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Effect of depletion of pre-existing senescent cells in aged hamstrers on gene expression in lungs

ABSTRACT: Effect of depletion of pre-existing senescent cells in aged hamstrers on gene expression in lungs

PROVIDER: PRJNA967282 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24442400_1.fastq.gz	Fastqsanger.gz
	SRR24442400_2.fastq.gz	Fastqsanger.gz
	SRR24442401_1.fastq.gz	Fastqsanger.gz
	SRR24442401_2.fastq.gz	Fastqsanger.gz
	SRR24442402_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of pre-existing senescent cells in aged hamstrers on gene expression in lungs

Project description:To investigate the potential role of senescent cells in COVID19-like pathology, aged hamsters were treated with the senolytics ABT-263 one day prior to a SARS-CoV-2 infection

2023-05-19 | GSE231673 | GEO

Transcriptome profiling of lungs from young and aged hamster

Project description:Older age is one of the strongest risk factors for COVID-19 morbidity and mortality. Here, we sought to determine whether age-associated cellular senescence contributes to the severity of COVID-19 by studying the well-established golden hamster model of SARS-CoV-2-driven lung disease. We found that aged hamsters (22 months of age) accumulate senescent cells in the lungs and that the senolytic drug ABT-263 depletes these cells at baseline and during a SARS-CoV-2 infection. Relative to young hamsters (2 months of age), aged hamsters had a greater viral load during the acute phase of infection and displayed higher levels of sequelae during the post-acute phase. Interestingly, early treatment with ABT-263 was associated with a significantly lower pulmonary viral load, an effect associated with lower angiotensin converting enzyme 2, the receptor for SARS-CoV-2, and an amelioration of COVID-19-like lung disease in aged (but not young) animals. ABT-263 treatment of aged animals was also associated with lower pulmonary and systemic levels of senescence-associated secretory phenotype factors. Furthermore, early removal of senescent cells reduced the longer-term pulmonary inflammation. These data demonstrate the causative role of age-associated pre-existing senescent cells on the pathologic severity of experimental COVID-19.

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Removal of senescent cells reduces the viral load and attenuates pulmonary and systemic inflammation in SARS-CoV-2-infected, aged hamsters

Project description:Older age is one of the strongest risk factors for COVID-19 morbidity and mortality. Here, we sought to determine whether age-associated cellular senescence contributes to the severity of COVID-19 by studying the well-established golden hamster model of SARS-CoV-2-driven lung disease. We found that aged hamsters (22 months of age) accumulate senescent cells in the lungs and that the senolytic drug ABT-263, a B cell lymphoma-2 family inhibitor, depletes these cells at baseline and during a SARS-CoV-2 infection. Relative to young hamsters (2 months of age), aged hamsters had a greater viral load during the acute phase of infection and displayed higher levels of sequelae during the post-acute phase. Interestingly, early treatment with ABT-263 was associated with a significantly lower pulmonary viral load, an effect associated with lower expression of angiotensin converting enzyme 2, the receptor for SARS-CoV-2, and an amelioration of COVID-19-like lung disease in aged (but not young) animals. ABT-263 treatment of aged animals was also associated with lower pulmonary and systemic levels of senescence-associated secretory phenotype factors. Furthermore, early removal of senescent cells reduced the longer-term pulmonary inflammation. These data demonstrate the causative role of age-associated pre-existing senescent cells on the pathologic severity of experimental COVID-19. As several senolytics have recently moved into early-stage clinical trials, our present findings have clear clinical relevance.

2023-07-03 | PXD041777 | Pride

Removal of senescent cells reduces the viral load and attenuates pulmonary and systemic inflammation in SARS-CoV-2-infected, aged hamsters

Project description:Older age is one of the strongest risk factors for COVID-19 morbidity and mortality. Here, we sought to determine whether age-associated cellular senescence contributes to the severity of COVID-19 by studying the well-established golden hamster model of SARS-CoV-2-driven lung disease. We found that aged hamsters (22 months of age) accumulate senescent cells in the lungs and that the senolytic drug ABT-263, a B cell lymphoma-2 family inhibitor, depletes these cells at baseline and during a SARS-CoV-2 infection. Relative to young hamsters (2 months of age), aged hamsters had a greater viral load during the acute phase of infection and displayed higher levels of sequelae during the post-acute phase. Interestingly, early treatment with ABT-263 was associated with a significantly lower pulmonary viral load, an effect associated with lower expression of angiotensin converting enzyme 2, the receptor for SARS-CoV-2, and an amelioration of COVID-19-like lung disease in aged (but not young) animals. ABT-263 treatment of aged animals was also associated with lower pulmonary and systemic levels of senescence-associated secretory phenotype factors. Furthermore, early removal of senescent cells reduced the longer-term pulmonary inflammation. These data demonstrate the causative role of age-associated pre-existing senescent cells on the pathologic severity of experimental COVID-19. As several senolytics have recently moved into early-stage clinical trials, our present findings have clear clinical relevance.

2023-07-03 | PXD041973 | Pride

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2016-06-27 | E-GEOD-64754 | biostudies-arrayexpress

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Pre-existed senescent fibroblasts in aged bladder create tumor-permissive niche via CXCL12 secretion

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scRNA-seq of young and aged lungs following influenza A virus infection

Project description:Aging is known to alter the host repsonse to influenza infection. Here, we use single-cell RNA sequencing (scRNA-seq) to identify cellular changes in the lungs of young (16-week-old) and aged (80-week-old) mice following influenza infection.

2023-09-05 | GSE202325 | GEO

Senescent Cells Contribute to the Physiological Remodeling of Aged Lungs.

Project description:Age-associated decline in organ function governs life span. We determined the effect of aging on lung function and cellular/molecular changes of 8- to 32-month old mice. Proteomic analysis of lung matrix indicated significant compositional changes with advanced age consistent with a profibrotic environment that leads to a significant increase in dynamic compliance and airway resistance. The excess of matrix proteins deposition was associated modestly with the activation of myofibroblasts and transforming growth factor-beta signaling pathway. More importantly, detection of senescent cells in the lungs increased with age and these cells contributed toward the excess extracellular matrix deposition observed in our aged mouse model and in elderly human samples. Mechanistic target of rapamycin (mTOR)/AKT activity was enhanced in aged mouse lungs compared with those from younger mice associated with the increased expression of the histone variant protein, MH2A, a marker for aging and potentially for senescence. Introduction in the mouse diet of rapamycin, significantly blocked the mTOR activity and limited the activation of myofibroblasts but did not result in a reduction in lung collagen deposition unless it was associated with prevention of cellular senescence. Together these data indicate that cellular senescence significantly contributes to the extracellular matrix changes associated with aging in a mTOR 1-dependent mechanism.

| S-EPMC4861645 | biostudies-literature

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