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The Aggregates of Mesenchymal stem cell with Cadherin/IGF1 Functionalized PLGA composite Microparticles Improve Systemic Lupus Erythematosus Treatment in MRL/lpr mice

ABSTRACT: Mesenchymal stem cell (MSC) therapy is a promising candidate for systemic lupus erythematosus (SLE), while more researches are needed to further improve therapeutic efficacy. In this study, engineered MSC aggregates are composited with MSC and cadherin/IGF1 functionalized PLGA composite microparticles, and are able to stimulate the microenvironment in vivo and enhance MSC functions of immunoregulation and cytokine secretion. Comprehensive characterization of these PLGA composite microparticles coated with E-cadherin/N-cadherin, enhancing MSC viability and cytokine secretion, followed by transcriptomic analysis to evaluate their potential advantages. We detected engineered MSC aggregates further ameliorated skin and lupus nephritis, compared with MSCs in MRL/lpr mice. In addition, engineered MSC aggregates enhanced Treg differentiation in vitro and in the spleen and lumph node of MRL/lpr mice. These findings suggested that engineered MSC aggregates represented a promising bioengineered approach for treating SLE, broadening the clinical applications of MSC-based therapies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE276961 | GEO | 2024/10/01

REPOSITORIES: GEO

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The Aggregates of Mesenchymal stem cell with Cadherin/IGF1 Functionalized PLGA composite Microparticles Improve Systemic Lupus Erythematosus Treatment in MRL/lpr mice

Project description:The Aggregates of Mesenchymal stem cell with Cadherin/IGF1 Functionalized PLGA composite Microparticles Improve Systemic Lupus Erythematosus Treatment in MRL/lpr mice

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Evaluation of microRNA levels in recipient BMMSCs of MRL/lpr mice after cell therapy (miRNA)

Project description:Mesenchymal stem cell transplantation (MSCT) has been widely used to treat a variety of human diseases. However, the detailed mechanisms underlying its success are not fully understood. Here we show that MSCT rescues recipient bone marrow mesenchymal stem cell (BMMSC) function in Fas-deficient-MRL/lpr systemic lupus erythematosus (SLE) mice via a miR-29b/Dnmt1/Notch epigenetic cascade. Using the microRNA microarray, we found that MSCT could rescue the high level of miR-29b in the recipient BMMSCs of MRL/lpr mice. In the present study, mesenchymal stem cell transplantation (MSCT) was used to treat MRL/lpr mice. One week after the treatment, normal control MSCs from C3H/HeJ mice (C3H), recipient MSCs from untreated MRL/lpr mice (LPR) and recipient MSCs from MSCT-treated MRL/lpr mice (MSC) were used for total RNA extraction and microRNA microarray for analysis of microRNA expressions.

2014-03-20 | E-GEOD-55971 | biostudies-arrayexpress

Evaluation of global methylation profile in recipient BMMSCs of MRL/lpr mice after cell therapy (MeDip)

Project description:Mesenchymal stem cell transplantation (MSCT) has been widely used to treat a variety of human diseases. However, the detailed mechanisms underlying its success are not fully understood. Here we show that MSCT rescues recipient bone marrow mesenchymal stem cell (BMMSC) function in Fas-deficient-MRL/lpr systemic lupus erythematosus (SLE) mice via rescuing their hypomethylated DNA profile. Using the methylation microarray, we found the global hypomethylation pattern in the recipient BMMSCs of MRL/lpr mice could be rescued by MSCT. In the present study, mesenchymal stem cell transplantation (MSCT) was used to treat MRL/lpr mice. One week after the treatment, normal control MSCs from C3H/HeJ mice (C3H), recipient MSCs from untreated MRL/lpr mice (LPR) and recipient MSCs from MSCT-treated MRL/lpr mice (MSC) were used for total DNA extraction and DNA methylation microarray for analysis of global genome methylation patterns.

2014-03-20 | E-GEOD-55970 | biostudies-arrayexpress

RNA Sequencing Facilitates Quantitative Analysis of Lupus (MRL/lpr) and Control（MRL/mpj）Mouse Microglia Tanscriptomes

Project description:Up to 75% of systematic lupus erythematosus (SLE) patients experience neuropsychiatric (NP) symptoms, called neuropsychiatric SLE (NPSLE), yet the underlying mechanisms remain elusive. Microglia control synaptic pruning during early postnatal brain development. The process in NPSLE remains unclear. Here, we show that microglia-coordinated elimination of synaptic terminals participated in NPSLE in MRL/lpr mice, a lupus-prone murine model. We elucidated that lupus mice developed increased depression- and anxiety-like behaviors and persistent phagocytic microglia reactivation before overt peripheral lupus pathology. Microglial engulfment of synapses explained behavioral disorders. To elucidate the mechanism of synaptic pruning by microglia, we sequenced the gene expression in sorted microglia from both lupus (MRL/lpr) mice and the wild-type (MRL/mpj) controls.

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Remodeling of Neurotransmission and Chemokine Signaling Genomic Fabrics in Neuropsychiatric Systemic Lupus Erythematosus

Project description:Cognitive dysfunction and mood changes are prevalent and especially taxing issues to patients with systemic lupus erythematosus (SLE). TNF-like weak inducer of apoptosis (TWEAK) and its cognate receptor Fn14 have been shown to play an important role in neurocognitive dysfunction in murine lupus. We profiled and compared gene expression in the cortices of MRL/+, MRL/lpr and MRL/lpr-Fn14 knockout (Fn14ko) adult female mice to determine the transcriptomic impact of TWEAK/Fn14 on cortical gene expression in lupus. We found that the TWEAK/Fn14 pathway strongly affects the expression level, variability and coordination of the genomic fabrics responsible for neurotransmission and chemokine signaling. Dysregulation of the PI3K-Akt pathway in the MRL/lpr lupus strain compared with the MRL/+ control and Fn14ko mice was particularly prominent and therefore promising as a potential therapeutic target, although the complexity of the transcriptomic fabric highlights important considerations in in vivo experimental models.

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IKBKE contributes to neuropsychiatric manifestations in lupus-prone mice

Project description:Objectives. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by multi-organ dysfunction. Neuropsychiatric SLE (NPSLE) occurs in 30~40% of patients with lupus and is the most severe presentation of SLE, frequently resulting in limitation of daily life. Recent studies have shown that microglia, tissue-resident macrophages in the central nervous system, are involved in the pathogenesis of NPSLE. Herein, we explored new therapeutic targets for NPSLE focusing on microglia. Methods. RNA sequencing of microglia in MRL/lpr, lupus-prone mice, as well as that of microglia cultured in vitro with cytokines were performed. A candidate gene, which could be a therapeutic target for NPSLE, was identified and its role on microglial activation and phagocytosis was investigated using specific inhibitors and siRNA. The effect of intracerebroventricular administration of the inhibitor on the behavioural abnormalities of MRL/lpr was also evaluated. Results. Transcriptome analysis revealed the upregulation of Ikbke, which encodes the inhibitor of nuclear factor kappa-B kinase epsilon (IKBKE) in both microglia from MRL/lpr mice and cytokine-stimulated microglia in vitro. Intracerebroventricular administration of an IKBKE inhibitor ameliorated cognitive function and suppressed microglial activation in MRL/lpr mice. Mechanistically, IKBKE inhibition reduced glycolysis, which dampened microglial activation and phagocytosis. Conclusions. These findings suggest that IKBKE plays a vital role in the pathogenesis of NPSLE via microglial activation, and it could serve as a therapeutic target for NPSLE.

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2024-10-01 | E-MTAB-13838 | biostudies-arrayexpress

DNA Methylation-dependent regulation of Cathepsin E gene expression by the transcription factor Kaiso in MRL/lpr mice.

Project description:Global DNA hypomethylation in CD4+ cells in SLE patients was suggested to play a key role in the pathogenesis. To identify new methylation-sensitive genes, we integrated genome-wide DNA methylation and mRNA profiling in CD4+ cells of MRL/lpr (MRL) and C57BL6/J (B6) mice. We identified Ctse, in which 13 methyl-CpGs within 583 bp region of intron 1 were hypomethylated, and mRNA upregulated in MRL compared with B6 mice. One of methyl-CpGs, mCGCG was hypomethylated and mutated to CGGG in MRL mice. Kaiso is known to bind mCGCG and we hypothesized that it represses expression of Ctse. The binding of Kaiso to mCGCG site in B6 was reduced in MRL mice revealed by ChIP-PCR. EL4 cells treated with 5-azaC and/or TSA showed the suppression of the binding of Kaiso to mCGCG motif and the overexpression of Ctse was demonstrated by qPCR. Ctse gene silencing by siRNA in EL4 cells resulted in reduction of IL-10 secretion. Accordingly, IL10 and CTSE mRNAs up-regulated in CD4+ T cells both in MRL mice and the patients with SLE. The hypomethylation of mCGCG motif, reduced recruitment of Kaiso, and increased expression of Ctse and Il-10 in CD4+ cells may be involved in the pathogenesis of SLE.

2017-08-13 | GSE102421 | GEO

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