Survival and proliferation of liver stem/progenitor cells by liver endothelial cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1081758 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28144918_1.fastq.gz | Fastqsanger.gz | |||
| SRR28144918_2.fastq.gz | Fastqsanger.gz | |||
| SRR28144919_1.fastq.gz | Fastqsanger.gz | |||
| SRR28144919_2.fastq.gz | Fastqsanger.gz | |||
| SRR28144920_1.fastq.gz | Fastqsanger.gz |
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Project description:Adult liver stem/progenitor cells (LPCs) exhibit robust proliferation upon impaired hepatocyte-mediated liver regeneration. However, the regenerative capacity becomes compromised in chronic liver diseases. Consequently, the promotion of liver regeneration through the utilization of LPCs emerges as a promising alternative therapeutic strategy for patients with chronic liver diseases. LPCs can be massively expanded in vitro as self-renewing organoids, however, lack of the niche cell interactions with LPCs is a major limitation. In this study, we highlight the role of liver endothelial cells (LiECs), as a part of LPC niche cells, in supporting the hepatobiliary organoids (HOs) in long-term culture even in the absence of key growth factors, such as Wnt agonists. Furthermore, LiECs altered the gene expression profile of HOs involved in inflammation, migration, extracellular matrix organization, and receptor signaling pathway through paracrine factors. Our findings expand the role of LiECs for regulating stemness of LPCs and provide a new organoid co-culture model using reduced growth medium.
2025-02-10 | GSE259435 | GEO
Project description:While others have reported that fetal liver contains a population of endothelial progenitors based on expression of cell surface markers or culture assays, this is the first proof of a CD31+Sca1+ progenitor by demonstrating highly efficient in vivo angiogenesis and a direct connection to the host vasculature. We have developed a novel isolation method based on collagenase digestion and culture on a fetal liver-derived feeder layer and demonstrate that the feeder cells or their supernatants are required for endothelial progenitor survival and proliferation. Proteogenomic profiling of the endothelial progenitors and the feeder cells was done with tandem mass spectrometry proteomics using MudPIT and gene transcript expression profiling using high density DNA microarrays. This approach identified a number of gene transcripts, proteins and candidate growth factor pathways that are likely to be involved in endothelial progenitor growth, differentiation and angiogenesis.
2007-12-15 | E-GEOD-1727 | biostudies-arrayexpress
Project description:Since human fetal liver progenitor cells (hFLPC) can differentiate into multiple liver cell types in vitro and in vivo, hFLPC may be a suitable source for cell therapy and regeneration strategies. Imperative for effective clinical applications of hFLPC is the enhanced knowledge of growth factors that mediate and improve migration and proliferation. The canonical wingless/int-1 (Wnt) signal transduction pathway is known to play a key role in proliferation and migration of stem cells. So, we investigated a role for Wnt3a and Wnt5a ligands in regulating the proliferation and migration of hFLPC. We used alamarBlue assay and transwell migration assay and examined proliferation and migration of hFLPC to Wnt3a and Wnt5a. In addition, the target genes of Wnt signal transduction pathway was identified using microarray analysis and validated by quantitative real-time polymerase chain reaction (qPCR). We found that Wnt3a or Wnt5a independently significantly increased migration and proliferation in a dose-dependent manner which was significantly inhibited by Wnt inhibitors Wnt-C59 or KN-62. Addition of Wnt3a to hFLPC resulted in increased mRNA expression of the known Wnt target genes Axin-2, DKK2, while Wnt5a increased CXCR7, all of which are closely associated with an enhanced proliferation capacity of stem cells. Thus, we report that Wnt3a and Wnt5a may play an important role in the proliferation and migration of hFLPC by possibly regulating key target genes-involved in these processes. Incorporating recombinant human Wnt3a and Wnt5a in regenerative strategies using liver stem/progenitor cells might improve the process of liver regeneration.
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Project description:Wnt ligands 3a and 5a regulate proliferation and migration in human fetal liver progenitor cells
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Project description:Surgical resection remains the gold standard for liver tumor treatment, yet the emergence of post-operative liver failure, known as the small for size syndrome (SFSS), poses a significant challenge. The activation of hypoxia sensors in a SFSS liver remnant initiated early angiogenesis, improving vascular architecture, safeguarding against liver failure and reducing mortality. The study aimed to elucidate vascular remodeling mechanisms in SFSS, its impact on hepatocyte function and subsequent liver failure. Mice underwent extended partial hepatectomy to induce SFSS, with a subset exposed to hypoxia immediately after surgery. Hypoxia bolstered post-hepatectomy survival rates. Early proliferation of liver sinusoidal cells coupled with recruitment of putative endothelial progenitor cells (EPC) via the VEGF/SDF-1α pathway, increased vascular density, improved lobular perfusion, and limited hemorrhagic events in the regenerating liver under hypoxia. Administration of G-CSF in hepatectomized mice mimicked the effects of hypoxia on vascular remodeling and EPC recruitment, but failed to rescue survival. Compared to normoxia, hypoxia favored hepatocyte function over proliferation, , promoting functional preservation in the regenerating remnant. Injection of AAV8-TBG-HNF4α virus for hepatocyte-specific overexpression of HNF4α, the master regulator of hepatocyte function, enforced functionality in proliferating hepatocytes but did not rescue survival. Only the combination of HNF4α overexpression and G-CSF treatment rescued survival afterSFSS-setting hepatectomy. In summary, SFSS arises from an imbalance and desynchronized interplay between functional regeneration and vascular restructuring. To enhance survival following SFSS-hepatectomy, a two-pronged strategy is essential, addressing the preservation of function in the proliferating parenchymal cells alongside the simultaneous mitigation of vascular harm.
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Project description:Hepatocyte-derived liver progenitor-like cells (HepLPCs) can reversibly differentiate into mature hepatocytes and play important roles in liver regeneration following acute liver failure. However, the mechanisms by which HepLPCs exert these regulatory effects are unclear. Herein, we report that HepLPCs participate in reinitiating liver regeneration and improving survival during acute liver failure, at least in part, via miRNA-183-5p, which is released from HepLPCs in extracellular vesicles. Thus, these findings may identify novel targets and strategies for the treatment of acute liver failure.
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Project description:This SuperSeries is composed of the following subset Series:; GSE6942: Transcriptional profiling of bipotential embryonic liver cells to identify liver progenitor cell surface markers (moe430a). GSE6957: Transcriptional profiling of bipotential embryonic liver cells to identify liver progenitor cell surface markers (mouse4302). Experiment Overall Design: Refer to individual Series
2008-06-15 | E-GEOD-6966 | biostudies-arrayexpress
Project description:Human liver progenitor cells (LPCs) show therapeutic potential, however, their in vitro culture results in inadequate function and phenotypic instability reflecting incomplete understanding of in vivo processes. Foetal LPCs capable of differentiation to a hepatocyte phenotype were isolated and mRNA expression profiling carried out using Affymetrix HGU133plus2 microarrays. This was compared to profiles from mature human hepatocytes and human embryonic stem cells undergoing hepatocytic differentiation. Foetal LPCs exhibit a distinct molecular profile consistent with a stem cell signature, cell division, and some liver-specific functions. 9 independent samples of second trimester liver progenitor cells were profiled along with 3 independent mature hepatocyte samples and 3 each of embryonic stem cells at day 9 and day 17 of differentiation to hepatocyte like cells.
2015-05-01 | E-GEOD-57812 | biostudies-arrayexpress
Project description:Heterochromatin stability is crucial for progenitor proliferation during early neurogenesis. It relays on the maintenance of local hubs of H3K9me. However, the current understanding of the processes involved in the formation of efficient localized levels of H3K9me remains limited. To address this intriguing question, we used a neural stem cell (NSC) to analyze the function of the H3K9me2 demethylase PHF2, which is crucial for progenitor proliferation. Through mass spectroscopy and genome-wide assays, we uncovered that PHF2 interacts with heterochromatin components and it is enriched at pericentromeric heterochromatin (PcH) boundaries. This binding is essential for maintaining silenced the satellite repeats thereby preventing DNA damage and genome instability. Depletion of PHF2 led to increased transcription of heterochromatic repeats, accompanied by a decrease in H3K9me3 levels and alterations in PcH organization. Further analysis revealed that PHF2's PHD and catalytic domains are crucial for maintaining PcH stability and preventing unscheduled repeat transcription, thereby safeguarding genome integrity. These results highlight the multifaceted nature of PHF2's functions in maintaining heterochromatin stability and regulating gene expression during neural development. Altogether, our study unravels the intricate relationship between heterochromatin stability and progenitor proliferation during mammalian neurogenesis, shedding light on its potential as a therapeutic target for neurodevelopmental disorders
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