR23168575_2.fastq.gz	Fastqsanger.gz
	SRR23168576_1.fastq.gz	Fastqsanger.gz

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Improved Efficacy of MSCs stably expressing CXCR4 and IL-10 in a xenogeneic Graft versus Host Disease Mouse Model

Project description:Previous clinical trials have shown that mesenchymal stromal cells (MSCs) can modulate graft versus host disease (GvHD) after allogeneic hematopoietic transplantation, although with variable efficacy. To improve the anti-GvHD effect of these cells, adipose tissue derived-human MSCs (Ad-MSCs) were transduced with a lentiviral vector conferring stable expression of CXCR4, a molecule involved in cell migration to inflamed sites, and IL-10, a cytokine with potent anti-inflammatory properties. In vitro experiments showed that the expression of these molecules in Ad-MSCs (named CXCR4-IL10-MSCs) efficiently enhanced their migration towards SDF‐1α and also improved their immunomodulatory properties compared to unmodified Ad‐MSCs (WT‐MSCs). Moreover, using a humanized GvHD mouse model, CXCR4-IL10-MSCs showed improved therapeutic effects, which were confirmed by histopathologic analysis in the target organs. Additionally, compared to WT-MSCs, CXCR4-IL10-MSCs induced a more marked reduction in the number of pro-inflammatory Th1 and Th17 cells, a higher polarization towards an anti-inflammatory T cell profile (CD3+-IL10+ cells), and increased the number of regulatory T and B cells. Our in vitro and in vivo studies strongly suggest that CXCR4-IL10-MSCs should constitute an important new generation of MSCs for the treatment of GvHD in patients transplanted with allogeneic hematopoietic grafts.

2023-01-25 | GSE223390 | GEO

Improved efficacy of mesenchymal stromal cells stably expressing CXCR4 and IL-10 in a xenogeneic graft versus host disease mouse model.

Project description:Previous clinical trials have shown that mesenchymal stromal cells (MSCs) can modulate graft versus host disease (GvHD) after allogeneic hematopoietic transplantation, although with variable efficacy. To improve the anti-GvHD effect of these cells, adipose tissue derived-human MSCs (Ad-MSCs) were transduced with a lentiviral vector conferring stable expression of CXCR4, a molecule involved in cell migration to inflamed sites, and IL-10, a cytokine with potent anti-inflammatory properties. In vitro experiments showed that the expression of these molecules in Ad-MSCs (named CXCR4-IL10-MSCs) efficiently enhanced their migration towards SDF-1α and also improved their immunomodulatory properties compared to unmodified Ad-MSCs (WT-MSCs). Moreover, using a humanized GvHD mouse model, CXCR4-IL10-MSCs showed improved therapeutic effects, which were confirmed by histopathologic analysis in the target organs. Additionally, compared to WT-MSCs, CXCR4-IL10-MSCs induced a more marked reduction in the number of pro-inflammatory Th1 and Th17 cells, a higher polarization towards an anti-inflammatory T cell profile (CD3+-IL10+ cells), and increased the number of regulatory T and B cells. Our in vitro and in vivo studies strongly suggest that CXCR4-IL10-MSCs should constitute an important new generation of MSCs for the treatment of GvHD in patients transplanted with allogeneic hematopoietic grafts.

| S-EPMC9929539 | biostudies-literature

Tissue factor pathway inhibitor promotes the migration, proliferation and colonization of MSCs by regulating CXCL12/CXCR4 signaling pathway

Project description:MSCs (mesenchymal stem cells) can promote the structural and functional recovery of lung injury, but most of MSCs do not retain in the injury sites. TFPI (tissue factor pathway inhibitors) can promote stem/progenitor cell migration and homing. The objective of this study was to explore investigate the feasibility and efficacy of TFPI combined therapy with MSCs to alleviate lung injury and the possible mechanism. rhTFPI or (and) MSCs were administered via tail vein to LPS-induced ALI mice. Lung H&E, coagulation function, TFPI, TNF-α, IL-1β, CXCL12 and CXCR4 in BALF and plasma, 7-day survival rate, and colonization of MSC in lung were observed. Transmembrane migration assay, CCK-8 and EdU assay were used to determine the migration, viability and proliferation of MSCs. RNA sequencing was performed to find differentially expressed genes. The lentivirus transfection technique was used to infect MSCs to overexpession and knockdown TFPI of MSCs. The data demonstrated that rhTFPI could promote cell viability, proliferation and migration of MSCs to improve lung injury. RNA sequence indicated that CXCL12 was in top 40 DEGs and up-regulated after the combination treatment of rhTFPI and MSCs. LPS dampened TFPI, CXCL12/CXCR4 levels in a dose- and time- dependent manner, but can restored by rhTFPI. The level of TFPI expressed by MSCs affected the levels of CXCL12/CXCR4 in MSCs, and migration, proliferation and colonization of MSCs. The results indicated that TFPI may promote the migration, proliferation and colonization of MSCs by regulating CXCL12/CXCR4 signaling pathway.

2025-05-03 | GSE295816 | GEO

CXCL12 Stimulation of CXCR4-WHIM Transduced Waldenstrom's Macroglobulinemia cell line BCWM.1

2016-06-10 | GSE83150 | GEO

CXCL12 Stimulation of CXCR4-WHIM Transduced Waldenstrom's Macroglobulinemia cell line BCWM.1

Project description:CXCR4 cDNA transcripts were subcloned into plenti-IRES-GFP vectors, and stably transduced using a lentiviral system In addition to wild-type CXCR4, vectors with the mutations c.1013C>G (p.Ser338*), c.932_933insT (p.Thr311fs), and c.1030_1041delinsGT (p.Ser344fs) were generated. Cell lines were stimulated with 50nM of the CXCR4 ligand CXCL12 (SDF1A) (R&D Systems, Minneapolis MN) for two hours. RNA from each sample was extracted at baseline and at 2 hours. At baseline and following stimulation, RNA was extracted and processed for analysis using Affymetrix Human Gene ST 2.0 arrays (Affymetrix, Santa Clara, CA). Data was analyzed using Oligo and Limma bioconductor packages in R using TMM normalization.

2016-06-10 | E-GEOD-83150 | biostudies-arrayexpress

Gene expression pattern in CXCR4+ and CXCR4- subpopulation of breast cancer cells

Project description:The goal of this study was to identify signalling molecules downstream of CXCR4 in breast cancer cells. For this purpose, we sorted CXCR4-positive and CXCR4-negative cells from MDA-MB-231 breast cancer cell line by flow cytometry and performed microarrays analysis. Three sets of samples, each in quadruplicate, were analyzed. These include CXCR4-positive subpopulation, CXCR4-positive subpopulation treated with SDF-1 (ligand for CXCR4, also called CXCL12) for one hour and CXCR4-negative subpopulation.

2010-04-28 | E-GEOD-15893 | biostudies-arrayexpress

Regulation of Gene Expression by Connective Tissue Growth Factor (CTGF) in Mesenchymal Stromal Cells (MSCs)

Project description:mRNA from bone marrow-derived MSCs stably expressing CTGF-specific shRNA (or empty vector control) was analyzed for differential gene expression. Significant differences were found in cell proliferation-related genes, especially genes related to the M phase of the cell cycle, which were down-regulated in CTGF-knockdown-MSCs compared to control MSCs. Bone marrow-derived MSCs were stably transduced with lentivirus expressing CTGF-specific shRNA or an empty vector control. After antibiotic selection, total RNA was amplified and hybridized to Illumina HT12 version 3 human whole-genome arrays (Illumina, San Diego, CA).

2013-08-05 | E-GEOD-47575 | biostudies-arrayexpress

Regulation of Gene Expression by Connective Tissue Growth Factor (CTGF) in Mesenchymal Stromal Cells (MSCs)

2013-08-05 | GSE47575 | GEO

Gene expression pattern in CXCR4+ and CXCR4- subpopulation of breast cancer cells

Project description:The goal of this study was to identify signaling molecules downstream of CXCR4 in breast cancer cells. For this purpose, we sorted CXCR4-positive and CXCR4-negative cells from MDA-MB-231 breast cancer cell line by flow cytometry and performed microarrays analysis.

2010-04-20 | GSE15893 | GEO

LC-MS characterization of anti-PD-L1 and CXCR4 bispecific nanobodies

Project description:Antibodies and derivative drugs targeting immune checkpoints have been approved for the treatment of several malignancies, but there are fewer responses in patients with pancreatic cancer. Here, we designed a nanobody molecule with bi-targeting on PD-L1 and CXCR4, as both targets are overexpressed in many cancer cells and play important roles in tumorigenesis. The nanobody sequences targeting PD-L1 and CXCR4 were linked by the (G4S)3 flexible peptide to construct the anti-PD-L1/CXCR4 bispecific nanobody. The bispecific nanobody was expressed in E. coli cells and purified by affinity chromatography. The purified nanobody was biochemically characterized by mass spectrometry, Western blotting and flow cytometry to confirm the molecule and its association with both PD-L1 and CXCR4. The biological function of the nanobody and its anti-tumour effects were examined.

2023-03-11 | PXD037102 | Pride

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