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Genome wide map of chromatin state during early development of TrkC neurons of the DRG

ABSTRACT: We isolated E11.5 TrkC neurons and profiled ATAC and H3K27ac genomic regions

ORGANISM(S): Mus musculus

PROVIDER: GSE162471 | GEO | 2020/12/02

REPOSITORIES: GEO

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Genome wide map of Runx3, Brn3a, Islet1 binding, chromatin accessibility (ATAC) and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

Project description:We isolated E11.5 TrkC neurons and profiled chromatin accessibility (ATAC), Runx3, Brn3a, Islet1 binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons by Cut&Run

2024-11-03 | GSE252398 | GEO

Genome wide map of Runx3, Brn3a binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

Project description:We isolated E12.5 TrkC neurons and profiled Runx3, Brn3a binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons by Cut&Run

2024-11-06 | GSE253172 | GEO

RNA-seq of E11.5 TrkC neurons of Runx3-P2+/- and Runx3-P2-/- mice

Project description:To gain insight into the role of Runx3 in TrkC neurons we performed RNA-seq on E11.5 TrkC neurons isolated from cervical ganglia of Runx3-P2+/- and Runx3-P2-/- mice

2016-11-20 | GSE81140 | GEO

Genome wide map of chromatin state during early development of TrkC neurons of the DRG

Project description:Genome wide map of chromatin state during early development of TrkC neurons of the DRG

| PRJNA681913 | ENA

Novel role of TrkC in diabetic nephropathy and cross-talk of TrkC with insulin-related signaling

Project description:Diabetic nephropathy is a major cause of end-stage renal disease. Kidney podocytes play a central role in the pathogenesis of diabetic nephropathy. With their intercellular contacts they assemble part of the kidney filter. Many molecular mechanisms of the pathogenesis of diabetic nephropathy are not elucidated and targeted therapies are lacking. Nephron-specific TrkCknockout (TrkC-KO) and TrkC overexpressing mice exhibit features of diabetic nephropathy such as enlarged glomeruli with mesangial proliferation, basement membrane thickening, albuminuria and podocyte loss when aging. Insulin-like growth factor 1 receptor (Igf1R)- associated gene expression was regulated in TrkC-KO mice glomeruli by qPCR. Phosphoproteins associated with insulin, erb-b2 receptor tyrosine kinase (Erbb) and Toll-like receptor signaling were enriched in lysates of podocytes treated with the TrkC ligand neurotrophin-3(Nt-3) in a mass spectrometry analysis. Activation of TrkC by Nt-3 resulted in phosphorylation of the Igf1R on activating tyrosine residues in podocytes. Our results identify TrkC to be a potentially targetable mediator of diabetic nephropathy.

2021-09-10 | PXD017960 | Pride

Genome wide map of Runx3, Brn3a, Islet1 binding, chromatin accessibility (ATAC) and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

Project description:Genome wide map of Runx3, Brn3a, Islet1 binding, chromatin accessibility (ATAC) and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

| PRJNA1060332 | ENA

Genome wide map of Runx3, Brn3a binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

Project description:Genome wide map of Runx3, Brn3a binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

| PRJNA1064151 | ENA

RNA-seq of human neurons derived from mutant embryonic stem cell line lacking the BDNF receptor TrkB treated with the natural TrkC receptor agonist Neurotrophin-3

Project description:RNAseq data indicate that in the human brain, most neurons co-express the brain-derived neurotrophic factor (BDNF) receptor TrkB and the Neurotrophin-3 (NT3) receptor TrkC. Because NT3 can also activate TrkB and TrkB is expressed at higher levels compared with TrkC, it has been difficult thus far to explore TrkC-mediated signaling. To this end, neurons were generated from human embryonic stem cells lacking the BDNF receptor TrkB using CRISPR/Cas9. These neurons were found to respond to very low concentrations of NT3, lower than the concentrations of BDNF needed to activate TrkB. In order to compare the transcriptional changes following treatment with NT3 RNA-seq analysis was performed and the results compared with those previously obtained following treatment of wild-type neurons with BDNF Merkouris et al. PMID: 29987039. The results indicate that downstream of TrkC activation, most of the changes in gene expression are similar to those seen after TrkB activation. The results also show that exposure to sub-saturating concentrations of either BDNF or NT3 does not cause receptor downregulation as seen with saturating ligand concentrations and that the receptors can be re-activated.

2022-03-22 | E-MTAB-11566 | biostudies-arrayexpress

Next-generation sequencing facilitates quantitative analysis of T1-T4 sympathetic ganglia transcriptomes from TRKC+/-, AdNTF3-Tg and their respective wild type control mice after 1 day cold exposure at 5℃

Project description:Activation of brown fat thermogenesis increases energy expenditure and alleviates obesity. Sympathetic nervous system (SNS) is important in brown/beige adipocyte thermogenesis. Here we discover a novel fat-derived “adipokine” neurotrophic factor neurotrophin 3 (NTF3) and its receptor Tropomyosin receptor kinase C (TRKC) as key regulators of SNS growth and innervation in adipose tissue. NTF3 is highly expressed in brown/beige adipocytes, and potently stimulates sympathetic neuron neurite growth. NTF3/TRKC regulates a plethora of pathways in neuronal axonal growth and elongation. Adipose tissue sympathetic innervation is significantly increased in mice with adipocyte-specific NTF3 overexpression, but profoundly reduced in mice with TRKC haploinsufficiency (TRKC+/-). Increasing NTF3 via pharmacological or genetic approach promotes beige adipocyte development, enhances cold-induced thermogenesis and protects against diet-induced obesity (DIO); whereas TRKC+/- mice or SNS TRKC deficient mice are cold intolerant and prone to DIO. Thus, NTF3 is an important fat-derived neurotrophic factor regulating SNS innervation, energy metabolism and obesity.

2021-07-15 | GSE173503 | GEO

NT-3 contributes to chemotherapy-induced neuropathic pain by TrkC-mediated CCL2 elevation in DRG

Project description:Cancer patients undergoing treatment with antineoplastic drugs often experience chemotherapy-induced neuropathic pain (CINP), and therapeutic options for managing CINP are limited. Here, we show that systemic paclitaxel administration upregulates the expression of neurotrophin-3 (Nt3) mRNA and NT3 protein in the neurons of dorsal root ganglia (DRG), but not in the spinal cord. Blocking NT3 upregulation attenuates paclitaxel-induced mechanical, heat, and cold nociceptive hypersensitivities and spontaneous pain without altering acute pain and locomotor activity in male and female mice. Conversely, mimicking this increase produces enhanced responses to mechanical, heat, and cold stimuli and spontaneous pain in naïve male and female mice. Mechanistically, NT3 triggers tropomyosin receptor kinase C (TrkC) activation and participates in the paclitaxel-induced increases of C-C chemokine ligand 2 (Ccl2) mRNA and CCL2 protein in the DRG. Given that CCL2 is an endogenous initiator of CINP and that Nt3 mRNA co-expresses with TrkC and Ccl2 mRNAs in DRG neurons, NT3 likely contributes to CINP through TrkC-mediated activation of the Ccl2 gene in DRG neurons. NT3 may be thus a potential target for CINP treatment.

| S-SCDT-10_1038-S44319-024-00133-6 | biostudies-other

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