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Transcriptome analysis of myeloid cells (CD11b) and astrocytes (ACSA2) from the striatum and midbrain of control and parkinsonian animals

ABSTRACT: Transcriptome analysis of myeloid cells (CD11b) and astrocytes (ACSA2) from the striatum and midbrain of control and parkinsonian animals

PROVIDER: PRJNA789843 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17259555.fastq.gz	Fastqsanger.gz
	SRR17259556.fastq.gz	Fastqsanger.gz
	SRR17259557.fastq.gz	Fastqsanger.gz
	SRR17259558.fastq.gz	Fastqsanger.gz
	SRR17259559.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of myeloid cells (CD11b) and astrocytes (ACSA2) from the striatum and midbrain of control and parkinsonian animals

Project description:Inflammation is a common feature in neurodegenerative diseases that participates in the process of neuronal loss. Here, we questioned whether the inflammatory reaction generated in Parkinson´s disease (PD) by dopaminergic neuron degeneration would trigger specific inflammatory reactions in the midbrain and in the striatum that could modify the course of neuronal death. Experimental parkinsonism was induced by overexpressing α-synuclein in the substantia nigra with a viral vector. Bulk RNA sequencing of purified midbrain microglia/myeloid cells showed a phagocytic and anti-inflammatory M2 phenotype, while midbrain astrocytes presented a pro-inflammatory state. In the striatum, microglia but not astrocytes presented a pro-inflammatory state.

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Transcriptional profiling of myeloid cells (CD11b) and astrocytes (ACSA2) from the striatum and the midbrain of control and parkinsonian animals in the MPTP mouse model

Project description:Neuroinflammation is a common hallmark of neurodegenerative diseases such as Parkinson’s disease (PD). Here, we questioned about the activation state of glial cells along the degeneration process of dopaminergic terminals in the striatum and loss of neuronal cell bodies in the midbrain. We hypothesized that MPTP administration pattern would produce different inflammatory responses that could modify the course of nigrostriatal degeneration. To reproduce the dopaminergic impairment in a PD experimental mouse model, we used two different MPTP-administration patterns: subacute (sMPTP) and chronic (cMPTP). Bulk RNA sequencing of purified midbrain microglia/myeloid cells of sMPTP mice showed an anti-inflammatory phenotype, while midbrain microglia/myeloid cells of cMPTP mice showed a pro-inflammatory and phagocytic phenotype. Midbrain astrocytes presented a phagocytic phenotype in sMPTP mice. In the striatum, microglia presented a continuous pro-inflammatory state in sMPTP and cMPTP conditions. In this region, astrocytes presented a remarkable activated and phagocytic state in sMPTP mice which was attenuated with the chronicity of MPTP administration.

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Transcriptome analysis of purified microglial cells from striatum and midbrain

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