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Biological processes in hind paws, dorsal root ganglia and spinal cord of PTX (the short model) and lymphotoxin-beta receptor (LTβR) antagonist treated mice

ABSTRACT: We investigated biological processes in hind paw, dorsal root ganglion (DRG) and spinal cord (SC) associated with lymphotoxin-beta receptor (LTβR) antagonist treatment of chemotherapy modeled mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE302021 | GEO | 2026/03/02

REPOSITORIES: GEO

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Biological processes in hind paws, dorsal root ganglia and spinal cord of lymphotoxin-beta receptor (LTβR) agonist treated mice

Project description:We investigated biological processes in hind paw, dorsal root ganglion (DRG) and spinal cord (SC) associated with lymphotoxin-beta receptor (LTβR) agonist treatment.

2026-03-02 | GSE302020 | GEO

Biological processes in hind paws, dorsal root ganglia and spinal cord after PTX treatment (the short model)

Project description:We investigated biological processes in hind paw, dorsal root ganglion (DRG) and spinal cord (SC) associated with chemotherapy treatment.

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Biological processes in hind paws and dorsal root ganglia in males and females after PTX treatment (the intermediate model)

Project description:We investigated biological processes in hind paw and dorsal root ganglion (DRG) of male and female mice associated with chemotherapy treatment

2026-03-02 | GSE302110 | GEO

Biological processes in hind paw skin fibroblasts, keratinocytes and immune cells after PTX treatment (the short model)

Project description:We investigated biological processes in hind paw skin fibroblasts, keratinocytes and immune cells associated with chemotherapy treatment.

2026-03-02 | GSE302111 | GEO

Inhibition of LTβR-signalling blocks epithelial apoptosis and activates endogenous Wnt-induced regeneration

Project description:Lymphotoxin β-receptor-signalling orchestrates lymphoid neogenesis and subsequent tertiary lymphoid structures (TLS) associated with severe chronic inflammatory diseases spanning multiple organ systems. How LTβR-signalling drives chronic tissue damage particularly in the lung, which mechanism(s) regulate this process, and whether LTβR-blockade might be of therapeutic value has remained unclear. Here we demonstrate increased lymphotoxin expression of LTbR-ligands on myeloid and adaptive and innate immune-cells, enhanced non-canonical NF-κB signalling and enrichment of LTβR-target gene expression in epithelial cells of lungs from patients and mice with smoking-associated chronic obstructive pulmonary disease (COPD). Accordingly, Therapeutic inhibition of LTβR-signalling in young and aged mice with COPD disrupted TLS, reverted lung tissue destruction, airway-fibrosis and systemic muscle wasting. Mechanistically, we identified that LTβR-signalling blockade leads to diminished cell-death, concomitantly reactivated endogenous Wnt/β-catenin-signalling in alveolar epithelial cells and reduced TGFβ-signalling in airways. These findings highlight LTβR as a viable therapeutic target against TLS induced tissue damage that translates into novel anti-inflammatory, regenerative strategies to treat COPD.

2020-07-10 | GSE125521 | GEO

RelA and RelB-dependent transcriptome analysis in lymphotoxin-ß receptor stimulated mouse embryonic fibroblasts

Project description:Background: Lymphotoxin signaling via the lymphotoxin-β receptor (LTβR) has been implicated in several biological processes, ranging from development of secondary lymphoid organs, maintenance of splenic tissue, host defense against pathogens, autoimmunity, and lipid homeostasis. The major transcription factor that is activated by LTβR crosslinking is NF-κB. Two signaling pathways have been described that result in the activation of classical p50-RelA and alternative p52-RelB NF-κB heterodimers. Results: Using microarray analysis, we investigated the transcriptional response downstream of the LTβR in mouse embryoni fibroblasts (MEF) and its regulation by the RelA and RelB subunits of NF-κB. We describe novel LTβR-responsive genes that are regulated by RelA and/or RelB. Interestingly, we found that the majority of LTβR-regulated genes require the presence of both RelA and RelB, suggesting significant crosstalk between the two NF-κB activation pathways. Gene Ontology (GO) analysis confirmed that LTβR-NF-κB target genes are predominantly involved in the regulation of immune responses. However, other biological processes, such as apoptosis/cell death, cell cycle, angiogenesis, and taxis were also regulated by LTβR signaling. Moreover, we show that activation of the LTβR inhibits the expression of a key adipogenic transcription factor, peroxisome proliferator activated receptor-γ (pparg), suggesting that LTβR signaling may interfere with adipogenic differentiation. Conclusions: Thus, microarray analysis of LTβR-stimulated fibroblasts revealed further insight into the transcriptional response of LTβR signaling and its regulation by the NF-κB family members RelA and RelB. Keywords: cell type comparison (wt vs relA-/- vs relB-/-) after genetic modification using a time course for each cell type (wt, relA-/-, relB-/-) two time points were analysed (0h as control and 10h) using 3 technical replicates resulting in 18 samples in total

2008-12-17 | E-GEOD-11963 | biostudies-arrayexpress

RelA and RelB-dependent transcriptome analysis in lymphotoxin-ß receptor stimulated mouse embryonic fibroblasts

2008-12-18 | GSE11963 | GEO

LTβR controls thymic portal endothelial cells for hematopoietic progenitor cell homing and T cell regeneration

Project description:Continuous thymic homing of hematopoietic progenitor cells (HPCs) via the blood is critical for normal T cell development. However, the nature and the differentiation program of the specialized thymic endothelial cells (ECs) controlling this process remain poorly understood. Here, using conditional gene-deficient mice, we find that lymphotoxin beta receptor (LTβR) directly controls thymic ECs to guide HPC homing. Interestingly, T cell deficiency or conditional ablation of T-cell-engaged LTβR signaling results in a defect in thymic HPC homing, suggesting the feedback regulation of thymic progenitor homing by thymic products. Furthermore, we identify and characterize a special thymic portal EC population with features that guide HPC homing. LTβR is essential for the differentiation and homeostasis of these thymic portal ECs. Finally, we show that LTβR is required for T cell regeneration upon irradiation-induced thymic injury. Together, these results uncover a cellular and molecular pathway that governs thymic EC differentiation for HPC homing.

2017-02-09 | GSE83114 | GEO

RNA-Seq of Ribosomal prophiling in mice 2h post Hind-Paw Formalin injection

Project description:The goal was to identify actively translated sequences in Dorsal spinal cord from Mice 2hours after Hind-Paw 20% formalin injection. Ipsi and Contralateral sides were compared to identify transcriptional changes after acute pain. Tissue was collected and ribosomes were pulled-down in the presence of CHX, RNA was purified and sequenced afterwards.

2024-01-30 | E-MTAB-13734 | biostudies-arrayexpress

Transcription profiling by array of mouse hind paws after receiving KRN T cells from K/BxN mice

Project description:K/BxN mice were generated by crossing KRN males with NOD females, and it was these mice that served as the source for the T cells adoptively transferred. Male B6.TCR.Ca-/-H-2b/g7 (recipient) mice age 10-14 weeks old were used in this model and are the source of the paw tissue profiled in this study.

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