Wild type (WT), partial hepatectomy, and lncHand2 KO chip
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE98357 | GEO | 2017/04/29
SECONDARY ACCESSION(S): PRJNA384804
REPOSITORIES: GEO
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Project description:The goal of this study is to obtain an expression profile of regenerating mouse livers. We used microarray analysis to study the gene groups coordinately expressed temporally during mouse a liver regeneration. One of the syn-expression groups that showed a sharp rise in gene expression immediately after hepatectomy contains a set pancreatic exocrine genes. The syn-expression profile of pancreatic genes and the pancreatic-specific transcription factors Ptf1a and Ipf1 was confirmed using real-time PCR. Electron microscopic examination showed the presence of morphological features reminiscent of pancreatic acinar cells with the presence of characteristic zymogen granules and ER organization. These results indicate that there is a transient liver-to-pancreas transdifferentiation event at the beginning of liver regeneration. A strong coordinated up-regulation of pancreatic genes was found to accompany the injury response in the pancreas, suggesting a compensatory mechanism for pancreatic functions. There seems to be a relationship between the induction of pancreatic genes and acute phase response at the beginning of liver regeneration. Experiment Overall Design: Total RNA was extracted from livers of mice recovered at Experiment Overall Design: various hours after partial hepatectomy (PHx 4h, 8h, 12h, 36h, Experiment Overall Design: 48h, 72h). We grouped livers of four to six mice together for Experiment Overall Design: RNA extraction. Genes showed differentially up- or downregulated Experiment Overall Design: by two-fold with respect to the normal mouse livers Experiment Overall Design: were identified using GeneSpring software version 7.2 (Silicon Experiment Overall Design: Genetics, Agilent Technologies).
2008-06-13 | E-GEOD-4528 | biostudies-arrayexpress
Project description:Adult male Sprague-Dawley rats (275-350 g) were anesthetized and subjected to two-thirds PHx. Liver sections removed by partial hepatectomy (PHx) were collected and used both as controls (time=0) and as individual reference material for each animal to reduce the error introduced by animal-to-animal variability. At 1, 2, 4, and 6 hours following PHx, rats were killed and liver samples were harvested. Keywords: Time series PHx (1, 2, 4, 6h)
2007-04-06 | GSE7415 | GEO
Project description:The liver possesses remarkable regenerative capacity in response to injury. Upon partial hepatectomy (PHx), terminally differentiated hepatocytes in the remaining liver enter the cell cycle and restore the liver mass and function within weeks. However, liver regeneration is often impaired in livers with chronic diseases. Survivin, an inhibitor of apoptosis protein (IAP) and member of chromosome passenger complex (CPC), plays versatile roles in cell mitosis and apoptosis. We and others found that the expression of Survivin was highly increased in liver during PHx-induced liver regeneration, which indicated that Survivin played important roles in this process. However, the function of Survivin in liver regeneration remains largely undefined. Here, using mice with genetic deletion of Survivin, we found that during PHx-induced liver regeneration Survivin regulated both hepatocyte G1/S phase transition by inhibiting the expression of p21 and G2/M phase transition by regulating the localization of CPC. Moreover, restoration of Survivin expression in Survivin-deficient hepatocytes inhibited p21 expression and promote both hepatocyte G1/S and G2/M transition during PHx-induced liver regeneration.
2017-01-01 | GSE83598 | GEO
Project description:The liver has a remarkable ability to regenerate, with the best experimental model for regeneration being partial hepatectomy (PHx), in which up to two-thirds of the liver may be removed, and the residual lobes enlarge to make up for the missing mass in a few days’ time. Liver regeneration has been extensively studied, mainly in rodent models, and characterized in terms of transcriptional regulation of gene expression. However, little is known regarding regulation of gene expression in a human model of regeneration following PHx. We used microarrays to follow gene expression changes shortly following PHx. Experiment Overall Design: Liver tissues were collected from patients undergoing a PHx surgery (1.5, 42 and 81 years) under an IRB approval, at the onset (T0) and shortly after PHx (0.5hr, 1hr and 1.5hrs) for RNA extraction and hybridization on Affymetrix microarrays.
2009-10-10 | E-GEOD-15239 | biostudies-arrayexpress
Project description:The liver has a remarkable ability to regenerate, with the best experimental model for regeneration being partial hepatectomy (PHx), in which up to two-thirds of the liver may be removed, and the residual lobes enlarge to make up for the missing mass in a few days’ time. Liver regeneration has been extensively studied, mainly in rodent models, and characterized in terms of transcriptional regulation of gene expression. However, little is known regarding regulation of gene expression in a human model of regeneration following PHx. We used microarrays to follow gene expression changes shortly following PHx.
2009-10-01 | GSE15239 | GEO
Project description:Our aim was to study the impact of bleeding and red blood cell (RBC) resuscitation on liver regeneration. We assessed the impact of RBC storage time on liver regeneration following 50% partial hepatectomy (PHx) in rats, and explored possible contributing molecular mechanisms using immunohistochemistry, RNA-Seq, and macrophage depletion.
2022-11-14 | GSE216924 | GEO
Project description:Arid1a is the subunit of SWI/SNF complex, which was reported to guide SWI/SNF to DNA. Here, we found that loss of Arid1a in the liver results in improved liver regeneration after partial hepatectomy.Genome-wide analysis showed that after hepatectomy,loss of Arid1a reduces the recruitment and activity of E2F4 on target promoters, resulting in expression programs that favor regeneration during injury.RNAseq shows transcriptional profiling in WT and Arid1a LKO livers pre- and post-hepatectomy, which confirmed the E2F4 target genes and cell cycle genes were upregulated after hepatectomy. After partial hepatectomy, liver transcriptional profiling in WT and Arid1a liver specific KO mice were generated by RNA-seq analysis.
2016-03-30 | E-GEOD-76926 | biostudies-arrayexpress
Project description:Deletion of the RPS6 gene in mouse liver results in the inhibition of 40S ribosome biogenesis and the failure of hepatocytes to enter S-phase following partial hepatectomy. This microarray experiment was designed to assess the effects of RPS6 deletion on the expression of genes involved in liver regeneration following partial hepatectomy. Keywords: time course, liver RNA was isolated from mouse livers at different time-points following partial hepatectomy. Conditional deletion of the RPS6 gene was perfomed by injecting polyinosinic-polycytidylic acid in mice harbouring a floxed version of the RPS6 gene and a cre recombinase under the regulation of an interferon responsive promoter (MX-CRE). The mice used a control have also a floxed version of the RPS6 gene but lack the cre recombinaste transgene.
2009-05-01 | E-GEOD-13864 | biostudies-arrayexpress
Project description:Background & Aims. Resection of hepatocellular carcinoma (HCC) tumors by partial hepatectomy (PHx) is associated with promoting hepatocarcinogenesis. We have previously reported that PHx promotes hepatocarcinogenesis in the Mdr2-knockout (Mdr2-KO) mouse, a model for inflammation-mediated HCC. Now, we explored the molecular mechanisms underlying the tumor-promoting effect of PHx in these mice. Methods. Using microarrays-based techniques, we compared genomic and transcriptomic profiles of HCC tumors developing in the Mdr2-KO mice either spontaneously or following PHx. Results. PHx accelerated HCC development in these mice by four months. PHx-induced tumors had only amplifications affecting multiple chromosomes and locating mainly near the acrocentric centromeres of murine chromosomes. Four different chromosomal regions were amplified each in at least three tumors. All tumors of untreated mice had chromosomal aberrations, including both deletions and amplifications. Comparison of gene expression profiles revealed a significantly enriched expression of oncogenes, chromosomal instability markers and E2F1 targets in the post-PHx compared to spontaneous tumors. Both tumor groups shared the same frequent amplification at chromosome 18. Here, we demonstrated that one of the regulatory genes encoded by this amplified region, Crem, was over-expressed in the nuclei of murine and human HCC cells in vivo, and that it stimulated proliferation of human HCC cells in vitro. Conclusions: PHx of a chronically inflamed liver directed tumor development to a discrete pathway characterized by amplification of specific chromosomal regions and expression of specific tumor-promoting genes. Crem is a new candidate HCC oncogene frequently amplified in this model and frequently over-expressed in human HCC. To explore the mechanisms of the accelerated HCC development by PHx, we compared liver tumors and their matched non-tumor liver tissues between 9-month-old hepatectomized and 13-14-month-old untreated Mdr2-KO mice. RNA was isolated from frozen liver tissues and subjected to gene expression profiling using GeneChip Mouse Gene 1.0 ST Array
2015-04-01 | E-GEOD-61422 | biostudies-arrayexpress
Project description:The cellular and molecular mechanisms involved in liver regeneration following partial hepatectomy (PHx) are complicated. Liver sinusoidal endothelial cells (LSECs) play key roles in orchestrating liver regeneration, especially during the inductive phase and angiogenic phase post PHx (from day 0 to day 8). However, the expression profile of LSECs during the late phase of regeneration remains poorly explored. Thus, we purified LSECs from mice underwent PHx or sham operation at day 14 to unravel their transcriptome changes in the late phase of liver regeneration.
2021-08-06 | GSE181482 | GEO