Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Caulis Polygoni Multiflori accelerates megakaryopoiesis and thrombopoiesis via activating PI3K/Akt and MEK/ERK (MAPK) signaling pathways

ABSTRACT: Caulis Polygoni Multiflori accelerates megakaryopoiesis and thrombopoiesis via activating PI3K/Akt and MEK/ERK (MAPK) signaling pathways

PROVIDER: PRJNA874815 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21307865_1.fastq.gz	Fastqsanger.gz
	SRR21307865_2.fastq.gz	Fastqsanger.gz
	SRR21307866_1.fastq.gz	Fastqsanger.gz
	SRR21307866_2.fastq.gz	Fastqsanger.gz
	SRR21307867_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Caulis Polygoni Multiflori accelerates megakaryopoiesis and thrombopoiesis via activating PI3K/Akt and MEK/ERK (MAPK) signaling pathways

Project description:In vtro and in vivo experiments revealed that Caulis Polygoni Multiflori (CPM) significantly induced megakaryocyte (MK) differentiation and maturation. To investigate the underlying mechanism of action of CPM in promoting MK differentiation, RNA-seq was performed to reveal the gene expression profile in MK differentiation induced by CPM. Our results showed that CPM up-regulated 850 differentially expressed genes (DEGs), down-regulated 1100 DEGs. Disease Ontology (DO) enrichment analysis revealed that CPM could regulate thrombocytopenia, blood platelet disease and blood coagulation disease. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome pathway enrichment analysis suggested that CPM regulated PI3K/Akt and ERK/MEK (MAPK) signaling pathways.

2022-08-31 | GSE212290 | GEO

<i>Caulis Polygoni Multiflori</i> Accelerates Megakaryopoiesis and Thrombopoiesis via Activating PI3K/Akt and MEK/ERK Signaling Pathways.

Project description:Thrombocytopenia is one of the most common complications of cancer therapy. Until now, there are still no satisfactory medications to treat chemotherapy and radiation-induced thrombocytopenia (CIT and RIT, respectively). Caulis Polygoni Multiflori (CPM), one of the most commonly used Chinese herbs, has been well documented to nourish blood for tranquilizing the mind and treating anemia, suggesting its beneficial effect on hematopoiesis. However, it is unknown whether CPM can accelerate megakaryopoiesis and thrombopoiesis. Here, we employ a UHPLC Q-Exactive HF-X mass spectrometer (UHPLC QE HF-X MS) to identify 11 ingredients in CPM. Then, in vitro experiments showed that CPM significantly increased megakaryocyte (MK) differentiation and maturation but did not affect apoptosis and lactate dehydrogenase (LDH) release of K562 and Meg-01 cells. More importantly, animal experiments verified that CPM treatment markedly accelerated platelet recovery, megakaryopoiesis and thrombopoiesis in RIT mice without hepatic and renal toxicities in vivo. Finally, RNA-sequencing (RNA-seq) and western blot were used to determine that CPM increased the expression of proteins related to PI3K/Akt and MEK/ERK (MAPK) signaling pathways. On the contrary, blocking PI3K/Akt and MEK/ERK signaling pathways with their specific inhibitors suppressed MK differentiation induced by CPM. In conclusion, for the first time, our study demonstrates that CPM may be a promised thrombopoietic agent and provide an experimental basis for expanding clinical use.

| S-EPMC9607024 | biostudies-literature

Inhibition of O-GlcNAcylation via O-GlcNAc transferase fosters megakaryopoiesis and induces thrombopoiesis

Project description:We report that cellular O-GlcNAcylation levels decline along the course of megakaryocyte (MK) differentiation from human-derived hematopoietic stem and progenitor cells (HSPCs) and that inhibition of O-GlcNAc transferase (OGT), of which catalyzes O-GlcNAcylation, prolongedly decreases O-GlcNAcylation and induces megakaryopoiesis and thrombopoiesis. To gain the better insight into the potential mechanisms underlying platelet regulation by O-GlcNAcylation ,we compared the genome-wide transcription profiles of megakaryblastic MEG-01 cells with decreased O-GlcNAcylation (OGTi) and its control counterpart using RNA sequencing. Gene ontology and enrichment analysis of differentially expressed genes suggest that platelet formation might be regulated through the perturbation in cell adhesion molecules, i.e. integrin-a4 and b7, downstream of O-GlcNAc/c-Myc axis.

2020-08-06 | GSE150880 | GEO

Inhibition of O-GlcNAcylation via O-GlcNAc transferase fosters megakaryopoiesis and induces thrombopoiesis

Project description:Inhibition of O-GlcNAcylation via O-GlcNAc transferase fosters megakaryopoiesis and induces thrombopoiesis

| PRJNA633908 | ENA

Gastrophysa polygoni

Project description:Gastrophysa polygoni overview

| PRJNA1002044 | ENA

A Novel Antithrombocytopenia Agent, <i>Rhizoma cibotii</i>, Promotes Megakaryopoiesis and Thrombopoiesis through the PI3K/AKT, MEK/ERK, and JAK2/STAT3 Signaling Pathways.

Project description:BackgroundCibotii rhizoma (CR) is a famous traditional Chinese medicine (TCM) used to treat bleeding, rheumatism, lumbago, etc. However, its therapeutic effects and mechanism against thrombocytopenia are still unknown so far. In the study, we investigated the effects of aqueous extracts of Cibotii rhizoma (AECRs) against thrombocytopenia and its molecular mechanism.MethodsGiemsa staining, phalloidin staining, and flow cytometry were performed to measure the effect of AECRs on the megakaryocyte differentiation in K562 and Meg-01 cells. A radiation-induced thrombocytopenia mouse model was constructed to assess the therapeutic actions of AECRs on thrombocytopenia. Network pharmacology and experimental verification were carried out to clarify its mechanism against thrombocytopenia.ResultsAECRs promoted megakaryocyte differentiation in K562 and Meg-01 cells and accelerated platelet recovery and megakaryopoiesis with no systemic toxicity in radiation-induced thrombocytopenia mice. The PI3K/AKT, MEK/ERK, and JAK2/STAT3 signaling pathways contributed to AECR-induced megakaryocyte differentiation. The suppression of the above signaling pathways by their inhibitors blocked AERC-induced megakaryocyte differentiation.ConclusionsAECRs can promote megakaryopoiesis and thrombopoiesis through activating PI3K/AKT, MEK/ERK, and JAK2/STAT3 signaling pathways, which has the potential to treat radiation-induced thrombocytopenia in the clinic.

| S-EPMC9694118 | biostudies-literature

YAP1 regulates thrombopoiesis by binding to MYH9 in immune thrombocytopenia

Project description:Immune thrombocytopenia (ITP) is a complicated bleeding disease characterized by sharp platelet reduction. As a dominating element involved in ITP, megakaryocytes (MKs) are responsible for thrombopoiesis. However, the mechanism behind the dysregulation of thrombopoiesis in ITP remains undetermined. In this study, we examined the role of YAP1, Yes-associated protein 1, in thrombopoiesis during ITP. We observed a reduced YAP1 expression with cytoskeletal actin misalignment in MKs of ITP patients. Using experimental ITP mice, we showed that YAP1 reduction induced aberrant MK distribution, reduced the percentage of late MKs in total MKs, and caused submaximal platelet recovery. Mechanistically, YAP1 upregulation by GATA1 binding to its promoter promoted MK maturation. Phosphorylated YAP1 facilitated cytoskeletal activation by binding of its WW2 domain to MYH9, facilitating thrombopoiesis. Targeting YAP1 by its activator XMU-MP-1 was sufficient to rescue cytoskeleton defects and thrombopoiesis in YAP1+/- ITP mice and ITP patients. Taken together, these results demonstrate a crucial role for YAP1 in thrombopoiesis, providing a potential for the development of diagnostic markers and therapeutic options for ITP.

2024-12-22 | GSE250220 | GEO

YAP1 regulates thrombopoiesis by binding to MYH9 in immune thrombocytopenia [scRNA-seq]

2024-12-31 | GSE251704 | GEO

Paenibacillus polygoni strain:C31

Project description:Paenibacillus polygoni strain:C31 Genome sequencing

| PRJNA977379 | ENA

RUVBL1 accelerates tongue squamous cell carcinoma by mediating CRaf/MEK/ERK pathway

Project description: Not available

| S-EPMC10960137 | biostudies-literature