Proliferation-correlated expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE139594 | GEO | 2019/10/31
REPOSITORIES: GEO
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Project description:Our earlier study demonstrated that when CFSE-labeled LCMV-or Pichinde virus-immune spleen leukocytes were transferred into T cell-deficient hosts, the bona fide virus-specific memory cells underwent relatively limited cell division and were substantially diluted in frequency by other more extensively proliferating cells originating from that donor cell population. We questioned how the slowly dividing population, which contained bona fide memory cells, differed from the rapidly dividing cells, which contained âmemory-likeâ cells. As a preliminary screen we performed a comparative genome-wide microarray analysis of genes expressed on sorted rapidly proliferating (CFSE-low) and slowly proliferating (CFSE-high) CD8 cell populations Experiment Overall Design: 2x10^7 CFSE-labeled, Ly5.1+, LCMV-Immune splenocytes were adoptively transferred into congenic T cell ko hosts. Splenocytes were harvested 12 days post-transfer and stained with anti-CD8 Ab, anti-Ly5.1 Ab and 7AAD. 7AAD negative cells were gated, and CFSE-low (> eight divisions) and CFSE-high (0-6 divisions) cells were sorted by flow cytometry using a FACStarPLUS sorter (BD Bioscience, Mountain View, CA). Total RNA was extracted from both CFSE-low and CFSE-high CD8+Ly5.1+ donor populations to compare rapidly vs. slowly dividing CD8 T cells during acute homeostatic proliferation via Affymetrix gene analysis.
2008-10-18 | E-GEOD-8584 | biostudies-arrayexpress
Project description:Our earlier study demonstrated that when CFSE-labeled LCMV-or Pichinde virus-immune spleen leukocytes were transferred into T cell-deficient hosts, the bona fide virus-specific memory cells underwent relatively limited cell division and were substantially diluted in frequency by other more extensively proliferating cells originating from that donor cell population. We questioned how the slowly dividing population, which contained bona fide memory cells, differed from the rapidly dividing cells, which contained “memory-like” cells. As a preliminary screen we performed a comparative genome-wide microarray analysis of genes expressed on sorted rapidly proliferating (CFSE-low) and slowly proliferating (CFSE-high) CD8 cell populations Keywords: Division profile comparison
2008-07-25 | GSE8584 | GEO
Project description:Analysis of primary human CD4+ T cells stained with the proliferation tracker CFSE and stimulated with anti-CD3, anti-CD28, and PDL1 or PDL2 for 5 days. Cells were sorted at the end of stimulation based on number of proliferative doublings prior to RNA isolation. Results provide insight into the PD-1 response pathway in CD4+ T cells that are proliferating or non-proliferating following stimulation.
2021-10-20 | GSE159774 | GEO
Project description:We identified slow-cycling cells (SCCs) in Ewing sarcoma using a label retention assay with CFSE. We labeled cells of SK-ES-1, an Ewing sarcoma cell line, with CFSE. After 5 days culture, we isolated cells retaining strong fluorescence (upper, ~10%) as SCCs and other cells (lower, ~90%) as non-slow-cycling cells (non-SCCs) using FACS AriaTM Ⅲ cell sorter.
2022-10-17 | GSE204671 | GEO
Project description:Resistance against chemotherapy remains a major obstacle in treating patients with acute myeloid leukemia (AML). Novel therapeutic concepts are especially desired to target and eliminate resistant AML stem cells. Here we show that AML stem cells harbor the plasticity to switch from a low-cycling, therapy resistant state into an actively proliferating state associated with treatment response. We used patient-derived xenograft (PDX) cells from patients with high risk or relapsed AML, which were lentivirally transduced for marker expression, stained with the proliferation-sensitive dye Carboxyfluorescein succinimidyl ester (CFSE), and re-transplanted into next-recipient mice. A rare subpopulation of AML cells displayed reduced proliferation in vivo, associated with increased treatment resistance. The proportion of AML cells with stem cell potential was identical in both, the highly and lowly proliferative sub-fraction. In re-transplantation experiments, proliferation behavior proved reversible, and AML stem cells were able to switch between a high and low proliferation state. Our data indicate that AML stem cells display functional plasticity in vivo, which might be exploited for therapeutic purposes, to prevent AML relapse and ultimately improve the prognosis of patients with AML.
2020-09-03 | GSE141627 | GEO
Project description:Proliferation-correlated expression
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Project description:Background: CD72 is a highly required regulatory molecule in B cells. Its sufficient expression is crucial for maintaining self-tolerance. In contrast, soluble CD72 (sCD72) is reported to be increased in the serum of autoimmune diseases such as systemic lupus erythematosus and primary Sjogren's syndrome (pSS). Objective: We wanted to assess the biological effect of sCD72 on CD4+T cells. Methods: We performed mass spectrometry and co-immunoprecipitation experiments to look for a sCD72 receptor on activated CD4+T cells. Afterward, to explore the biological functions of sCD72, we used flow cytometry for the cytokine secretion profile, a phosphorylation assay for the signaling pathway, and a CFSE dye-based assay for cell proliferation. Results: We found and validated the sCD72 and CD6 interaction as a possible ligand-receptor interaction. We also demonstrated that sCD72 significantly increases the expression of pro-inflammatory cytokines, namely IL-17A and IFN-γ, in activated CD4+T cells and increases the proliferation of CD4+T cells, possibly through its activation of the SLP-76-AKT-mTOR pathway. Conclusion: The sCD72-CD6 axis on activated CD4+T cells is probably a new signaling pathway in the induction of immune-mediated diseases. Therefore, targeting sCD72 may become a valuable therapeutic tool in some autoimmune disorders.
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Project description:Slow-cycling/dormant cancer cells (SCCs) are thought to cause cancer relapse, but the underlying biology remains obscure. A subpopulation of SCCs has been found even in rapidly growing tumors and cancer cell lines. To investigate the mechanism underlying cellular dormancy, we obtained SCCs from three NSCLC cell lines (H460, H1299, and SK-MES-1) and PDX tumor by using a cell proliferation-dependent fluorescent dye (CSFE).
2020-08-31 | GSE141218 | GEO
Project description:Proliferating germ cells in C. elegans provide a useful model system for deciphering fundamental mechanisms underlying the balance between proliferation and differentiation. Using gene expression profiling of mutants with excess germ cell proliferation, we identified approximately 200 genes expressed in the proliferating germ cells of C. elegans. RNA isolated from young adult C. elegans hermaphrodites of the genotype unc-32(e189) (control) and from unc-32(e189)glp-1(oz112gf) (excess germ cell proliferation) was directly compared on DNA arrays representing >90% of C. elegans genes. Four biological replicates were performed, with balanced dye swaps.
2010-04-29 | E-GEOD-21531 | biostudies-arrayexpress
Project description:When Trypanosoma brucei parasites, the causative agent of sleeping sickness, colonize the adipose tissue, they rewire gene expression. Whether this adaptation affects population behavior and disease treatment remained unknown. By using a mathematical model, we estimate that the population of adipose tissue forms (ATFs) proliferates slower than blood parasites. Analysis of the ATFs proteome, measurement of protein synthesis and proliferation rates confirm that the ATFs divide on average every 12hr, instead of 6hr in the blood. Importantly, the population of ATFs is heterogeneous with parasites doubling times ranging between 5hr and 35hr. Slow-proliferating parasites remain capable of reverting to the fast proliferation profile in blood conditions. Intravital imaging shows that ATFs are refractory to drug treatment. We propose that in adipose tissue, a subpopulation of T. brucei parasites acquire a slow growing behavior, which contributes to disease chronicity and treatment failure.
2022-11-17 | PXD014958 | Pride