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Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity

ABSTRACT: Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity

PROVIDER: PRJNA817155 | ENA |

REPOSITORIES: ENA

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Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity [scRNA-seq]

Project description:Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity [scRNA-seq]

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Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity [Bulk RNA-seq]

Project description:Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity [Bulk RNA-seq]

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Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity

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

2023-01-23 | GSE197082 | GEO

Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity [scRNA-seq]

Project description:To explore the link between Alzheimer's disease (AD) and obisity, we profiled the transcriptional changes of the co-morbidites as well as indivitual morbidities on brain, immune and adipose tissue, at the single cell level. We observed effects of both morbidities, including AD-associated alterations in microglia and astrocytes in AD mice, and HFD-associated transcriptional changes in teh brain and the adipose. See details in: doi: https://doi.org/10.1101/2022.02.05.479219

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Hippocampus and visceral adipose tissues cellular landscape profiling to characterize the effects of obesity-amyloidosis comorbidity [Bulk RNA-seq]

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Exercise suppresses mouse systemic AApoAII amyloidosis through enhancement of the p38 MAPK signaling pathway

Project description:Exercise interventions are beneficial for reducing the risk of age-related diseases, including amyloidosis, but the underlying molecular links remain unelucidated. Here, we investigated the protective role of interval exercise training in a mouse model of age-related systemic apolipoprotein A-II amyloidosis (AApoAII) and elucidated potential mechanisms. Mice subjected to sixteen weeks of exercise improved whole-body physiologic functions and exhibited substantial inhibition of amyloidosis, particularly in the liver and spleen. Exercise activated the hepatic p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway and the downstream transcription factor tumor suppressor p53. This activation resulted in elevated expression and phosphorylation of heat shock protein beta-1 (HSPB1), a chaperone that defends against protein aggregation. In the amyloidosis-induced mice, the hepatic p38 MAPK-related adaptive responses were additively enhanced by exercise. We observed that with exercise, greatly increased amounts of phosphorylated HSPB1 accumulated at amyloid deposition areas, which we suspect to inhibit amyloid fibril formation. Collectively, our findings conclude exercise-activated, specific chaperone prevention of amyloidosis, and suggest that exercise may amplify intracellular stress-related protective adaptation pathways against age-associated disorders such as amyloidosis.

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An early inflammatory gene profile in visceral adipose tissue in children

Project description:The aim of this study was to characterize expression profiles of visceral and subcutaneous adipose tissue in children. Adipose tissue samples were collected from children having elective surgery (n=71, [54 boys], 6.0 +- 4.3 years). Affymetrix microarrays (n=20) were performed to characterize the functional profile and identify genes of interest in adipose tissue. Visceral adipose tissue had an overrepresentation of Gene Ontology themes related to immune and inflammatory responses and subcutaneous adipose tissue had an overrepresentation of themes related to adipocyte growth and development. Likewise, qPCR performed in the whole cohort showed a 30-fold increase in haptoglobin (P < 0.005), 7-fold increase in IL-10 (P < 0.001), 8-fold decrease in VEGF (P < 0.01) and a 28-fold decrease in TBOX15 (P < 0.001) in visceral compared to subcutaneous adipose tissue.The inflammatory pattern in visceral adipose tissue may represent an early stage of the adverse effects of this depot, and combined with chronic obesity, may contribute to increased metabolic and cardiovascular risk. 20 human samples from pre-pubertal boys and girls were assessed for differences in expression between subcutaneous (n=15) and visceral fat (n=5), with 1 microarray per subject

2011-06-04 | E-GEOD-29718 | biostudies-arrayexpress

An early inflammatory gene profile in visceral adipose tissue in children

2011-06-04 | GSE29718 | GEO

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Copy number analysis of plasma cells from AL amyloidosis patients

Project description:Immunoglobulin light chain (AL) amyloidosis is characterized by deposition of abnormal amyloid fibrils in multiple organs impairing their function. CD138-purified plasma cells producing these fibrils are investigated regarding chromosomal alterations by interphase fluorescence in situ hybridization (iFISH) using a multiple myeloma specific probe set for the IgH translocations as well as recurrent numerical aberrations. Aberrations genuine to AL amyloidosis cannot be detected due to the inherent limitation of this probe panel to known loci. We analyzed 118 AL amyloidosis patients by high-density copy number array to quantitatively detect genome-wide chromosomal imbalances. Most prevalent gains affected chromosomes 1q (37%), 9 (24%), 11q (24%), and 19 (16%). The most frequent deletion was monosomy 13 (28%) followed by partial deletions on 14q (21%), 16q (14%), and 13q (12%). The results were analyzed with respect to cytogenetic subgroups. In 88% of patients with translocation t(11;14) and concomitant gain of 11q22.3/11q23 detected by iFISH, the latter aberration was not due to trisomy of chromosome 11 but part of the unbalanced translocation der(14)t(11;14)(q13;q32) with breakpoint in the CCND1/MYEOV gene region. Partial loss of chromosomes 14q and 16q were significantly associated to patients with gain 1q. Our iFISH probe set is highly concordant with copy number results as it detects the most common cytogenetic aberrations present in AL amyloidosis. Beyond that, the probe panel is also the method of choice to detect translocations involving the IgH locus. In contrast to the results of our iFISH panel the frequency of hyperdiploidy detected by copy number array analysis is higher.

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