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Altered granulopoiesis aggravates stroke in the elderly [bulk RNA-seq]

ABSTRACT: Altered granulopoiesis aggravates stroke in the elderly [bulk RNA-seq]

PROVIDER: PRJNA730092 | ENA |

REPOSITORIES: ENA

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Altered granulopoiesis aggravates stroke in the elderly.

Project description:Altered granulopoiesis aggravates stroke in the elderly.

| PRJNA729965 | ENA

Altered granulopoiesis aggravates stroke in the elderly [bulk RNA-seq]

Project description:Ischemic stroke is one of the leading causes of disability and mortality worldwide, recognizing aging as a prominent risk factor and determinant of dismal outcome. Aging is known to lead to overall frailty due to multifactorial changes, but pathogenic mechanisms underlying poor outcome remain unclear. Here we show that deterioration in elderly stroke is preceded by neutrophil accumulation and clogging in the ischemic brain microcirculation leading to a worse no-reflow phenomenon. With high-dimensional single-cell profiling over time of the brain's, blood's, and bone marrow's immune response, we could delineate after stroke four main neutrophil clusters in the blood whose quantitative and temporal dynamic of release is deranged in the bone marrow of the old. In the elderly, stroke triggers an early surge in the blood of the CD62Llo neutrophil subset characterized by a signature of bone marrow proximity, senescence, and oxidative stress. Functionally, transfer of this neutrophil subset displaying prominent thrombogenic features in young stroke mice leads to increased clogging of the ischemic brain microcirculation, worse no-reflow and outcome. Interrogating the blood leukocyte landscape of a large human stroke cohort with extensive single-cell proteome analyses, we confirmed that older stroke patients display a similar precocious accumulation of blood CD62Llo neutrophil subset, worse reperfusion and outcome. Our results demonstrate how age-related alterations in the process of neutrophil differentiation and release from the bone marrow have a relevant pathogenic role in the major cerebrovascular disorder affecting the world population, that unleash emergency granulopoiesis.

2023-05-16 | GSE174438 | GEO

Altered granulopoiesis aggravates stroke in the elderly.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-05-16 | GSE174440 | GEO

Age-induced alterations of granulopoiesis generate atypical neutrophils that aggravate stroke pathology. [scRNA-Seq 2]

Project description:Stroke in aging leads to a dysregulated emergency granulopoiesis impacting neurological outcome.

2023-05-16 | GSE231822 | GEO

Age-induced alterations of granulopoiesis generate atypical neutrophils that aggravate stroke pathology [scRNA-Seq 1]

Project description:Stroke in aging leads to a dysregulated emergency granulopoiesis impacting neurological outcome.

2023-05-16 | GSE174439 | GEO

Altered lncRNAs transcriptomic profiles in atherosclerosis-induced ischemic stroke

Project description:Altered lncRNAs transcriptomic profiles in atherosclerosis-induced ischemic stroke

| PRJNA612294 | ENA

Age-induced alterations of granulopoiesis generate atypical neutrophils that aggravate stroke pathology [scRNA-Seq 1]

Project description:Age-induced alterations of granulopoiesis generate atypical neutrophils that aggravate stroke pathology [scRNA-Seq 1]

| PRJNA730093 | ENA

Age-induced alterations of granulopoiesis generate atypical neutrophils that aggravate stroke pathology. [scRNA-Seq 2]

Project description:Age-induced alterations of granulopoiesis generate atypical neutrophils that aggravate stroke pathology. [scRNA-Seq 2]

| PRJNA967740 | ENA

Photothrombotic Cerebral Stroke as a Model of Post-Stroke Seizures/Epilepsy in aged mice

Project description:Stroke is a prevalent disorder representing the third leading cause of death and major cause of disability. Post-stroke epilepsy (PSE) has been recognized as a common clinical issue after stroke, accounting for 30-40% of the causes of epilepsy among older adults. In this study, we determined GABAA receptor-mediated seizure susceptibility after PT cerebral stroke in aged mice. Young adult mice around 10 weeks of age are widely used in stroke experiments. However, as most strokes are diagnosed in the elderly and PSE has been recognized as a common clinical incidence after stroke, we utilized photothrombosis (PT) model of cerebral ischemia and examined seizure susceptibility and brain injury using combined behavioral (video) and EEG monitoring and histological (MRI) assessments. To investigate GABAA receptor-mediated convulsive/non-convulsive seizures, lower-doses of pentylenetetrazol (PTZ) was injected. PTZ susceptibility in aging mice increased compared to young adults. One month after PT stroke, aged PT stroke mice exhibited severe convulsive seizures (late-onset). These findings exhibited the increase of GABAA receptor-mediated seizures susceptibility in PT stroke aging mice, but not in young adults.

2023-11-27 | GSE241528 | GEO

Changes in gene expression during G-CSF-induced emergency granulopoiesis in humans

Project description:Emergency granulopoiesis refers to the increased production of neutrophils in bone marrow and their release into circulation induced by severe infection. Several studies point to a critical role for granulocyte colony-stimulating factor (G-CSF) as the main mediator of emergency granulopoiesis. However, the consequences of G-CSF stimulation on the transcriptome of neutrophils and their precursors have not yet been investigated in humans. Here, we examine the changes in mRNA expression induced by administration of G-CSF in vivo, as a model of emergency granulopoiesis in humans. Blood samples were collected from healthy individuals after five days of G-CSF administration. Neutrophil precursors were sorted into discrete stages of maturation by flow cytometry, and RNA was subjected to microarray analysis. mRNA levels were compared to previously published expression levels in corresponding populations of neutrophil precursors isolated from bone marrow of untreated, healthy individuals. 1110 mRNAs were differentially expressed more than 2-fold throughout terminal granulopoiesis. Major changes were seen in pathways involved in apoptosis, cytokine signaling, and Toll-like receptor pathways. In addition, G-CSF treatment reduced the levels of four out of five measured granule proteins in mature neutrophils including the proantibacterial protein hCAP-18, which was completely deficient in neutrophils from G-CSF-treated donors. These results indicate that multiple biological processes are altered in order to satisfy the increased demand for neutrophils during G-CSF-induced emergency granulopoiesis in humans.

2017-04-04 | E-MTAB-4668 | biostudies-arrayexpress

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