The influence of LIF (Leukemia Inhibitory Factor) on the functional status of R1 mouse embryonic stem cells

Lobanok, E. S.; Mezhevikina, L. M.; Belyanovich, L. M.; Petrova, R. R.; Василевич, И. Б.; Volotovsky, I. D.; Фесенко, Е. Е.

doi:10.1134/s1990750809010077

Cited by 3 publications

(4 citation statements)

References 11 publications

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“…These facts tell some other (not receptor based) mechanisms of LIF mouse ESC regulation. Possibility of direct effects of recombinant LIF on properties of biological membranes is evidenced by our investigations with bilayer lipid membranes (Borisova et al, 2009), and membranes of intact cells highly dependent on the protein (Lobanok et al, 2008(Lobanok et al, , 2009. We found that LIF acts as a membranotropic agent: it affects viscosity of membrane lipids, surface charge and conductivity of cell membranes.…”

Section: Introductionmentioning

confidence: 57%

“…For example, our investigations showed that 5-10 ng/ml concentrations of LIF decrease share of apoptotic cells in R1 population to 2.0% in comparison with 7.2 % following 18 hours of incubation in LIF-free medium (Lobanok et al, 2008(Lobanok et al, , 2009). At 5 ng/ml concentration LIF is more effective as anti-apoptotic agent than at 10 ng/ml.…”

Section: Effects On Cell Death (Apoptosis) and Cell Cyclesmentioning

confidence: 99%

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Effects of Recombinant Leukemia Inhibitory Factor (LIF) on Functional Status of Mouse Embryonic Stem Cells

Mezhevikina¹,

Petrova²,

Borisova³

et al. 2011

Embryonic Stem Cells: The Hormonal Regulation of Pluripotency and Embryogenesis

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Section: Introductionmentioning

confidence: 57%

Section: Effects On Cell Death (Apoptosis) and Cell Cyclesmentioning

confidence: 99%

Effects of Recombinant Leukemia Inhibitory Factor (LIF) on Functional Status of Mouse Embryonic Stem Cells

Mezhevikina¹,

Petrova²,

Borisova³

et al. 2011

Embryonic Stem Cells: The Hormonal Regulation of Pluripotency and Embryogenesis

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“…Our PCR array analysis identified genes important in cellular proliferation (Lif) (Lobanok et al, 2008;Schraml et al, 2008) and apoptosis (Gdf5 and cmtm5) (Shao et al, 2007). Pathway analysis of the PCR array data using GNCpro software (SA Bioscience, Frederick, MD) generated the gene network, implicating the NF-kB and STAT3 pathways in our DNFB-induced MBL2 tumors (Supplementary Figure S5 online).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Inflammatory Cytokines and Oncogenic Signal Pathways Preceding Tumor Formation in a Murine Model of T-Cell Lymphoma in Skin

Sells

Hwang

2011

Journal of Investigative Dermatology

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The tumor microenvironment, including its inflammatory components, regulates tumor progression. Herein, we explore the relationship between inflammation and the progression of T-cell lymphoma in the cutaneous microenvironment. Injection of MBL2 murine T lymphoma cells into ear skin of C57BL/6 and immunodeficient SCID/Beige mice resulted in tumor formation in only the latter group. However, induction of skin inflammation by one topical application of DNFB following MBL2 inoculation in C57BL/6 mice resulted in progressive high-grade lymphoma. The DNFB-regulated tumor formation was blocked by early, but not late, application of a potent topical corticosteroid. At 2 days after implantation, a 10-fold decrease in MBL2 cell apoptosis was detected in DNFB-treated ears compared with vehicle control. After DNFB treatment, Gr-1(high) neutrophils and F4/80(+) macrophages constituted the majority of tumor-infiltrating CD45(+) leukocytes. Depletion of macrophages by clodronate-containing liposomes blocked the tumor-promoting effect of DNFB. Transcriptional profiling of inflammatory cytokines and chemokines after DNFB treatment revealed robust changes in genes that are important in chemotaxis, proliferation, and apoptosis. Activation of oncogenic signal pathways, including NF-κB, was also detected. This work provides insights into the cellular and molecular pathways that mediate lymphoma progression and may have applicability to human cutaneous T-cell lymphomas.

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“…Our data supports this concept, since we detected several proteins associated with mRNA splicing at the Nanog promoter. Besides proteins related to transcriptional regulation, we found many proteins associated with nuclear division, DNA replication and double strand break repair some of which might be explained by the fact that the cells were potentially at many different stages of the cell cycle at the point of analysis, as ESCs are self-renewing and constantly proliferating (Lobanok et al 2009). Additionally, our TINC data provides plausible explanations for several previously published observations.…”

Section: Discussionmentioning

confidence: 99%

TINC - a method to dissect transcriptional complexes at single locus resolution - reveals novelNanogregulators in mouse embryonic stem cells

Knaupp

Mohenska

Larcombe

et al. 2020

Preprint

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Cellular identity is ultimately controlled by transcription factors (TFs), which bind to specific regulatory elements (REs) within the genome to regulate gene expression and cell fate changes. While recent advances in genome-wide epigenetic profiling techniques have significantly increased our understanding of which REs are utilized in which cell type, it remains largely unknown which TFs and cofactors interact with these REs to modulate gene expression. A major hurdle in dissecting the whole composition of a multi-protein complex formed at a specific RE is the shortage of appropriate techniques. We have developed a novel method termed TALE-mediated Isolation of Nuclear Chromatin (TINC). TINC utilizes epitope-tagged TALEs to isolate a specific genomic region from the mammalian genome and includes a nuclei isolation and chromatin enrichment step for increased specificity. Upon crosslinking of the cells and isolation of the chromatin, the target region is purified based on affinity purification of the TALE and associated nucleic acid and protein molecules can be subjected to further analyses. A key TF in the pluripotency network and therefore in embryonic stem cells (ESCs) is NANOG. It is currently not fully understood how Nanog expression is regulated and consequently it remains unclear how the ESC state is maintained. Using TINC we dissected the protein complex formed at the Nanog promoter in mouse ESCs and identified many known and numerous novel factors. Enrichment and other statistical analysesProtein classification analyses were performed with Panther ( Thomas et al. 2003), and all other ontology analyses were performed with Metascape (Zhou et al. 2019). Transcription factors were defined by collected annotation from Riken and fantom five mouse TF datasets (Carninci et al. 2005;Kanamori et al. 2004). All other epigenetic modifiers and respective metadata were obtained from the epifactors database (Medvedeva et al. 2015). The pluripotency network was obtained from ESCAPE (Embryonic Stem Cells Atlas of Pluripotency Evidence) (Xu et al. 2013(Xu et al. , 2014. Enrichment of TINC proteins within the pluripotency network was calculated with Fisher's exact test. RNA-seq data of reprogramming fibroblasts into iPSCs was obtained from Knaupp et al. 2017. Raw sequencing files were processed to raw counts as described in the original publication. The raw counts were then TMM normalized and converted to log2 CPM for all analyses. The standardized log2CPM values were centred to the mean expression for each gene. Pearson's correlation coefficients were calculated on standardized log2CPM values for all genes corresponding to proteins identified in all three TINC replicates. Protein-protein enrichment networks were visualized with Cytoscape v3.7.1 (Shannon et al. 2003). ComplexHeatmap was used for any visualization of heatmaps with default clustering parameters and all other analyses outputs were graphed using GGplot2 unless otherwise stated (Gu, Eils, and Schlesner 2016;Wickham 2016). A set seed of 123 was used in all analys...

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The influence of LIF (Leukemia Inhibitory Factor) on the functional status of R1 mouse embryonic stem cells

Cited by 3 publications

References 11 publications

Effects of Recombinant Leukemia Inhibitory Factor (LIF) on Functional Status of Mouse Embryonic Stem Cells

Effects of Recombinant Leukemia Inhibitory Factor (LIF) on Functional Status of Mouse Embryonic Stem Cells

Upregulation of Inflammatory Cytokines and Oncogenic Signal Pathways Preceding Tumor Formation in a Murine Model of T-Cell Lymphoma in Skin

TINC - a method to dissect transcriptional complexes at single locus resolution - reveals novelNanogregulators in mouse embryonic stem cells

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