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Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Fe treatment WT-KO]

ABSTRACT: Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Fe treatment WT-KO]

PROVIDER: PRJNA1228621 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32501155.fastq.gz	Fastqsanger.gz
	SRR32501156.fastq.gz	Fastqsanger.gz
	SRR32501157.fastq.gz	Fastqsanger.gz
	SRR32501158.fastq.gz	Fastqsanger.gz
	SRR32501159.fastq.gz	Fastqsanger.gz

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Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis

Project description:This study aimed to investigate impact of myeloid ferritin heavy chain (FtH) deletion on iron trafficking in kidney health and disease. Myeloid FtH deletion (FtHΔ/Δ) led to upregulation of synuclein-α (Snca) as the only iron-binding protein. When exposed to kidney injury, FtHΔ/Δ mice exhibited significantly worse kidney function. Transcriptome analysis identified ferroptosis as a key pathway triggered by FtH deletion. This was confirmed by elevated expression of ferroptosis-related genes, oxidative stress markers, and increased iron deposition in the kidneys. The latter was mediated via reprogramming of macrophages to an iron-recycling phenotype by inducing Spic. Mechanistically, we demonstrate ferrireductase activity of monomeric Snca acts as a catalyst triggering oxidative stress and ferroptosis. Moreover, kidney accumulation of Snca is promoted in kidney diseases marked by heavy leukocyte infiltration in both mice and humans. These findings emphasize role of FtH in regulating iron metabolism and promoting kidney repair by suppressing Snca and Spic.

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Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis

Project description:Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis

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Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Fe treatment WT-KO]

Project description:Following kidney injury, we observed increased iron depsoition in kidneys of myeloid specific FtH deficient (FtHΔ/Δ) mice when compared to wild-type (FtHfl/fl) kidneys. To explore mechanisms coordinating increased iron accumulation in FtHΔ/Δ kidneys, we employed a parenterally induced iron overload model by injecting 10–12-week-old male FtHfl/fl (wild-type) and FtHΔ/Δ (myeloid-specific FtH-deficient) mice with 0.4 mg/g body weight iron dextran via five intraperitoneal injections on consecutive days. Three days after the final injection, kidneys were harvested and sent for bulk RNA sequencing to assess transcriptional changes underlying tissue iron deposition due to FtH deletion in myeloid cells.

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Project description:To investigate impact of myeloid ferritin heavy chain (FtH) deletion in kidney iron metabolism under baseline conditions, we performed bulk RNA sequencing on kidney tissues from FtHfl/fl (wild-type) and FtHΔ/Δ (myeloid-specific FtH-deficient) mice.

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Project description:Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Baseline WT-KO]

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