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Targeting JNK Pathway Expands Human Hematopoietic Stem Cells

ABSTRACT: Targeting JNK Pathway Expands Human Hematopoietic Stem Cells

PROVIDER: PRJNA471685 | ENA |

REPOSITORIES: ENA

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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

Transient inhibition of JNK pathway improves hematopoietic stem cell engraftment

Project description:Transient inhibition of JNK pathway improves hematopoietic stem cell engraftment

| PRJNA694702 | ENA

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 promotes human hematopoietic stem cell expansion.

Project description: Not available

| S-EPMC6323118 | biostudies-literature

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

Targeting Hedgehog pathway by Smoothened Antagonist

Project description:Targeting Hedgehog pathway by Smoothened Antagonist

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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

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

Project description:Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

| PRJNA494503 | ENA

Loss of JNK in Breast Epithelium Accelerates Tumor Formation

Project description:Members of the JNK pathway have been found to be mutated in human breast cancer. Mouse studies examining JNK loss in different tissues have demonstrated that the JNK pathway can play a role in cancer. Using and autochthonous mouse model, we found that JNK deficiency on a p53-null background resulted in more rapid tumor onset. To learn more about these tumors we generated cells lines and performed various in vitro assays, as well as RNAseq in hope of finding differentially expressed genes that may explain the differences we observed in vivo.

2018-05-29 | GSE92560 | GEO

Regulation of the Golgi apparatus by p38 and JNK kinases during cellular stress responses

Project description:p38 and JNK are activated in response to acute stress and inflammatory signals. Through modification of a plethora of substrates, these kinases profoundly re-shape cellular physiology for the optimal response to a harmful environment and/or an inflammatory state. Here, we utilized phospho-proteomics to identify several hundred substrates for both kinases. Our results indicate that the scale of signaling from p38 and JNK are of a similar magnitude. Among the many new targets, we highlight the regulation of the transcriptional regulators GIGYF1 and 2 by p38-dependent MK2 phosphorylation and 14-3-3 binding. We also show that the Golgi apparatus contains numerous substrates, and is a major target for regulation by p38 and JNK. When activated, these kinases mediate structural rearrangement of the Golgi apparatus which positively affects protein flux through the secretory system. Our work expands on our knowledge about p38 and JNK signaling with important biological ramifications.

2021-09-13 | PXD028151 | Pride

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