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Transcription profiling of human aging hematopoietic progenitor/stem cells

ABSTRACT: To determine how aging impacts gene expression in hematopoietic stem cells (HSCs), human CD34+ cells from bone marrow (34BM) and mobilized stem cell products (34P38NPBSC) were examined using microarray-based expression profiling. Differential expression changes were confirmed by microarray comparisons of younger and older expanded T-cell populations. Experiment Overall Design: We compared gene expression profiles between younger and older human CD34+ cells from bone marrow (34BM) and CD34+CD38- cells from mobilized stem cell products(34P38NPBSC). We also examined gene expression changes associated with aging in human expanded T-cells. For 34BM and T-cells, biotin-labeling of total RNA (5 Âµg) was performed as per standard Affymetrix protocol. For the 34P38NPBSC arrays, the single-stranded linear amplification protocol was used to process total RNA (100 nanograms) for the microarrays. Both protocols are described in detail in PMID14706461.

ORGANISM(S): Homo sapiens

SUBMITTER: Derek Stirewalt

PROVIDER: E-GEOD-13496 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Decreased IRF8 expression found in aging hematopoietic progenitor/stem cells.

Stirewalt D L DL Choi Y E YE Sharpless N E NE Pogosova-Agadjanyan E L EL Cronk M R MR Yukawa M M Larson E B EB Wood B L BL Appelbaum F R FR Radich J P JP Heimfeld S S

Leukemia 20080703 2

PMID: 18596738

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Aging hematopoietic progenitor/stem cells

Project description:To determine how aging impacts gene expression in hematopoietic stem cells (HSCs), human CD34+ cells from bone marrow (34BM) and mobilized stem cell products (34P38NPBSC) were examined using microarray-based expression profiling. Differential expression changes were confirmed by microarray comparisons of younger and older expanded T-cell populations.

2008-12-01 | GSE13496 | GEO

Age-associated changes in human CD4+ T cells point to mitochondrial dysfunction consequent to impaired autophagy

Project description:To gain understanding on the mechanisms that drive immunosenescence in humans, we examined CD4+ T cells obtained from younger (20-39 years-old) and older (70+ years-old) healthy participants of the Baltimore Longitudinal Study on Aging (BLSA). We found that mitochondrial proteins involved in the electron transport chain were overrepresented in cells from older participants, with prevalent dysregulation of oxidative phosphorylation and energy metabolism molecular pathways. Surprisingly, gene transcripts coding for mitochondrial proteins pertaining to oxidative phosphorylation and electron transport chain pathways were underrepresented in older individuals. Paralleling the observed decrease in gene expression, mitochondrial respiration was impaired in CD4+ T cells from older subjects. Though mitochondrial number in both naïve and memory cells visualized with electron microcopy was similar in older versus younger participants, there were a significantly higher number of autophagosomes, many of them containing undegraded mitochondria, in older individuals. The presence of mitochondria inside the accumulated autophagic compartments in CD4+ T cells from older individuals was confirmed by immunofluorescence. These findings suggest that older age is associated with persistence of dysfunctional mitochondria in CD4+ T lymphocytes caused by defective mitochondrial turnover by autophagy, which may trigger chronic inflammation and contribute to the impairment of immune defense in older persons.

2019-11-27 | PXD016039 | Pride

Normal Muscle - Female , Effect of Age

Project description:Healthy younger (20-29 yr) and older (65-71 yr) women donated vastus lateralis muscle under standard conditions. Keywords = muscle Keywords = aging Keywords: time-course

2003-09-22 | GSE674 | GEO

Resistance Exercise Reverses Aging in Human Skeletal Muscle

Project description:Human aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training. Keywords: resistance exercise, muscle, aging

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snRNA-Seq from Younger and Older human abdominal subcutaneous white adipose tissue

Project description:Abstract White adipose tissue (WAT) is a robust energy storage and endocrine organ critical for maintaining metabolic health as we age. Our aim was to identify cell-specific transcriptional aberrations that occur in WAT with aging. We leveraged full-length snRNA-Seq and histology to characterize the cellular landscape of human abdominal subcutaneous WAT in a prospective cohort of 10 younger (≤30 years) and 10 older individuals (≥65 years) balanced for sex and body mass index (BMI). The older group had greater cholesterol, very-low-density lipoprotein, triglycerides, thyroid stimulating hormone, and aspartate transaminase compared to the younger group (p< 0.05). We highlight that aging WAT is associated with adipocyte hypertrophy, increased proportions of lipid-associated macrophages and mast cells, an upregulation of immune responses linked to fibrosis in pre-adipocyte, adipocyte, and vascular populations, and highlight CXCL14 as a biomarker of these processes. We show that older WAT has elevated levels of senescence marker p16 in adipocytes and identify the adipocyte subpopulation driving this senescence profile. We confirm that these transcriptional and phenotypical changes occur without overt fibrosis and in older individuals that have comparable WAT insulin sensitivity to the younger individuals.

2024-07-31 | GSE235529 | GEO

AMD3100 and G-CSF Mobilize Different CD34+ Cell Populations Based on Gene and miRNA Expression

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2009-12-05 | GSE16936 | GEO

The biological age linked with oxidative estress modifies breast cancer aggressiveness

Project description:The incidence of breast cancer increases with age until menopause, and breast cancer is more aggressive in younger women. The existence of epidemiological links between breast cancer and aging indicates that both processes possibly share some common mechanisms of development. Oxidative stress is associated with both cancer susceptibility and aging. Here we observed that ERBB2-positive breast cancer, developed from genetically different ERBB2-positive transgenic mice generated by a backcross, is more aggressive in younger than in older mice, similar to what occurs in humans. In this cohort, we estimated the oxidative biological age using a mathematical model that integrated several subphenotypes directly or indirectly related to oxidative stress. This model included the serum levels of HDL-cholesterol and magnesium that were determined at a disease-free stage, and total AKT1 and glutathione concentrations in the liver at the time of necropsy. Later we defined the grade of aging due to oxidative stress as the increment of aging, which was the difference between the predicted biological age and the chronological age. This comparison permitted the identification of the biologically younger mice with less oxidative stress and older mice with more oxidative stress than would be expected according to their chronological age. Interestingly, biologically older mice developed more aggressive breast cancer than the biologically younger mice. We identified genomic regions on chromosomes 2 and 15 that were linked to the grade of oxidative aging. The levels of expression of Zbp1 located on chromosome 2, a gene related to necroptosis and inflammation, positively correlated with the grade of oxidative aging and tumour aggressiveness. This study shows part of the complex interactions between breast cancer and aging.

2017-06-14 | GSE99962 | GEO

Age-associated changes in human CD4+ T cells point to mitochondrial dysfunction consequent to impaired autophagy.

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2015-03-23 | E-GEOD-51954 | biostudies-arrayexpress

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2022-03-15 | PXD030463 | Pride

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