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HuR coordinates systemic aging through platelet infiltration.

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE304047 | GEO | 2026/07/22

REPOSITORIES: GEO

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Similar Datasets

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

Platelet factor 4 (PF4) is induced by klotho and rejuvenates cognition and its molecular signature in the aging hippocampus

Project description:Platelet factors regulate wound healing and also signal from the blood to the brain. However, whether platelet factors modulate cognition, a highly valued and central manifestation of brain function, is unknown. Here, we show that systemic platelet factor 4 (PF4) modulates cognition and its molecular signature. Klotho, a longevity and cognition-enhancing protein, acutely activated platelets and increased circulating platelet factors, most robustly platelet factor 4 (PF4). To directly test PF4 effects on the brain, we treated mice with vehicle or systemic PF4. In young mice, PF4 enhanced synaptic plasticity and cognition. In aging mice, PF4 restored cognitive deficits and rejuvenated a molecular signature of cognition in the aging hippocampus. Augmenting platelet factors such as PF4, a possible messenger of klotho, may enhance cognition in the young brain and rejuvenate cognitive deficits in the aging brain.

2023-06-24 | GSE171929 | GEO

Aging Experiment

Project description:Lifelong murine gene expression profiles in relation to chronological and biological aging in multiple organs Five tissues: Kidney, Liver, Lung, Spleen, Brain. Six timepoints: 13wks, 26 wks, 52wks, 78wks, 104wks, 130wks. One Genotype: C57Bl/6, 3 replicates

2013-07-10 | E-GEOD-34378 | biostudies-arrayexpress

Young blood-derived platelet factors abate inflammation and rescue recognition in aging.

Project description:We show that platelet factors transfer rejuvenating effects of young plasma to the aging brain. Proteomic analysis of plasma from young and aged mice identified age-related changes in platelets. Systemic exposure of aged animals to the platelet fraction of young plasma decreased hippocampal neuroinflammation at a transcriptional and cellular level and ameliorated cognitive impairments. We identified the platelet-derived chemokine CXCL4/Platelet Factor-4 (PF4) as a pro-youthful circulating factor. Systemic PF4 administration decreased age-related neuroinflammation, restored the aging peripheral immune system to a more youthful state, and improved hippocampal-dependent learning and memory in aged mice.

2023-06-20 | GSE173254 | GEO

HuR coordinates systemic aging through platelet infiltration

Project description:HuR coordinates systemic aging through platelet infiltration

| PRJNA1184739 | ENA

Deciphering the Transcriptomic Signatures of Aging Across Organs in Mice

Project description:Aging is a key risk factor for disease in mammals, yet its molecular basis across organs remains unclear. Here, we performed bulk RNA sequencing on eight organs (brain, heart, kidney, liver, lung, skeletal muscle, spleen, testis) from male C57BL/6J mice at distinct life stages. Our analysis revealed that age-related transcriptomic shifts vary in timing and magnitude: early in lung, spleen, testis; mid-life in heart, kidney, skeletal muscle; and late in brain and liver. Magnitude ranged from very low (testis), low (brain, heart), moderate (lungs, skeletal muscle) to high (kidneys, liver, spleen). We uncovered organ-specific aging signatures, for instance, mitochondrial and epigenetic regulation in the kidney, metabolic/detoxification in the lung, and angiogenesis as well as ribosome biogenesis in the spleen). We also identified shared transcriptomic signatures, such as cellular senescence in the kidney and skeletal muscle, ECM remodeling in the heart, skeletal muscle and spleen), or inflammation in the heart, kidney, liver and lungs. These findings highlight unique and overlapping transcriptomic aging signatures, informing future therapeutic strategies to improve healthspan.

2026-02-06 | GSE291420 | GEO

Hepatic HuR protects against atherosclerosis through bile acid production

Project description:Hepatocyte-specific HuR knockout mice exhibit a lean MAFLD (metabolic-associated fatty liver disease)-like phenotype in response to high-fat diet. However, if this phenotype further impacts the development of atherosclerosis (AS) remains to be studied. Here, we report that HuR represses the production of chenodeoxycholic acid (CDCA) and taurocholic acid (TCA) in the liver through repressing the expression of CYP7A1, the rate-limiting enzyme for the central pathway of BA production. HuR destabilizes Cyp7a1 mRNA by associating with its 3’UTR. In response to high-cholesterol diet (HCD), hepatic HuR increases the expression of CYP7A1 in the liver, thereby increasing the levels of CDCA and TCA in the liver and serum, activating HuR-PSPF (platelet-secreted pro-inflammatory factors) regulatory process, and aggravating HCD-induced AS in APOE (-/-) mice. Administration of TCA and CDCA activates HuR-PSPF regulatory process and at the same time aggravates HCD-induced AS. Platelet HuR ablation mitigates the effect of hepatic HuR ablation in aggravating HCD-induced AS. In the liver tissues from patients with lean MAFLD, the reduction of HuR expression, the induction of CYP7A1 expression and the activation of HuR-PFPF regulatory process, are concurrently observed. Our findings suggest an important role of hepatic HuR-CYP7A1 regulatory process in the development of AS in lean MAFLD-like lipid dysregulation.

2026-05-31 | GSE326269 | GEO

Direct Signaling Between Platelets and Cancer Cells Induces an Epithelial-Mesenchymal-Like Transition and Promotes Metastasis

Project description:Interactions of cancer cells with the primary tumor microenvironment are important determinants of cancer progression towards metastasis but it is unknown whether additional prometastatic signals are provided during the intravascular transit to the site of metastasis. Here, we show that transient platelet-tumor cell interactions are sufficient to prime tumor cells for subsequent metastasis. Platelet-derived TGF-beta and direct platelet-tumor cell contacts synergistically activate the TGF-beta/Smad and NF-kappaB pathways in cancer cells, resulting in their transition to an invasive mesenchymal-like phenotype and enhanced metastasis in vivo. Inhibition of NF-kappaB signaling in cancer cells or ablation of TGF-beta1 expression solely in platelets protects against lung metastasis in vivo. Thus, cancer cells rely on platelet-derived signals outside of the primary tumor for efficient metastasis. MoEx-1_0-st: Five replicates of Ep5 tumor cells cultured alone, five replicates of tumor cells cultured in combination with platelets, and three replicates of tumor cells combined with platelets just prior to RNA isolation to control for the presence of platelet RNAs. MoGene-1_0-st: Three replicates of tumor cells cultured alone, three replicates of tumor cells cultured in combination with platelets, three replicates of tumor cells cultured with centrifuged platelets and three replicates of tumor cells cultured with supernate (releasate) from centrifuged platelets.

2011-12-13 | E-GEOD-27456 | biostudies-arrayexpress

Ten Mouse Organs Proteome and Metabolome Atlas from Adult to Aging

Project description:<p>The complexity of the aging process, encompassing numerous organs and systems, poses a significant challenge in identifying and targeting key factors that drive age-related decline. The multi-organ synchronous molecular intricacies underlying natural aging remain elusive. Here we presented a data resource for proteomics and metabolomics analyses on ten organs (brain, heart, intestine, kidney, liver, lung, muscle, skin, spleen and stomach) of mice spanning from youth to aging (4, 8, 12 and 20 months, n = 10). We detected and quantified 14,763 protein groups (PGs) and 4,779 metabolites across the ten organs. We found immunoregulation was deeply involved in multi-organ aging. Specifically, 18 immune-related proteins including Ighm showed significant expression changes in all ten organs. Besides, aging organs also expressed age-attributed proteins such as App, Plg and Saa1. Our study revealed that age-related metabolite changes are primarily concentrated in purine, pyrimidine and nicotinate-nicotinamide metabolism, and further constructed a differential proteins-metabolites network. These data highlight the dynamic molecular changes during organ aging, offering insights into geriatric health decline.</p>

2025-08-29 | MTBLS10642 | MetaboLights

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

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