Partial Hepatectomy Induced Long Noncoding RNA Inhibits Hepatocyte Proliferation during Liver Regeneration
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Sagar Damle
PROVIDER: E-GEOD-70283 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
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:In this study, we analyzed the effects of chronic alcohol consumption on liver repair and regeneration after partial hepatectomy (PHx). Rats were fed a liquid diet containing 36% of total calories derived from ethanol for 5 weeks; corresponding pair-fed calorie-matched controls were fed diets in which ethanol calories were replaced either by carbohydrate or by fat. After 5 weeks, rats were subjected to 70% PHx and liver samples were collected at 1, 6 and 24h after the surgery. The excised liver samples at t=0 served as within-animal controls. We used Affymetrix Rat Gene 1.0 ST arrays to obtain global gene expression data from each liver sample (n=4 replicate rats, 72 arrays total). Gene expression was profiled in the chronic ethanol-fed (EtOH) and carbohydrate control pair-fed (CHO) liver prior to (control) and 1 h, 6 h, 12 h, and 24 h after partial hepatectomy (PHx).
2012-07-23 | E-GEOD-33785 | biostudies-arrayexpress
Project description:In this study, we analyzed the role of miR-21 in liver regeneration after partial hepatectomy (PHx) in chronic ethanol-treated rats. Male Sprague-Dawley rats were fed a liquid diet containing 36% of total calories derived from ethanol for 5 weeks; corresponding pair-fed calorie-matched controls were fed diets in which ethanol calories were replaced by carbohydrate. After 5 weeks, locked nucleic acid (LNA)-modified oligo antisense to miR-21 (AM21, Exiqon, Vedbaek, Denmark) was used to inhibit miRNA in vivo, and rats were subjected to 70% PHx. Liver samples were collected at 24h after the surgery. The excised liver samples at t=0 served as within-animal controls. Rat Gene 2.0 ST (Affymetrix, Santa Clara, CA) arrays were used to obtain global gene expression data from pooled liver samples (pools of 3 or 4 biological replicates/array, total 8 arrays). Gene expression was profiled in AM21 treated or untreated chronic ethanol-fed (EtOH) and carbohydrate control pair-fed (CHO) rat liver prior to (control, t=0) and 24 h after 70% partial hepatectomy (PHx).
2015-09-01 | E-GEOD-67242 | biostudies-arrayexpress
Project description:miRNA expression was profiled before and during liver regeneration following 2/3 partial hepatectomy (PHx) in chronic ethanol-fed (EtOH) and pair-fed carbohydrate control (CHO) rats. Prior to PHx, EtOH animals were fed a liquid diet containing 36% of the calories from ethanol for 5 weeks. Left lateral and medial (LLM) lobes were removed at time of PHx and used as t = 0 biological controls. Remnant liver tissue (PHx) was harvested 1 h, 6 h, 12 h, and 24 h after PHx. RNA from 4 biological replicates was pooled for profiling miRNA expression on Agilent Rat miRNA Microarrays v1.0. miRNA expression was profiled in the chronic ethanol-fed (EtOH) and carbohydrate control pair-fed (CHO) liver prior to (LLM) and 1 h, 6 h, 12 h, and 24 h after partial hepatectomy (PHx).
2012-07-22 | E-GEOD-34057 | 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.
2015-04-01 | E-GEOD-61423 | biostudies-arrayexpress
Project description:Genome-wide expression analysis revealed that 3653 mRNAs and 465 putative lncRNAs were differentially expressed compared to transcripts isolated from livers of control sham operated mice. Analysis was done using the NCode Mouse Non-coding RNA Microarray (Invitrogen), which contains 25,179 coding featues and 10,802 noncoding features. To identify lncRNAs that regulate cell proliferation during liver regeneration, we analysed lncRNA expression profiles in mouse liver tissue collected at 4, 12, 36, and 72 hours after PHx, using Sham operated mouse livers as control. -------------------------- submitter cannot locate original raw data files
2015-07-07 | E-GEOD-70593 | 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:To understand the mechanisms that regulate the renewal and maintenance of taste cells we performed RNA-sequencing analysis on isolated taste cells from 2 and 6 month old mice to determine how alterations in the taste cell-transcriptome regulate taste cell maintenance and function in adults. We found that the Activator Protein-1 (AP1) transcription factors (c-Fos, Fosb and c-Jun) and genes associated with this pathway were significantly downregulated in taste cells from 6 month old mice and further declined at 12 months. We generated conditional c-Fos- knockout mice to target K14-expressing cells, including differentiating taste cells. c-Fos deletion caused a severe perturbation in taste bud structure and resulted in a significant reduction in the taste bud size. c-Fos deletion also affected taste cell turnover as evident by, a decrease in proliferative markers, and upregulation of the apoptotic marker cleaved-PARP. Thus, AP1 factors are important regulators of adult taste cell renewal and their downregulation negatively impacts taste maintenance. Comparison of genes responsible for peripheral Taste system maintenance at age, 3 and 6 months. processed_data.txt: List of B vs S gene expression data gene_exp.diff: cuffdiff data for 2 and 6 month taste cells
2016-08-16 | E-GEOD-85308 | biostudies-arrayexpress
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Project description:Laparoscopic Gastric Plication (LGP) is a relatively new bariatric surgery procedure unique by not removing any part of the stomach. To bring new insights into the underlying molecular mechanism, we here present the first hypothesis-free analysis of the impact of LGP on the inflammatory and metabolic state as reflected by the serum proteome. A label-free quantitative shotgun proteomics approach was used to compare the serum proteome of 16 obese individuals before surgery with the serum of same individuals 1 to 2 months (timepoint T1) and 4 to 5 months (timepoint T2) post-surgery.
2019-06-06 | PXD010528 | Pride