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Transcriptional abnormalities in iPSC-derived oligodendrocytes of individuals with primary progressive multiple sclerosis

ABSTRACT: Transcriptional abnormalities in iPSC-derived oligodendrocytes of individuals with primary progressive multiple sclerosis

PROVIDER: PRJNA871916 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21152813_1.fastq.gz	Fastqsanger.gz
	SRR21152813_2.fastq.gz	Fastqsanger.gz
	SRR21152814_1.fastq.gz	Fastqsanger.gz
	SRR21152814_2.fastq.gz	Fastqsanger.gz
	SRR21152815_1.fastq.gz	Fastqsanger.gz

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Transcriptional abnormalities in iPSC-derived oligodendrocytes of individuals with primary progressive multiple sclerosis

Project description:Multiple sclerosis (MS) is the most common neurological disorder in young adults and is classically defined as a chronic inflammatory demyelinating disease of the central nervous system (CNS). Although MS affects millions of people worldwide, its underlying cause remains unknown making discovery of effective treatments challenging. Whether intrinsic or extrinsic factors contribute to MS initiation and progression is still unclear. This is especially true for primary progressive MS (PPMS), the rarest form of the disease, in which progressive and irreversible loss of neurological function is often observed in the absence of an overt immune-inflammatory response. To test the hypothesis that intrinsic dysfunction in oligodendrocytes (OLs), the primary targets of damage in MS, may contribute to PPMS etiopathology, we differentiated human induced pluripotent stem cell (hiPSC) lines derived from PPMS and healthy individuals into mature OLs to compare their transcriptional profile. PPMS derived OLs displayed hundreds of differentially expressed genes compared to control OLs, many associated with cell adhesion, apoptosis and inflammation, including the inflammasome component Nlrp2, which was highly upregulated. NLRP2 immunoreactivity in OLs was confirmed in post-mortem PPMS brain tissues, with higher expression than in control tissues. Altogether, our findings suggest that mature OLs in PPMS affected individuals carry intrinsic abnormalities that could contribute, at least in part, to the pathophysiology of this form of the disease.

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Project description:Multiple Sclerosis is a complex neurological disorder characterised by inflammation, demyelination, and neurodegeneration of the central nervous system. While treatments exist for relapsing-remitting multiple sclerosis, therapeutic options for the progressive forms remain limited, highlighting the need to understand their distinct pathological mechanisms. To identify subtype specific molecular signatures in patients with multiple sclerosis, bulk RNA sequencing was performed in 90 brain tissue samples from donors with relapsing-remitting, secondary progressive, and primary progressive multiple sclerosis, as well as controls without the disease. This study provides open access to transcriptomic data from multiple sclerosis tissue samples, enabling other researchers to perform independent analyses, validate findings, and generate new hypotheses.

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Project description:Chemokine-like factor-like MARVEL-transmembrane domain containing protein 5 (CMTM5) is a tetraspan-transmembrane protein highly enriched in oligodendrocytes and central nervous system (CNS) myelin. We analyzed the proteome of myelin biochemically purified from mouse brains upon genetic disruption of the Cmtm5-gene specifically in myelinating cells. An ion mobility-enhanced version of data-independent acquisition (DIA) workflow with alternating low and elevated energy (referred to as UDMSE) was used to compare protein abundance in Cmtm5 cKO and CTRL samples by label-free quantification. Specifically, dynamic range enhancement (DRE)-UDMSE was applied as a dedicated data acquisition mode recently introduced for routine differential myelin proteome profiling. We found that Cmtm5 cKO mice displayed a largely similar myelin proteome composition as control mice and, together with other data such as electron micrographs, concluded that CMTM5 is not essential for myelin biogenesis and composition. However, oligodendroglial Cmtm5-deficiency causes an early-onset progressive axonopathy, presumably following a Wallerian-like pathomechanism. These results indicate that CMTM5 is involved in the function of oligodendrocytes to maintain axonal integrity rather than myelin biogenesis.

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