FGF9 Promotes Mouse Spermatogonial Stem Cell Proliferation Mediated by p38 MAPK Signaling [bulk RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA671713 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12893200.fastq.gz | Fastqsanger.gz | |||
| SRR12893201.fastq.gz | Fastqsanger.gz | |||
| SRR12893202.fastq.gz | Fastqsanger.gz | |||
| SRR12893203.fastq.gz | Fastqsanger.gz | |||
| SRR12893204.fastq.gz | Fastqsanger.gz |
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Project description:Objectives: Fibroblast growth factor 9 (FGF9) is expressed by somatic cells in the seminiferous tubules, yet little information exists about its role in regulating spermatogonial stem cells (SSCs). Materials and Methods: Fgf9 overexpression lentivirus was injected into mouse testes, and PLZF immunostaining was performed to investigate the effect of FGF9 on spermatogonia in vivo. Effect of FGF9 on SSCs was detected by transplanting cultured germ cells into tubules of testes. RNA-seq of bulk RNA and single-cell was performed to explore FGF9 working mechanisms. SB203580 was used to disrupt p38 MAPK pathway. p38 MAPK protein expression was detected by western blot and qPCR was performed to determine different gene expression. Small interfering RNA (siRNA) was used to knock down Etv5 gene expression in germ cells. Results: Overexpression of Fgf9 in vivo resulted in arrested spermatogenesis and accumulation of undifferentiated spermatogonia. Exposure of germ cell cultures to FGF9 resulted in larger numbers of SSCs over time. Inhibition of p38 MAPK phosphorylation negated the SSC growth advantage provided by FGF9. Etv5 and Bcl6b gene expression was enhanced by FGF9 treatment. Gene knockdown of Etv5 disrupted the growth effect of FGF9 in cultured SSCs along with downstream expression of Bcl6b. Conclusions: Taken together, this data indicates that FGF9 is an important regulator of SSC proliferation, operating through p38 MAPK phosphorylation and upregulating Etv5 and Bcl6b in turn.
2020-10-26 | GSE160062 | GEO
Project description:Objectives: Fibroblast growth factor 9 (FGF9) is expressed by somatic cells in the seminiferous tubules, yet little information exists about its role in regulating spermatogonial stem cells (SSCs). Materials and Methods: Fgf9 overexpression lentivirus was injected into mouse testes, and PLZF immunostaining was performed to investigate the effect of FGF9 on spermatogonia in vivo. Effect of FGF9 on SSCs was detected by transplanting cultured germ cells into tubules of testes. RNA-seq of bulk RNA and single-cell was performed to explore FGF9 working mechanisms. SB203580 was used to disrupt p38 MAPK pathway. p38 MAPK protein expression was detected by western blot and qPCR was performed to determine different gene expression. Small interfering RNA (siRNA) was used to knock down Etv5 gene expression in germ cells. Results: Overexpression of Fgf9 in vivo resulted in arrested spermatogenesis and accumulation of undifferentiated spermatogonia. Exposure of germ cell cultures to FGF9 resulted in larger numbers of SSCs over time. Inhibition of p38 MAPK phosphorylation negated the SSC growth advantage provided by FGF9. Etv5 and Bcl6b gene expression was enhanced by FGF9 treatment. Gene knockdown of Etv5 disrupted the growth effect of FGF9 in cultured SSCs along with downstream expression of Bcl6b. Conclusions: Taken together, this data indicates that FGF9 is an important regulator of SSC proliferation, operating through p38 MAPK phosphorylation and upregulating Etv5 and Bcl6b in turn.
2020-10-26 | GSE160061 | GEO
Project description:FGF9 Promotes Mouse Spermatogonial Stem Cell Proliferation Mediated by p38 MAPK Signaling
| PRJNA671712 | ENA
Project description:FGF9 Promotes Mouse Spermatogonial Stem Cell Proliferation Mediated by p38 MAPK Signaling [single-cell RNA-seq]
| PRJNA671714 | ENA
Project description:ObjectivesFibroblast growth factor 9 (FGF9) is expressed by somatic cells in the seminiferous tubules, yet little information exists about its role in regulating spermatogonial stem cells (SSCs).Materials and methodsFgf9 overexpression lentivirus was injected into mouse testes, and PLZF immunostaining was performed to investigate the effect of FGF9 on spermatogonia in vivo. Effect of FGF9 on SSCs was detected by transplanting cultured germ cells into tubules of testes. RNA-seq of bulk RNA and single cell was performed to explore FGF9 working mechanisms. SB203580 was used to disrupt p38 MAPK pathway. p38 MAPK protein expression was detected by Western blot and qPCR was performed to determine different gene expression. Small interfering RNA (siRNA) was used to knock down Etv5 gene expression in germ cells.ResultsOverexpression of Fgf9 in vivo resulted in arrested spermatogenesis and accumulation of undifferentiated spermatogonia. Exposure of germ cell cultures to FGF9 resulted in larger numbers of SSCs over time. Inhibition of p38 MAPK phosphorylation negated the SSC growth advantage provided by FGF9. Etv5 and Bcl6b gene expressions were enhanced by FGF9 treatment. Gene knockdown of Etv5 disrupted the growth effect of FGF9 in cultured SSCs along with downstream expression of Bcl6b.ConclusionsTaken together, these data indicate that FGF9 is an important regulator of SSC proliferation, operating through p38 MAPK phosphorylation and upregulating Etv5 and Bcl6b in turn.
| S-EPMC7791179 | biostudies-literature
Project description:Mitogen-activated protein kinases (MAPKs) regulate cardiomyocyte growth and apoptosis in response to extracellular stimulation, but the downstream effectors that mediate their pathophysiological effects remain poorly understood. We determined the targets and role of p38 MAPK in the heart in vivo by using local adenovirus-mediated gene transfer of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38α in rats. DNA microarray analysis of animals with cardiac-specific overexpression of p38 MAPK revealed that 264 genes were upregulated more than 2-fold including multiple genes controlling cell division, cell signaling, inflammation, adhesion and transcription. Several previously unknown p38 target genes were found. Using gel mobility shift assays we identified several cardiac transcription factors that were directly activated by p38 MAPK. Finally, we determined the functional significance of the altered cardiac gene expression profile by histological analysis and echocardiographic measurements, which indicated that p38 MAPK overexpression induced gene expression results in cell proliferation, myocardial inflammation and fibrosis. In conclusion, we defined the novel target genes and transcription factors as well as the functional effects of p38 MAPK in the heart. Expression profiling of p38 MAPK overexpression identified cell cycle regulatory and inflammatory genes critical for pathological processes in the adult heart. Keywords: Gene transfer
2006-12-19 | GSE3866 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-10-26 | GSE160063 | GEO
Project description:Background: Magnesium transporter subtype 1 (MAGT1) is involved in animal development and cell differentiation. Thus far, researches on MAGT1 are mainly focused on Cardiomyocyte regulation and differentiation, but rare research has been reported on cell proliferation, especially concerning the underlying molecular mechanisms. Methods: HeLa cells were transiently knock down with different SiRNAs and processed for RNA sequencing and bioinformatics analysis, western blot, real-time PCR as well as cell cycle assays. Results: We showed that cell proliferation was significantly restricted with S-phase arrest in MAGT1 knock down cells, which was further confirmed by the up expression of p21, CCNA1 and CCNB1, while down expression of CCND1, CCNE1 and CDK4. Knocking down MAGT1 also resulted in significant transcriptional expression changes of 1599 target genes analyzed by RNA sequencing. The bioinformatics analysis showed that MAGT1 was related to MAPK signaling pathway. Western blot analysis confirmed that the phosphorylation of ERK1/2 and p38 exhibited a remarkable reduction in MAGT1 downregulated group. Conclusion: MAGT1 is critical in HeLa cell proliferation, S-phase progress and ERK/p38 MAPK signaling pathway, indicating that MAGT1 might be a novel target of anticancer research.
2022-02-02 | GSE166084 | GEO
Project description:SARS-CoV-2, the causative agent of the COVID-19 pandemic, drastically modifies the cells that it infects. One such effect is the activation of the host p38 mitogen-activated protein kinase (MAPK) pathway, which plays a major role in inflammation pathways that are dysregulated in severe COVID-19 cases. Inhibition of p38/MAPK activity in SARS-CoV-2-infected cells reduces both cytokine production and viral replication. Here, we applied a systems biology approach to better understand interactions between the p38/MAPK pathway and SARS-CoV-2 in human lung epithelial cells. We found several components of the p38/MAPK pathway positively and negatively impact SARS-CoV-2 infection and that p38ß is a required host factor for SARS-CoV-2 that acts by promoting viral protein translation in a manner that prevents innate immune sensing. Furthermore, we combined chemical and genetic perturbations of p38ß with quantitative phosphoproteomics to identify novel, putative p38ß substrates in an unbiased manner, with broad relevance beyond SARS-CoV-2 biology.
2022-01-21 | GSE183999 | GEO
Project description:Objective: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS), characterized by a global increasing incidence driven by relapsing-remitting disease in females. p38 MAP kinase (MAPK) has been described as a key regulator of inflammatory responses in autoimmunity, but its role in the sexual dimorphism in MS or MS models remains unexplored. Methods: Toward this end, we used experimental autoimmune encephalomyelitis (EAE), the principal animal model of MS, combined with pharmacologic and genetic inhibition of p38 MAPK activity and transcriptomic analyses. Results: Pharmacologic inhibition of p38 MAPK selectively ameliorated EAE in female mice. Conditional deletion studies demonstrated that p38M-NM-1 signaling in macrophages/myeloid cells, but not T cells or dendritic cells, recapitulated this sexual dimorphism. Analysis of CNS inflammatory infiltrates showed that female, but not male mice lacking p38M-NM-1 in myeloid cells exhibited reduced immune cell activation compared with controls, while peripheral T cell priming was unaffected in both sexes. Transcriptomic analyses of myeloid cells revealed differences in p38M-NM-1-controlled transcripts comprising female- and male-specific gene modules, with greater p38M-NM-1 dependence of pro-inflammatory gene expression in females. Interpretation: Our findings demonstrate a key role for p38M-NM-1 in myeloid cells in CNS autoimmunity and uncover important molecular mechanisms underlying sex differences in disease pathogenesis. Taken together, our results suggest that the p38 MAPK signaling pathway represents a novel target for much needed disease modifying therapies for MS WT vs. p38alphaCKO macrophages, male vs. female
2013-10-29 | E-GEOD-51707 | biostudies-arrayexpress