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Adenosine impairs the proliferative capacity of terminally mature NK cells

ABSTRACT: Adenosine impairs the proliferative capacity of terminally mature NK cells

PROVIDER: PRJEB22631 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2119810.fastq.gz	Fastqsanger.gz
	ERR2119811.fastq.gz	Fastqsanger.gz
	ERR2119802.fastq.gz	Fastqsanger.gz
	ERR2119812.fastq.gz	Fastqsanger.gz
	ERR2119803.fastq.gz	Fastqsanger.gz

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Conversion of terminally committed hepatocytes to culturable bipotent progenitor cells with regenerative capacity

Project description:A challenge for advancing approaches to liver regeneration is loss of functional differentiation capacity when hepatocyte progenitors are maintained in culture. Recent lineage-tracing studies have shown that mature hepatocytes (MHs) convert to an immature state during chronic liver injury, and we investigated whether this conversion could be recapitulated in vitro and if such converted cells could represent a source of expandable hepatocytes. We report that a cocktail of small molecules, Y-27632, A-83-01 and CHIR99021, can convert rat and mouse MHs in vitro into proliferative bipotent cells, which we term chemically induced liver progenitors (CLiPs). CLiPs can differentiate into both MHs and biliary epithelial cells that can form functional ductal structures. CLiPs in long-term culture did not lose their proliferative capacity or their hepatic differentiation ability, and rat CLiPs were shown to extensively repopulate chronically injured liver tissue. Thus our study advances the goals of liver regenerative medicine. Transcriptomic analyses for freshly isolated MHs and cells cultured for the designated periods with or without YAC stimulation (Matrix 1). Transcriptomic analysis for CLiPs which underwent hepatic induction (Matrix 2). Transcriptomic comparison of hepatic inducibility between CLiPs at early passage and those at late passages (Matrix 3). Transcriptomic comparison between chimera-derived rat cells (designated as “2nd”) and primary rat MH-derived cells (designated as “1st”) (Matrix 4).

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Small molecule oxybutynin rescues proliferative capacity of complex III-defective MPCs

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Diminished osteogenic capacity in mature periodontal ligament stem cells via RELB downregulation

Project description:Although periodontal ligament stem cells (PDLSCs) are pivotal for periodontal tissue regeneration, their regenerative capacity diminishes with the PDL maturity. This study aims to elucidate the mechanisms underlying this phenomenon.Single-cell RNA sequencing (scRNA-seq) was conducted on immature and mature human PDL tissues to characterize the heterogeneity and predict critical regulators affecting osteogenic capacity of PDLSCs. Subsequently, the predicted role of RELB was experimentally validated both in vitro and in vivo using small interfering RNA.Our scRNA-seq analysis revealed significant heterogeneity within the PDLSC population. Notably, PDLSC-5 subtype, which exhibited osteogenic potential and positioned at the terminus of the pseudotime trajectory, was markedly reduced in mature PDL tissues. RELB was specifically overexpressed in PDLSC_5 and identified as a key transcription factor (TF) for this subcluster. Knockdown of RELB significantly inhibited the osteogenic differentiation capacity of PDLSCs in vitro and bone formation potential in vivo at both developmental stages. This inhibitory effect appears to be mediated, at least in part, through the downregulation of its target gene, superoxide dismutase 2 (SOD2).This study demonstrates that the proportion of PDLSCs with osteogenic ability significantly declines with maturity, accounting for the diminished regeneration capacity of mature periodontal tissue. Furthermore, RELB was identified as a crucial TF for maintaining the osteogenic potential of PDLSCs. These findings provide a theoretical basis for strategies aimed at optimizing the bone regeneration capacity of PDLSCs.

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Identification of proliferative and mature Î²-cells in the islet of Langerhans

Project description:Insulin-dependent diabetes is a complex multifactorial disorder characterized by loss or dysfunction of Î²-cells. Pancreatic Î²-cells differ in size, glucose responsiveness, insulin secretion and precursor cell potential1-5, thus understanding the mechanisms underlying this functional heterogeneity might allow novel regenerative approaches. Here we discovered Flattop (Fltp) as a biomarker that distinguishes proliferative from mature Î²-cells. Genetic lineage tracing revealed that these Î²-cell subpopulations react differentially to environmental changes. Upon insulin resistance Fltp- Î²-cells undergo compensatory proliferation, whereas Fltp-lineage+ Î²-cells account for islet cell hypertrophy commonly associated with cytotoxic stress. The expression of the Wnt/planar cell polarity (PCP) effector gene Fltp increases when naÃ¯ve Î²-cells cluster together to form polarized and mature three-dimensional (3D) islet mini-organs6-8. We show that dispersed early postnatal islet cells, insulinoma cells and human Î²-cells all have the intrinsic ability to form polarized pseudo-islets in 3D cultures. Compaction and polarization correlates with the induction of maturation markers and can be enhanced by Wnt/PCP pathway activation. Finally, we show that Fltp is not only a marker for mature Î²-cells, but is also functionally required for proper insulin secretion in mouse and human. We conclude that planar cell polarity and 3D architecture underlie functional Î²-cell heterogeneity and report that Fltp is a biomarker that separates proliferative from mature Î²-cells. These findings establish novel molecular underpinnings of Î²-cells and enable targeting of subpopulations for the regeneration of functional Î²-cell mass in diabetic patients. We performed gene expression microarray analysis on two FACS-sorted pancreatic islet cell populations: flattop-positive and flattop-negative.

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Dietary cystine restriction increases the proliferative capacity of the small intestine of mice

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Diminished osteogenic capacity in mature periodontal ligament stem cells via RELB downregulation

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TIM-3 + CD8 T cells with a terminally exhausted phenotype retain functional capacity in hematological malignancies

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