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Clusterin is protective for liver fibrosis through mesothelial-specific LRP2 receptor mediated endocytosis

ABSTRACT: Clusterin is protective for liver fibrosis through mesothelial-specific LRP2 receptor mediated endocytosis

PROVIDER: PRJNA985580 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24969189_1.fastq.gz	Fastqsanger.gz
	SRR24969189_2.fastq.gz	Fastqsanger.gz
	SRR24969190_1.fastq.gz	Fastqsanger.gz
	SRR24969190_2.fastq.gz	Fastqsanger.gz
	SRR24969191_1.fastq.gz	Fastqsanger.gz

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Clusterin is protective for liver fibrosis through mesothelial-specific LRP2 receptor mediated endocytosis

Project description:During liver fibosis, the CLU protein was overexpressed of hepatocytes. Loss of function perform showed that CLU is protective for liver fibrosis. Mechanismly, we found LRP2 postive cells were increased after hrCLU administration in fibrotic CLUKO mice. Then single cell analysis domenstrated that LRP2 positive cells were mesothelial cells, which play a critical role of endocytosis during fibrosis resolution. Taken together, we identify clusterin as a protective chaperone that can reverse liver fibrosis and clear extracellular matrix, which targets LRP2 signaling mediated endocytosis.

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miRNAs in RPE cells treated by clusterin

Project description:Clusterin has been indicated to protect human retinal pigment epithelial (RPE) cells from oxidative stress-induced apoptosis. This study was conducted to identify aberrantly expressed microRNAs (miRNAs) downstream clusterin in RPE cells.

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Suppression of NCALD protects against spinal muscular atrophy by restoring impaired endocytosis

Project description:Spinal muscular atrophy (SMA) is a common genetic motor neuron (MN) disease caused by low levels of the ubiquitously expressed housekeeping survival motor neuron (SMN) protein, whereas concomitant overexpression of plastin 3 (PLS3) protects from SMA. Here we identify neurocalcin delta (NCALD), a neuronal calcium sensor, as a second fully protective SMA modifier, which counteracts SMA pathology when downregulated. We show reduced Ca2+ influx and impaired endocytosis in SMA, which are crucial processes in synaptic vesicle recycling and neurotransmission. Remarkably, both reduced NCALD or increased PLS3 restore endocytosis in cell culture and MN function across species in zebrafish, worm and mouse SMA models, whereas Ca2+ influx remains disturbed. Furthermore, NCALD physically binds clathrin in a Ca2+-dependent manner. We propose that NCALD acts as a Ca2+-regulated inhibitor of endocytosis, and that endocytosis is critically affected in SMA. This finding opens new therapeutic avenues for SMA. Multifactorial design comparing affected patients and unaffected disease carriers against severly affected control group to identify disease modifying transcripts

2015-01-01 | E-GEOD-58316 | biostudies-arrayexpress

Characterization of fibrosis and senescence of human omental peritoneal mesothelial cells

Project description:Primary human omental mesothelial cells from multiple donors in a young (=normal) phase and senescent phase were treated with or without TGF-ß to induce fibrosis. Senescence was induced by up to 9 passages and confirmed by stopped cell division and positive senescence-associated β-galactosidase staining.

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Identification of mesothelial-to-mesenchymal gene signature in ascitic fluid-isolated mesothelial cells through RNA-sequencing

Project description:RNA-sequencing analysis was carried out on ascetic fluid-isolated mesothelial cells from ovarian cancer patients compared to control human peritoneal mesothelial cells to identify a mesothelial-mesenchymal gene signature.

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RNA-seq gene expression profiles of primary murine peritoneal mesothelial cells.

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siRNA profiling of human synovial fibroblasts depleted for clusterin

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Expression data from fetal and adult mouse liver mesothelial cells

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