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Effect of long non-coding RNA LL35/Falcor depletion on gene expression in murine hepatocytes in vivo and in vitro

ABSTRACT: Effect of long non-coding RNA LL35/Falcor depletion on gene expression in murine hepatocytes in vivo and in vitro

PROVIDER: PRJNA840847 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19330378.fastq.gz	Fastqsanger.gz
	SRR19330379.fastq.gz	Fastqsanger.gz
	SRR19330380.fastq.gz	Fastqsanger.gz
	SRR19330381.fastq.gz	Fastqsanger.gz
	SRR19330382.fastq.gz	Fastqsanger.gz

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Effect of long non-coding RNA LL35/Falcor depletion on gene expression in murine hepatocytes in vivo and in vitro

Project description:To determine and compare a functional role of long non-coding RNA LL35/Falcor in murine hepatocytes in vitro and in vivo we performed a transcriptome analysis of AML12 hepatocytes cell line and murine liver after LL35 depletion.

2022-06-10 | GSE203431 | GEO

mRNA-seq data for DDX3 knockdown in murine hepatocytes in vivo and in vitro

Project description:A transcriptome analysis was performed to estimate a primary response of the hepatocytes to depletion of DDX3 RNA helicase both in vitro and in vivo. We used two siRNAs with different efficacy and demonstrated protein level-dependent effects on DDX3 RNA helicase depletion in the murine liver. We found that strong reduction of DDX3 protein (>85%) leads to similar changes in vitro and in vivo – we observed deregulation of cell cycle, Wnt and cadherin pathways. However, more modest downregulation of DDX3 protein (60-65%) resulted in discordant results between gene expression in vitro and in vivo – in vitro data were close to those under strong reduction, while in vivo phenotype was weak. These results demonstrate that the level of active DDX3 protein can dramatically influence on the phenotype in vivo, which should be taken into account during drug development.

2021-06-29 | GSE178618 | GEO

Effect of GCN5 depletion in hepatocytes in NAFLD

Project description:Effect of GCN5 depletion in hepatocytes in NAFLD

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Elucidation of the role of murine lncRNA LL35 in hepatocytes by LC-MSMS

Project description:Long non-coding RNAs (lncRNAs) play important roles in the regulation of many biological processes in the cell like transcription, translation, splicing, transport, etc. More than 10K lncRNAs are predicted in human, but functions for the majority remain unknown. LncRNAs may contribute to the development of multiple diseases that makes them perspective diagnostic and prognostic markers as well as drug targets [1]. Murine lncRNA Falcor/LL35 is a proposed functional analog of human lncRNA DEANR1, which is predominantly expressed in murine lungs and liver, intestine and pancreas [2, 3]. While the participation of LL35 in LL35–Foxa2 (transcription factor) regulatory loop during regeneration after lung injury was previously described by Swarr et al. [2], its functional role in murine liver remains unknown. In our work we focused on revealing the role of murine lncRNA LL35 in hepatocytes and in mouse liver. We analyzed changes in proteome of AML12 (normal hepatocytes) cell line on the 2nd day after LL35 depletion. [1] Morlando, M., Ballarino, M., & Fatica, A. (2015). Long non-coding RNAs: New players in hematopoiesis and leukemia. Frontiers in Medicine, Vol. 2. [2] Swarr, D. T., Herriges, M., Li, S., Morley, M., Fernandes, S., Sridharan, A., … Morrisey, E. E. (2019). The long noncoding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration. Genes & Development, 33(11-12), 656–668. [3] Sergeeva, O. V, Korinfskaya, S. A., Kurochkin, I. I., & Zatsepin, T. S. (2019). Long Noncoding RNA LL35 / Falcor Regulates Expression of Transcription Factor Foxa2 in Hepatocytes in Normal and Fibrotic Mouse Liver. Acta Naturae, 11(42), 66–74.

2022-08-11 | PXD033910 | Pride

RNA-seq transcriptional profiling in primary human hepatocytes, short- and long-term cultured Proliferating human hepatocytes (in vitro/in vivo)

Project description:One of the major challenges of cell therapy is manufacturing of the effective seed cells, which inevitably requires the expansion of cells in vitro. Although considerable progresses have been achieved in expansion of primary human hepatocytes (PHH) in vitro, the transplantation efficiency of proliferating human hepatocytes was decreased with the extended culture. The mechanism of declined transplantation is not clear.Here, we found that long-term cultured proliferating human hepatocytes (lc-ProliHH) significantly upregulated chemokines and proinflammatory cytokines associated with innate immune response. Moreover, lc-ProliHH elicited robust recruitment of macrophages and neutrophils at early stage of transplantation, and being cleared by macrophages caused the engraftment efficiency reduction.Based on these findings, we designed to treat recipient with Dexamethasone (Dex), which decreased the response of innate immune cells and significantly increased the transplantation efficiency to a level approximate to PHH in the liver-injured mice. Furthermore, ProliHH organoid reduced the expression of cytokine genes and behaved close to mature hepatocyte, and as a result, ameliorated their transplantation efficiency as well.

2024-01-25 | GSE184448 | GEO

Long-term Functional Maintenance of Primary Human Hepatocytes In Vitro

Project description:Functional maintenance of terminally differentiated cells outside the in vivo microenvironment has proved challenging. Current strategies that manipulate cell-cell or cell-matrix connections are difficult to constitute complex regulatory networks for cell function maintenance. Small molecules are easily combined for flexible spatiotemporal modulations, theoretically favorable for synergetic regulation of cell-innate signaling pathways to maintain cell function in vitro. Here, we developed small-molecule cocktails enabling robust maintenance of primary human hepatocytes (PHHs) longer than four weeks, with gene expression profiles, resembling those of freshly isolated PHHs; and prolong-cultured PHHs, for the first time, could maintain drug-metabolizing activities of enzymes accounting for over 80% of drug-oxidation and support hepatitis B virus infection in vitro for over one month. Our study demonstrates that this chemical approach effectively maintains terminally differentiated hepatocytes in vitro, which could be extended to various cell types.

2019-04-26 | GSE108198 | GEO

Study on expression of long non-coding RNA in colorectal cancer tissues and adjacent tissues

Project description:Interventions: Case series:No Primary outcome(s): long non-coding Ribonucleic Acid Study Design: Sequential

| 2725570 | ecrin-mdr-crc

StemNet - in vitro differentiation of human hepatocytes

Project description:Integrative epigenomic and transcriptomic characterization of hepatocyte-like cells differentiated in vitro from human induced pluripotent stem cells in comparison with primary human hepatocytes. This study comprises single cell RNA-seq, bulk mRNA-seq, ATAC-seq and RRBS.

| EGAS00001004201 | EGA

RNA-seq transcriptional profiling in primary human hepatocytes, short- and long-term cultured Proliferating human hepatocytes (in vitro/in vivo)

Project description:RNA-seq transcriptional profiling in primary human hepatocytes, short- and long-term cultured Proliferating human hepatocytes (in vitro/in vivo)

| PRJNA764688 | ENA

Level of Murine DDX3 RNA Helicase Determines Phenotype Changes of Hepatocytes In Vitro and In Vivo.

Project description:DDX3 RNA helicase is intensively studied as a therapeutic target due to participation in the replication of some viruses and involvement in cancer progression. Here we used transcriptome analysis to estimate the primary response of hepatocytes to different levels of RNAi-mediated knockdown of DDX3 RNA helicase both in vitro and in vivo. We found that a strong reduction of DDX3 protein (>85%) led to similar changes in vitro and in vivo-deregulation of the cell cycle and Wnt and cadherin pathways. Also, we observed the appearance of dead hepatocytes in the healthy liver and a decrease of cell viability in vitro after prolonged treatment. However, more modest downregulation of the DDX3 protein (60-65%) showed discordant results in vitro and in vivo-similar changes in vitro as in the case of strong knockdown and a different phenotype in vivo. These results demonstrate that the level of DDX3 protein can dramatically influence the cell phenotype in vivo and the decrease of DDX3, for more than 85% leads to cell death in normal tissues, which should be taken into account during the drug development of DDX3 inhibitors.

| S-EPMC8269429 | biostudies-literature

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