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Single, off-the-shelf treatment of Neuropathic Mucopolysaccharidoses with iPSC-derived microglia [scRNA-seq]

ABSTRACT: Single, off-the-shelf treatment of Neuropathic Mucopolysaccharidoses with iPSC-derived microglia [scRNA-seq]

PROVIDER: PRJNA929959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23289301.fastq.gz	Fastqsanger.gz
	SRR23289302.fastq.gz	Fastqsanger.gz
	SRR23289303.fastq.gz	Fastqsanger.gz
	SRR23289304.fastq.gz	Fastqsanger.gz
	SRR23289305.fastq.gz	Fastqsanger.gz

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Single, off-the-shelf treatment of Neuropathic Mucopolysaccharidoses with iPSC-derived microglia

Project description:Single, off-the-shelf treatment of Neuropathic Mucopolysaccharidoses with iPSC-derived microglia

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Single, off-the-shelf treatment of Neuropathic Mucopolysaccharidoses with iPSC-derived microglia [scRNA-seq]

Project description:Lysosomal storage disorders (LSDs) are a group of inherited metabolic disorders . A subgroup of LSDs is called Mucopolysaccharidoses (MPS), where accumulation of glycosaminoglycans causes a progressive degenerative disorder. The central nervous system (CNS) is particularly impacted with developmental delays, neurological regression, and early mortality. Current treatments are often insufficient to fully address the clinical need. Here we report the use of microglia derived from healthy human induced pluripotent stem cells (hiPSCs) as a potential one-time, allogeneic off-the-shelf cell therapy for several MPS. iPSC-derived microglia, termed MG01 , are replete with wild-type levels of lysosomal enzymes and we show that MG01 can deliver the functional enzyme into four different MPS knockout cell lines via mannose-6-phosphate receptor-mediated endocytosis in vitro. We then show that a single administration of MG01 provides sufficient enzyme to prevent behavioral deficits in two different animal models of MPS, efficacious to at least eight months after transplantation.

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Single, off-the-shelf treatment of Neuropathic Mucopolysaccharidoses with iPSC-derived microglia [bulk RNA-seq]

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Project description:Neuroinflammation is a major component in the transition to and perpetuation of neuropathic pain states. Spinal neuroinflammation involves activation of TLR4, localized to enlarged, cholesterol-enriched lipid rafts, designated here as inflammarafts. Conditional deletion of cholesterol transporters ABCA1 and ABCG1 in microglia, leading to inflammaraft formation, induced tactile allodynia in naïve mice. The apoA-I binding protein (AIBP) facilitated cholesterol depletion from inflammarafts and reversed neuropathic pain in a model of chemotherapy-induced peripheral neuropathy (CIPN) in wild-type mice, but AIBP failed to reverse allodynia in mice with ABCA1/ABCG1-deficient microglia, suggesting a cholesterol-dependent mechanism. An AIBP mutant lacking the TLR4-binding domain did not bind microglia nor reversed CIPN allodynia. The long-lasting therapeutic effect of a single AIBP dose in CIPN was associated with anti-inflammatory and cholesterol metabolism reprogramming and reduced accumulation of lipid droplets in microglia. These results suggest a cholesterol-driven mechanism of regulation of neuropathic pain by controlling TLR4 inflammarafts and gene expression program in microglia and blocking the perpetuation of neuroinflammation.

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