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SIX2-Mediated Microglial M2 Polarization and Exosomal miR-3470b Delivery Protect Dopaminergic Neurons in Parkinson's Disease [EV treatment]

ABSTRACT: SIX2-Mediated Microglial M2 Polarization and Exosomal miR-3470b Delivery Protect Dopaminergic Neurons in Parkinson's Disease [EV treatment]

PROVIDER: PRJNA1232054 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32574937.fastq.gz	Fastqsanger.gz
	SRR32574938.fastq.gz	Fastqsanger.gz
	SRR32574939.fastq.gz	Fastqsanger.gz
	SRR32574940.fastq.gz	Fastqsanger.gz
	SRR32574941.fastq.gz	Fastqsanger.gz

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Similar Datasets

SIX2-Mediated Microglial M2 Polarization and Exosomal miR-3470b Delivery Protect Dopaminergic Neurons in Parkinson's Disease [EV treatment]

Project description:Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons, with neuroinflammation playing a critical role in disease progression. The transcription factor SIX2 has been identified as an anti-inflammatory factor in microglial cells; however, the underlying mechanisms remain poorly understood. In this study, we demonstrated that SIX2 overexpression protects dopaminergic cells by promoting the polarization of microglial cells from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. Mechanistically, SIX2 upregulates DDIT4 expression by binding to its promoter region. DDIT4, in turn, facilitates microglial M2 polarization by inhibiting mTOR, thereby activating autophagy. Furthermore, SIX2-induced M2-polarized microglial cells secrete exosomes carrying miR-3470b. These exosomes are taken up by dopaminergic neurons, where miR-3470b inhibits GREM1 expression and enhances TGF-β signaling activity. Consequently, SIX2-mediated mechanisms prevent and restore damaged dopaminergic neurons in PD mice. Our findings reveal a novel regulatory mechanism of microglial M2 polarization and provide new insights into PD immunotherapy. Additionally, the discovery of exosome-mediated miR-3470b communication between microglia and dopaminergic neurons offers a theoretical foundation for developing exosome-based miRNA therapies.

2025-03-08 | GSE291127 | GEO

SIX2-Mediated Microglial M2 Polarization and Exosomal miR-3470b Delivery Protect Dopaminergic Neurons in Parkinson's Disease

2025-03-07 | GSE290896 | GEO

SIX2-Mediated Microglial M2 Polarization and Exosomal miR-3470b Delivery Protect Dopaminergic Neurons in Parkinson's Disease

Project description:SIX2-Mediated Microglial M2 Polarization and Exosomal miR-3470b Delivery Protect Dopaminergic Neurons in Parkinson's Disease

| PRJNA1230722 | ENA

Gene expression profiling of Six2-positive nephron progenitors from mouse embryo

Project description:Nephron progenitors in the embryonic kidney propagate while generating differentiated nephrons. However, the progenitors in mice terminally differentiate shortly after birth. We defined culture conditions to selectively propagated nephron progenitors in vitro in an undifferentiated state. To understand how expression profiles of Six2+ cells changed during culture in vitro compared with in vivo, we performed microarray analysis of Six2+ cells at E11.5 (starting material) and P0 (experiencing 8 days in vivo), and cultured Six2+ cells at E11.5 for 8 days or 19 days. Microarray analysis were performed with isolated Six2-positive nephron progenitors from transgenic mice embryo at E11.5 or P0, and cultured E11.5 Six2+ cells for 8 or 19 days in conditioned media. P0 non-progenitors represent Six2-GFP-negative cells at P0.

2016-04-14 | E-GEOD-79024 | biostudies-arrayexpress

Genome-wide maps of Six2 and b-catenin in mesenchymal nephron progenitors

Project description:Self-renewing undifferentiated nephron progenitors express Six2, a transcription factor that is required for their maintenance as undifferentiated progenitors. Differentiation of nephron progenitors is triggered by Wnt/b-catenin signaling. In order to understand how Six2 and Wnt signaling counteract each other, we performed ChIP-seq of Six2 and b-catenin in mesenchymal nephron progenitor cells. Nephron progenitors were FACS-isolated from BAC transgenic Six2GFPcre-positive embryonic kidneys at E16.5. For Six2 ChIP, freshly FACS isolated Six2+ cells were used. For b-catenin ChIP, FACS isolated Six2+ cells were aggregated by centrifugation at 850g for 5min and incubated in 10%FBS/DMEM containing 4uM BIO for 24hrs.

2012-09-11 | E-GEOD-39837 | biostudies-arrayexpress

RNA-seq Analysis in 4T07 Control (4T07-CTL) and Six2 Overexpression (4T07-Six2) cells

Project description:To determine the molecular mechanisms by which Six2 regulates metastatic colonization, we performed RNA-seq analysis on murine triple-negative 4T07 Control (4T07-CTL) and Six2 overexpressing (4T07-Six2) cells. Using both targeted and unbiased gene signature analyses, we found that Six2 differentially regulates gene signatures associated with stemness. Additionally, we confirmed that in several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes (identified as among the highest upregulated genes in response to Six2 overexpression) associated with embryonic stem cell programs. When combined with our in vitro and in vivo stemness-associated phenotypic assays, these data suggest that Six2 may play a similar role in mediating stemness characteristics during tumor progression as it does during development, and that this role may allow it to mediate late-stage metastasis by enhancing the ability of cells to self-renew and survive at secondary sites.

2020-01-30 | GSE123489 | GEO

Exploring Six2 distal enhancer interactome in developing mouse kidney

Project description:The Six2 distal enhancer regulates expression of the 60 kb-downstream gene Six2, but does not regulate the Six3 gene which is 70 kb further downstream. CTCF ChIP-Seq and Hi-C data points to a chromatin domain boundary between Six2 and Six3 which may intervene interaction between Six2-DE and Six3. The irradiation-induced Brachyrrhine (Br) mutant allele was found to carry a 320 kb genomic inversion that includes Six2 and Six3, but not Six2DE. This repositioned Six2 under Six3 enhancer control and Six3 under Six2 distal enhancer control. Consistent with this, Six3 is ectopically expressed in Br/+ kidneys and Six2 expression is reduced. To test whether there is a change of interaction between Six2 distal enhancer and Six2 or Six3 promoters, we performed 4C-Seq in E16.5 wildtyp or Br/+ mice nephron-genic zone cells.

2018-01-18 | GSE108102 | GEO

Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy

Project description:Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy

| PRJNA1068969 | ENA

Transcriptional responses in SIX2 nephron progenitor cells following mitochondrial complex III subunit 7 (Qpc) inactivation

Project description:To identify novel transcriptional targets following Qpc inactivation. We deleteted Qpc in SIX2 nephron progenitor cells using a Six2-eGFP/cre BAC transgene. We compared SIX2-expressing progenitors from Six2-Qpc-/- kidneys with control (Six2-Qpc+/-) embryonic kidneys at E18.5.

2022-06-29 | GSE158299 | GEO

Genome-wide map of SIX2 and SIX1 binding in human embryonic kidney cortex

Project description:Nephron endowment is determined by the self-renewal and induction of a nephron progenitor pool established at the onset of kidney development. In the mouse, the related transcriptional regulators Six1 and Six2 play non-overlapping roles in nephron progenitors. Transient Six1 activity prefigures, and is essential for, active nephrogenesis. In contrast, Six2 maintains later progenitor self-renewal from the onset of nephrogenesis. We compared Six2’s regulatory actions in mouse and human nephron progenitors by chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq). Surprisingly, SIX1 was identified as a SIX2 target unique to the human nephron progenitors. Further, RNA-seq and immunostaining revealed overlapping SIX1 and SIX2 progenitor activity in the 16 week human fetal kidney. Human SIX1 ChIP-seq revealed a similar set of targets to SIX2, and predicted both factors bind DNA through an identical recognition site. In contrast to the mouse where Six2 binds its own enhancers but doesn’t interact with DNA around Six1, both human SIX1 and SIX2 bind homologous SIX2 enhancers and putative enhancers positioned around SIX1. Transgenic analysis of a putative human SIX1 enhancer in the mouse revealed a transient, mouse-like, pre-nephrogenic, Six1 regulatory pattern. Together, these data demonstrate a divergence in SIX-factor regulation between mouse and human nephron progenitors. In the human, an auto/cross-regulatory loop drives continued SIX1 and SIX2 expression during active nephrogenesis. In contrast, the mouse establishes only an auto-regulatory Six2 loop. It is tempting to speculate that differential SIX-factor regulation may contribute to species differences in the duration of progenitor programs and nephron output.

2016-01-31 | GSE73865 | GEO

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