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Transient inhibition of JNK pathway improves hematopoietic stem cell engraftment

ABSTRACT: Transient inhibition of JNK pathway improves hematopoietic stem cell engraftment

PROVIDER: PRJNA694702 | ENA |

REPOSITORIES: ENA

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Transient inhibition of JNK pathway improves hematopoietic stem cell engraftment

Project description:We found that transient inhibition of JNK pathway increased short term-HSC frequency in cord blood CD34+ cells by 12.56 folds. Transcriptome analysis shows that inhibition of JNK pathway upregulated HSC-specific and anti-oxidative gene expression, prevented upregulation of cell cycle entry, oxidative phosphorylation and glycolysis related gene expression, and downregulated reactive oxygen species (ROS) active gene expression. Consistently, cell cycle and metabolic analysis show that inhibition of JNK pathway prevented HSC from cell cycle entry, glucose uptake increase and ROS accumulation. Accordingly, transient inhibition of JNK pathway also enhanced long term-HSC recovery during cord blood CD34+ cell collection. Collectively, these findings suggest that transient inhibition of JNK pathway could promote quiescent state of HSCs by preventing cell cycle entry and metabolic activation, thus improving HSC recovery and engraftment ability.

2022-06-29 | GSE165501 | GEO

Targeting JNK Pathway Expands Human Hematopoietic Stem Cells

Project description:The limited number of human hematopoietic stem cells (HSCs) has restrained their widespread clinical application. Despite great efforts in recent years, the in vitro expansion of HSCs remains a challenge due to incomplete understanding of the signaling networks underlying HSC self-renewal. Here we show that culturing human cord blood (CB) CD34+ cells with JNK-IN-8, an inhibitor of the JNK signaling pathway, can enhance the self-renewal of HSCs with a 6-fold increase in number. These expanded CD34+ cells repopulated recipient mice for 20 weeks and can form secondary engraftment that lasted for more than 21 weeks. Knockdown of c-Jun, a major downstream target in the JNK pathway, significantly promoted the expansion of hematopoietic stem and progenitor cells (HSPCs). Our findings demonstrate a critical role of JNK pathway in regulating HSC expansion, provide new insights into HSC self-renewal mechanism, and may lead to improved clinical application of HSCs.

2019-01-17 | GSE114524 | GEO

Stromal Repair via Long-term Engraftment of Primary Bone Marrow Stroma Improves Hematopoietic Stem Cell Transplantation

Project description:Stromal Repair via Long-term Engraftment of Primary Bone Marrow Stroma Improves Hematopoietic Stem Cell Transplantation

2017-07-02 | GSE79091 | GEO

Targeting JNK Pathway Expands Human Hematopoietic Stem Cells

Project description:Targeting JNK Pathway Expands Human Hematopoietic Stem Cells

| PRJNA471685 | ENA

JNK pathway blockade promotes HER2-driven breast cancer

Project description:JNK knockout cells proliferate more and forms bigger mulit acinar sturctures under normal conditions on 3D culture.

2022-12-21 | GSE196001 | GEO

Adipose-derived mesenchymal stem cells inhibit JNK-mediated mitochondrial retrograde pathway to alleviate acetaminophen-induced acute liver injury

Project description:Acetaminophen (APAP) is the major cause of drug-induced liver injury, with limited treatment options. APAP overdose invokes excessive oxidative stress that triggers mitochondria-to-nucleus retrograde pathways, contributing to APAP-induced liver injury (AILI). Mesenchymal stem cell therapy is a promising tool for acute liver failure. Therefore, the purpose of this study is to investigate the beneficial effects of adipose-derived mesenchymal stem cell (AMSC) therapy on AILI and reveal the potential therapeutic mechanisms. C57BL/6 mice are used as the animal model and AML12 normal murine hepatocytes as the cellular model of APAP overdose. Immunohistochemical staining, western blotting, immunofluorescence staining, and RNA sequencing assay are used for assessing the efficacy and validating mechanisms of AMSC therapy. We found AMSC therapy effectively ameliorated AILI, while delayed AMSC injection lost its efficacy related to the c-Jun N-terminal kinase (JNK)-mediated mitochondrial retrograde pathways. We further found that AMSC therapy inhibited JNK activation and mitochondrial translocation, reducing APAP-induced mitochondrial damage. The down-regulation of activated Ataxia telangiectasia mutated (ATM) and DNA damage response proteins in AMSC treated mice liver indicated AMSC blocked the JNK-ATM pathway. Overall, AMSC may be an effective treatment for AILI by inhibiting JNK-ATM mitochondrial retrograde pathway, which improves APAP-induced mitochondrial dysfunction and liver injury.

2022-12-17 | GSE218879 | GEO

Human hematopoietic stem cell engraftment in goat

Project description:Human hematopoietic stem cell engraftment in goat

| PRJNA90277 | ENA

JNK pathway blockade promotes HER2-driven breast cancer [RNA-seq_primary_mammary_tumor_cell_lines]

Project description:JNK deletion in MMTV-NIC mouse model promotes mammary gland tumor formation.

2022-12-21 | GSE200521 | GEO

JNK pathway blockade promotes HER2-driven breast cancer [RNA-seq]

Project description:JNK knockout cells proliferate more and forms bigger mulit acinar sturctures under normal conditions on 3D culture.

2022-12-21 | GSE196459 | GEO

The activation of the NF-κB-JNK pathway is independent of the PI3K-Rac1-JNK pathway involved in the bFGF-regulated human fibroblast cell migration

Project description:Wound healing is a complex process that repairs organ-tissues including skin after injury. Cell migration is an important process of wound healing and fibroblast growth factor bFGF has been reported to accelerate cell migration. However, knowledge of how bFGF regulates cell migration is limited. Here, we used human foreskin fibroblast primary cells and RNA-Seq based transcriptome analysis to isolate bFGF-regulating signal pathways that regulate cell migration. Among the many pathways identified, an inflammatory response pathway was further examined for its role in fibroblast cell migration through analysis of function by the key regulator NF-κB. Application of Bay11-7082 and LPS, a typical inhibitor and inducer of inflammatory response, promoted and inhibited cell migration, respectively. Biochemical data showed that Bay11-7082 treatment induces the phosphorylation level of JNK，but PI3K inhibitor LY294002 application did not alter the IκBα phosphorylation level. In addition, Bay11-7082 and JNK inhibitor SP600125 together inhibit while LY294002 together with Bay11-7082 maintains normal cell migration, indicating that NF-κB is independent of the PI3K pathway for regulation of JNK activity during cell migration. Taken together, the present study broadens our understanding of the bFGF-regulation mechanism and further identifies a new bFGF-regulating mechanism by which NF-κB regulates JNK during human fibroblast cell migration.

2018-01-22 | GSE65193 | GEO

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