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Platelet-derived thrombospondin 1 promotes immune cell liver infiltration and exacerbates diet-induced steatohepatitis.

ABSTRACT: Platelet-derived thrombospondin 1 promotes immune cell liver infiltration and exacerbates diet-induced steatohepatitis.

PROVIDER: PRJNA1051592 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27189302_1.fastq.gz	Fastqsanger.gz
	SRR27189302_2.fastq.gz	Fastqsanger.gz
	SRR27189303_1.fastq.gz	Fastqsanger.gz
	SRR27189303_2.fastq.gz	Fastqsanger.gz
	SRR27189304_1.fastq.gz	Fastqsanger.gz

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Platelet-derived thrombospondin 1 promotes immune cell liver infiltration and exacerbates diet-induced steatohepatitis.

Project description:Background and Aims: Recent studies have implicated platelets, particularly α-granules, in the development of steatohepatitis (NASH). However, the specific mechanisms involved have yet to be determined. Notably, thrombospondin 1 (TSP1) is a major component of the platelet α-granules released during platelet activation. The role of platelet-derived TSP1 in NASH remains unknown and was investigated in this study. Approach and Results: Platelet-specific TSP1 knockout mice (TSP1Δpf4) and their wild type littermates (TSP1F/F) were used. NASH was induced by feeding the mice a diet enriched in fat, sucrose, fructose, and cholesterol (AMLN diet). A human liver NASH organoid model was also employed. Although TSP1 deletion in platelets did not affect diet-induced steatosis, TSP1Δpf4 mice exhibited attenuated NASH and liver fibrosis, accompanied by improvements in plasma glucose and lipid homeostasis. Moreover, intrahepatic platelet accumulation, activation and chemokine production were reduced in TSP1Δpf4 mice, which was correlated with decreased immune cell infiltration into the liver. Consequently, this leads to diminished pro-inflammatory signaling in the liver and mitigated the progression of NAFLD. Moreover, in vitro data revealed that co-culturing TSP1-deficient platelets in a human liver NASH organoid model attenuated hepatic stellate cell activation and NASH progression. Additionally, TSP1 deficient platelets play a role in regulating brown fat endocrine function, specifically affecting Nrg4 production. Crosstalk between brown fat and the liver may also influence NAFLD progression. Conclusions: These data suggest that platelet α-granule-derived TSP1 is a significant contributor to diet-induced NASH and fibrosis, and may serve as a new therapeutic target for this severe liver disease.

2024-03-13 | GSE250004 | GEO

Platelet-derived thrombospondin 1 promotes immune cell liver infiltration and exacerbates diet-induced steatohepatitis.

Project description: Not available

| S-EPMC10918562 | biostudies-literature

HuR coordinates systemic aging through platelet infiltration

Project description:HuR coordinates systemic aging through platelet infiltration

| PRJNA1184739 | ENA

HuR coordinates systemic aging through platelet infiltration.

Project description:HuR coordinates systemic aging through platelet infiltration.

| PRJNA1298823 | ENA

HuR coordinates systemic aging through platelet infiltration

Project description:Aging involves morphological and functional changes across different organs, but how these changes are linked among the different organs remains to be elucidated. Here, we uncover a central role of platelets in sys temic aging. In aged mice, the levels of platelet secreted pro inflammatory factors (PSPF) increased greatly in the serum and platelets, leading to a diffuse increase of platelet infiltration in brain, liver, lung, kidney, and aortic root. The RNA binding protein HuR/ELAVL1, a major regulator of R NA metabolism, promoted the production of PSPF in platelets. Platelet specific deletion of HuR reduced the expression of PSPF in platelets, alleviated platelet infiltration in brain, liver, lung, kidney, and aortic root, and delayed systemic aging. Our findings highlight a role of platelets in coordinating aging traits across organs.

2024-11-16 | GSE281572 | GEO

HuR coordinates systemic aging through platelet infiltration.

Project description:Aging involves morphological and functional changes across different organs, but how these changes are linked among the different organs remains to be elucidated. Here, we uncover a central role of platelets in systemic aging. In aged mice, the levels of platelet-secreted pro-inflammatory factors (PSPF) increased greatly in the serum and platelets, leading to a diffuse increase of platelet infiltration in brain, liver, lung, kidney, and aortic root. The RNA-binding protein HuR/ELAVL1, a major regulator of RNA metabolism, promoted the production of PSPF in platelets. Platelet-specific deletion of HuR reduced the expression of PSPF in platelets, alleviated platelet infiltration in brain, liver, lung, kidney, and aortic root, and delayed systemic aging. By using single-nucleus sequencing, platelet-specific HuR ablation was found to alleviate p53 and pro-inflammatory signaling pathways in liver, lung, and brain tissues in aged mice. Our findings highlight a role of platelets in coordinating aging traits across organs.

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Cholesterol-rich diet exacerbates steatohepatitis in the STAM mouse model

Project description:Cholesterol-rich diet exacerbates steatohepatitis in the STAM mouse model

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Opisthorchis viverrini infection exacerbates kidney disease through gut dysbiosis and alteration of host proteome in nonalcoholic steatohepatitis hamsters

Project description:Non–alcoholic fatty liver disease (NAFLD) is high prevalent in worldwide and associated with chronic kidney disease (CKD). Infection with Opisthorchis viverrini (Ov) infection and consumption of high fat and high fructose (HFF) exacerbates NAFLD to nonalcoholic steatohepatitis in hamsters. Here, we aimed to investigate the effect a combination of HFF diet and Ov infection on kidney pathology via alteration of gut microbiome and proteome in hamster.

2024-09-12 | PXD045309 | JPOST Repository

Thrombin-reduced miR-27b attenuates platelet angiogenic activities via enhancing platelet de novo synthesis of anti-angiogenic thrombospondin-1

Project description:To identify if platelet activation would result in altered platelet miRNA profile, not only in total RNA sample, also in AGO2-immunoprecipitation(AGO2-IP) products. To determinate if altered platelet miRNAs could regulate de novo protein synthesis of angiogenic factors in activated platelets, and even more importantly, if miRNA-regulated platelet angiogenic factor synthesis could result in changes of platelet angiogenic activities.

2017-03-14 | GSE96533 | GEO

GP IIb/IIIa-ICAM-1 Mediated Platelet-Endothelial Adhesion Exacerbates Pulmonary Hypertension

Project description:GP IIb/IIIa-ICAM-1 Mediated Platelet-Endothelial Adhesion Exacerbates Pulmonary Hypertension

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