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Transcriptome analysis of in vitro hematopoietic stem cells (HSC) and stage 3 (ST3) NK cell progenitors cells expressing a TXNIP-specific shRNA.

ABSTRACT: To investigate the function of TXNIP in the regulation of natural killer (NK) cell differentiation, we established in vitro NK cell differentation cultures starting with cordblood derived HSC in which TXNIP has been knocked down with shRNA by lentiviral transduction. We then performed transcriptome analysis of the HSC population at day 3 and ST3 population at day 7.

ORGANISM(S): Homo sapiens

PROVIDER: GSE212024 | GEO | 2022/10/31

REPOSITORIES: GEO

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Transcriptome analysis of in vitro hematopoietic stem cells (HSC) and stage 3 (ST3) NK cell progenitors cells expressing a IRF2-specific shRNA.

Project description:To investigate the function of IRF2 in the regulation of natural killer (NK) cell differentiation, we established in vitro NK cell differentation cultures starting with cordblood derived HSC in which IRF2 has been knocked down with shRNA by lentiviral transduction. We then performed transcriptome analysis of the HSC population at day 3 and ST3 population at day 7.

2022-11-01 | GSE212023 | GEO

Transcriptome analysis of in vitro hematopoietic stem cells (HSC) and stage 3 (ST3) NK cell progenitors cells expressing a TXNIP-specific shRNA.

Project description:Transcriptome analysis of in vitro hematopoietic stem cells (HSC) and stage 3 (ST3) NK cell progenitors cells expressing a TXNIP-specific shRNA.

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Proteomic characterization of CD56posCD57 NK cell subsets

Project description:NK cells are lymphocytes that provide a first defense against viral infections and cancer. They act (i) cytotoxic by killing virus-infected and tumorigenic cells and (ii) immune regulatory by releasing cytokines and chemokines. These innate immune cells are commonly further classified as CD56bright and CD56dim NK cells. Former studies confirmed immune regulatory CD56bright NK cells as progenitors of cytotoxic CD56dim NK cells. CD57 was previously described as T cell marker for senescence and terminal differentiation. Recent studies detected CD57+ and CD57- NK cells among the CD56dim NK cell population and suggested a fully mature developmental status for CD57+ NK cells. The recent NK cell maturation model includes CD34+ hematopoietic stem cells (HSC), which develop into CD56bright NK cells, later into CD56dimCD57- and finally into terminally maturated CD56dimCD57+ (1) (2) (3). The molecular mechanisms of human NK cell differentiation and maturation remain unknown to this date. We performed for the first time a proteomic analysis of these distinct developmental stages of human primary NK cells, isolated from overall 10 healthy human blood donors. CD56bright NK cells versusCD56dim and CD56dimCD57- versus CD56dimCD57+ NK cells were analyzed by using quantitative peptide sequencing, which revealed individual protein signatures (3400 proteins) of these different NK cell developmental stages. Notably, our data support the current NK cell differentiation model by highlighting both strong distinctions between CD56dim/bright NK cells and close relationships between CD57+/- NK cells on the proteomic level. Among the most prominent and conserved regulated proteins, we detected myosin IIa, Calvasculin and Calcyclin with very similar expression patterns. We investigated their sub-cellular localization and observed specific recruitment- and accumulation-events at the NK cell immunological synapse (NKIS) after NK activation.

2013-01-23 | PRD000666 | Pride

TXNIP loss

Project description:TXNIP loss

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Transcriptome analysis of in vitro hematopoietic stem cells (HSC) and stage 3 (ST3) NK cell progenitors cells

Project description:Transcriptome analysis of in vitro hematopoietic stem cells (HSC) and stage 3 (ST3) NK cell progenitors cells

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Expression of thioredoxin-interacting protein (TXNIP) during megakaryopoiesis is indispensable for platelet biogenesis

Project description:Thioredoxin-interacting protein (TXNIP) is ubiquitously expressed in blood cells, including hematopoietic stem cells (HSCs), monocytes, and platelets. Here we report a novel finding that TXNIP plays a crucial role in megakaryopoiesis and platelet biogenesis via interacting with GATA1, a transcription factor for megakaryocyte-erythroid differentiation. Txnip-/- mice displayed immature megakaryocytes in the bone marrow with thrombocytopenia, which had gotten worse as the mice aged. Transcriptome analysis revealed that the transcriptional activity of GATA1 was significantly enhanced in the Txnip-/- megakaryocyte precursors (MkPs) than wild type (WT) cells. During megakaryopoiesis in ex vivo, Txnip-/- MkPs remained small in cell size with less mitochondrial mass, and more glycolysis for ATP production, as opposed to the normal megakaryocyte maturation. The effects of TXNIP in megakaryocytes were recapitulated in human cord blood CD34+ HSC-derived differentiation. Taken together, this study demonstrates the importance of spatiotemporal expression of TXNIP in platelet biogenesis. We propose for the first time that TXNIP might play a critical role in determining a lineage between megakaryocytes and erythroid cells from a common megakaryocyte-erythroid progenitor via regulation of transcriptional activity of GATA1.

2022-12-31 | GSE186400 | GEO

SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling (human data sets)

Project description:Among the features that distinguish type 1 innate lymphoid cells (ILC1s) from NK cells is a gene signature indicative of TGFb-family cytokine imprinting. To assess the impact of TGFb family cytokines on ILC1 differentation, we examined SMAD4- a transcription factor that facilitates the signaling pathway common to all TGFb family cytokines-was specifically ablated in ILCs and NK cells. While SMAD4 deficiency did not affect ILC1 differentation, NK cells paradoxically aquired an ILC1-like gene signature and were incapable of controlling tumor metastasis and viral infection. We used microarray to compare the transcriptional differences between human blood NK cells. NK cells from a patient with a deleterious SMAD4 mutation or control NK cells were cultured overnight with either IL-2 alone or TGFb1 and IL-2.

2017-07-31 | GSE100246 | GEO

SMAD4 impedes conversion of NK cells into ILC1-like cells by curtailing non-canonical TGFb signaling (mouse data sets)

Project description:Among the features that distinguish type 1 innate lymphoid cells (ILC1s) from NK cells is a gene signature indicative of TGFb-family cytokine imprinting. To assess the impact of TGFb family cytokines on ILC1 differentation, we examined SMAD4- a transcription factor that facilitates the signaling pathway common to all TGFb family cytokines-was specifically ablated in ILCs and NK cells. While SMAD4 deficiency did not affect ILC1 differentation, NK cells paradoxically aquired an ILC1-like gene signature and were incapable of controlling tumor metastasis and viral infection. We used microarray to define the transcriptional differences between splenic NK cells from WT and SMAD4F/F x Ncr1-Cre mice.

2017-07-31 | GSE100247 | GEO

Secretome from TXNIP knockout human colorectal cell line (DLD1)

Project description:Chemotherapy, the standard of care treatment for cancer patients with advanced disease, has been increasingly recognised to activate host immune responses to produce durable outcomes. Here, in colorectal adenocarcinoma (CRC) we identify oxaliplatin-induced Thioredoxin Interacting Protein (TXNIP), a MondoA-dependent tumor suppressor gene, as a negative regulator of Growth/Differentiation Factor 15 (GDF15). GDF15 is a negative prognostic factor in CRC and promotes the differentiation of regulatory T cells (Tregs), which inhibit CD8 T cell activation. Intriguingly, multiple models including patient-derived tumor organoids demonstrate that the loss of TXNIP and GDF15 responsiveness to oxaliplatin is associated with advanced disease or chemotherapeutic resistance, with transcriptomic or proteomic GDF15/TXNIP ratios showing potential as a prognostic biomarker. These findings illustrate a potentially common pathway where chemotherapy-induced epithelial oxidative stress drives local immune remodelling for patient benefit, with disruption of this pathway seen in refractory or advanced cases.

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TXNIP loss expands Myc transcriptome

Project description:To examine the generality of our finding where the gene expression profile of TXNIP knockout in MDA-MB-231 cells resembles of that Myc overexpression transcriptional program, our lab has generated TXNIP null HCC70 (HCC70:TKO) and MB135 (MB135:TKO) cells. We characterized the gene exrpession programs of these cells by RNA-seq.

2023-02-07 | GSE222693 | GEO

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