GEO DataSets

(Submitter supplied) How LTβR-signalling drives chronic tissue damage particularly in the lung, which mechanisms regulate this process, and whether LTβR-blockade might be of therapeutic value has remained unclear. To study the mechanisms underlying LTβR-inhibition, a transcriptional analysis was performed on lung tissue from B6 mice exposed to cigarette smoke for 6 months and treated therapeutically with LTβR-Ig from 4 to 6 months compared to mice exposed to cigarette smoke for 6 months and treated with control Ig from 4 to 6 months and filtered air control. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

13 Samples

Download data: MTX, TXT

(Submitter supplied) Extravasation of monocytes into tissue and to the site of injury is a fundamental immunological process underlying a variety of innate inflammatory responses across multiple organ systems, which requires rapid responses via post translational modifications (PTM) of proteins. Specifically, methylation of protein by arginine methyltransferases (PRMTs) is an epigenetic PTM implicated in inflammatory responses. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

16 Samples

Download data: H5AD, MTX, TXT

(Submitter supplied) 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). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6885

27 Samples

Download data: TXT

(Submitter supplied) Chronic Obstructive Pulmonary Disease, which is comprised of chronic bronchitis and emphysema, is a leading cause of morbidity and mortality. Because tissue destruction is the prominent characteristic of emphysema, extracellular proteinases, particularly those with elastolytic ability, are often considered to be key drivers in this disease. Several human and mouse studies have implicated roles for matrix metalloproteinases (MMPs), particularly macrophage-derived proteinases, in COPD pathogenesis. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6885

16 Samples

Download data: TXT

(Submitter supplied) Chronic obstructive pulmonary disease (COPD) is characterized by a progressive decline in lung function, caused by exposure to exogenous particles, mainly cigarette smoke (CS). COPD pathogenesis is initiated and perpetuated by an abnormal CS-induced inflammatory response of the lungs, involving both innate and adaptive immunity. Specifically, B cells organized in iBALT structures, as well as macrophages, accumulate in the lungs and contribute to CS-induced emphysema, but the mechanisms thereof remain unclear. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5438

Platform:

GPL6885

12 Samples

Download data: TXT

Analysis of lung from cigarette smoke (CS)-treated C57BL/6N females at 4 and 6 months of age. Tobacco smoking is a major cause of chronic obstructive pulmonary disease (COPD). Results provide insight into the molecular mechanisms underlying cigarette smoke-induced COPD.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 age, 2 stress sets

Platform:

GPL6885

Series:

GSE52509

12 Samples

Download data

(Submitter supplied) Atherosclerosis is a transmural chronic inflammatory condition of small and large arteries that is associated with adaptive immune responses at all disease stages. However, impacts of adaptive immune reactions on clinically apparent atherosclerosis such as intima lesion (plaque) rupture, thrombosis, myocardial infarction, and aneurysm largely remain to be identified. It is increasingly recognized that leukocyte infiltrates in plaque, media, and adventitia are distinct but their specific roles have not been defined. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL8321

19 Samples

Download data: CEL

(Submitter supplied) Cultured mouse aorta endothelial cells (from 8-12 weeks old C57BL/6J mice, passage 2-3) were exposed to phosphate buffered saline (control) or a combination of TNFalpha plus agonistic alpha-LTßR antibody for 24 hours as described in Lötzer et al. 2009. Arterioscler. Thromb. Vasc. Biol., in press. Total RNA was extracted and microarrays were prepared.

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3810

Platform:

GPL1261

5 Samples

Download data: CEL

(Submitter supplied) Mouse aorta smooth muscle cells (SMCs) express TNF receptor superfamily member 1A (TNFR1) and lymphotoxin ß receptor (LTßR). Circumstantial evidence has linked the SMC LTßR to tertiary lymphoid organogenesis in diseased aortae of hyperlipidemic mice. Here, we explored potential roles of TNFR1 and LTßR activation in cultured SMCs. TNFR1 signaling by TNF activated the classical RelA NF-κB pathway, whereas LTßR signaling by agonistic anti LTßR antibody activated both the classical RelA and alternative RelB NF-κB pathways. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3809

Platform:

GPL1261

21 Samples

Download data: CEL

Analysis of cultured aortic endothelial cells stimulated with a combination of tumor necrosis factor (TNF) and α-LTßR antibody for 24 hours. Unlike similarly-treated aortic smooth muscle cells (SMCs), the endothelial cells did not differentiate into a lymphoid tissue organizer (LTO) phenotype.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 agent sets

Platform:

GPL1261

Series:

GSE19139

5 Samples

Download data: CEL

Analysis of cultured aortic smooth muscle cells (SMCs) stimulated with a combination of tumor necrosis factor (TNF) and α-LTβR monoclonal antibody for up to 24 hours. SMCs stimulated by TNF/α-LTβR mAb, but not with either agent alone, differentiate into lymphoid tissue organizer (LTO)-like cells

Organism:

Mus musculus

Type:

Expression profiling by array, count, 4 agent, 3 time sets

Platform:

GPL1261

Series:

GSE15062

21 Samples

Download data: CEL

(Submitter supplied) Airway mucus obstruction triggers macrophage activation and MMP12-dependent emphysema

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

6 Samples

Download data: CEL

(Submitter supplied) Increased IGF1 signaling in p16 -/- lungs

Organism:

Mus musculus

Type:

Expression profiling by RT-PCR

Platform:

GPL26852

4 Samples

Download data: XLSX

(Submitter supplied) Wnt/β-catenin signaling regulates progenitor cell fate decisions during lung development and in various adult tissues. Ectopic activation of Wnt/β-catenin signaling promotes tissue repair in emphysema, a devastating lung disease with progressive loss of parenchymal lung tissue. The identity of Wnt/β-catenin responsive progenitor cells and the potential impact of Wnt/β-catenin signaling on adult distal lung epithelial progenitor cell function in emphysema, are poorly understood. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL20775

18 Samples

Download data: CEL, CHP

(Submitter supplied) Developmental signals are known to modulate inflammation. How ever, the mechanistic insight that links developmental and inflammatory signaling remains elusive. In the current study, we identifya critical role of NF-kB system in mediating stimulus specific crosstalk that allows developmental LTbR signals to sustain inflammatory TLR4 induced RelA/NF-kB response and gene expression. LTbR activated non-canonical signaling targets canonical TLR4 induced, nfkb2 encoded p100 not only to deplete inhibitory IkBd/(p100)2, but also to supplement RelA:p52/NF-kB dimers. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5655

Platform:

GPL6885

4 Samples

Download data: TXT

Analysis of MEFs treated for 24hrs with ligands lipopolysaccharide (LPS), lymphotoxin-β receptor agonist antibody (LTβR), and LPS+ LTβR. Results provide insight into molecular mechanisms underlying a potentially synergistic effect of LTβR signaling on LPS-TLR4 signaling.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 4 protocol sets

Platform:

GPL6885

Series:

GSE62301

4 Samples

Download data

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

35 Samples

Download data

(Submitter supplied) Purpose: The goal of this study is to address if in utero and early life nicotine exposure can prime the offspring to be more succetible to develop emphysema in adulthood Methods: A mouse model of two hits: a prenatal hit and a later insult delivered in adulthood was used in this study. In brief, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and until the post-natal day 16 (nicotine group). more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

21 Samples

Download data: TXT

(Submitter supplied) Purpose: The goal of this study is to address if in utero and early life nicotine exposure can affect genetic profile in early ephysema Methods: A mouse model of two hits: a prenatal hit and a later insult delivered in adulthood was used in this study. In brief, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and until the post-natal day 16 (nicotine group). more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

14 Samples

Download data: TXT

(Submitter supplied) HIV1+ smokers develop emphysema at an earlier age and with a higher incidence than HIV1- smokers. Based on the knowledge that human alveolar macrophages (AM) are capable of producing proteases that degrade extracellular matrix components, we hypothesized that upregulation of AM matrix metalloproteinases may be associated with the emphysema of HIV1+ smokers. To test this hypothesis, microarray analysis was used to screen which MMP genes were expressed by AM isolated by bronchoalveolar lavage (BAL) of HIV1+ smokers with early emphysema. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

11 Samples

Download data: CEL, CHP