Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1074424 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27915477_1.fastq.gz | Fastqsanger.gz | |||
| SRR27915477_2.fastq.gz | Fastqsanger.gz | |||
| SRR27915478_1.fastq.gz | Fastqsanger.gz | |||
| SRR27915478_2.fastq.gz | Fastqsanger.gz | |||
| SRR27915479_1.fastq.gz | Fastqsanger.gz |
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Project description:Lymphangioleiomyomatosis (LAM) is a metastasizing neoplasm of reproductive age women which causes cystic lung remodeling and progressive respiratory failure. While LAM lesions are known to contain abnormal smooth muscle-like cells which harbor mTOR activating mutations in TSC1 or TSC2, the tissue origins of the mutant “LAM cells” that invade the lung remain unclear. By employing single cell and single nuclear RNA sequencing on explanted LAM lungs, we identified a unique population of cells and associated signature genes and gene networks which were readily distinguished from those of endogenous lung cells. These unique LAMCORE cells shared closest transcriptomic similarity to normal uterus and share transcriptomic features with neural crest, as identified in uterine LAM lesions by single nuclear RNA-seq. Immunofluorescence microscopy demonstrated the expression of LAMCORE cell signature genes within LAM lesions in both lung and uterus. Serum aptamer proteomics and ELISA identified biomarkers consistent with the signature genes expressed and predicted to be secreted by LAMCORE cells. Single cell transcriptomics strongly supports a uterine neural crest origin of LAMCORE cells; providing insights into disease pathogenesis and informing future treatment strategies for LAM.
2020-07-11 | GSE135851 | GEO
Project description:Cultivated grapevine (Vitis vinifera) is susceptible to many pathogens which cause significant losses to viticulture worldwide. Chemical control is available, but agro-ecological concerns have raised interest in alternative methods, especially in elicitation of plant immunity by bio-molecules such as Pathogen Associated Molecular Patterns (PAMPs). We have demonstrated that the beta-glucan laminarin (Lam) and its sulfated derivative (PS3) induce a PAMP-triggered immunity in grapevine against downy mildew (Plasmopara viticola). However, if Lam elicits classical grapevine defenses, PS3 triggered grapevine resistance via a poorly understood priming phenomenon. The aim of this study was to discover the mechanism of the PS3-induced resistance. On uninfected grapevine, we first investigated defense signaling and performed microarray experiments to identify early events and genes directly triggered by PS3. Our results showed that PS3 i) was unable to elicit ROS and NO production, cytosolic Ca2+ variations, MAPK activation but triggered a long lasting plasma membrane depolarization in grapevine cells ii) up-regulated a stress-responsive transcriptome close to the one induced by Lam but only partly overlapping the ones triggered by salicylate (SA) or jasmonate (JA). Finally, in response to P. viticola infection, PS3 specifically primed the SA- and ROS-dependent defense pathways leading to grapevine triggered immunity against this biotroph. Keywords: cell death, induced resistance, oomycete, priming, reactive oxygen species, salicylate, sulfated laminarin, transcriptomics, Vitis vinifera. 6 samples (Adj, PS3, Lam, ctrl, SA, JA) were analized with 3 biological replicates each, Adj and ctrl samples are reference samples
2013-12-16 | E-GEOD-42972 | biostudies-arrayexpress
Project description:Lymphangioleiomyomatosis (LAM) is characterized by cystic lung destruction caused by smooth, muscle-like LAM cells which have mutations in the tumor suppressor genes Tuberous Sclerosis Complex (TSC) 1 or 2, and the capacity to metastasize. Since chemokines and their receptors function in chemotaxis of metastatic cells, we hypothesized that LAM cells may be recruited by chemokine(s) in the lung. Quantification of 25 chemokines in bronchoalveolar lavage fluid from LAM patients and healthy volunteers revealed that concentrations of MCP-1/CCL2, GROa/CXCL1 and ENA-78/CXCL5 were significantly higher in samples from LAM patients than healthy volunteers. In this transcript analysis, expression of chemokine and chemokine receptor mRNA in LAM cells differed from those in melanoma and smooth muscle cells. Subsequent immunohistochemistry of lung sections from 30 LAM patients confirmed protein expression of chemokines and these receptors varied among LAM patient and differed from that seen in breast cancer and melanoma cells. . In vitro, MCP-1/CCL2 induced selective migration of cells showing loss of heterozygosity of TSC2 from a heterogeneous populations of cells grown from explanted LAM lungs. In addition, the frequencies of single-nucleotide polymorphisms in the MCP-1 gene promoter region differed significantly in LAM patients and healthy volunteers (p=0.018), and one polymorphism was associated significantly more frequently with the decline of lung function. These observations are consistent with the notion that chemokines such as MCP-1 may serve to specify site of LAM cell metastasis. Keywords: Human patient sample comparison with cell lines The study is of case/control design with biological replication. Biopsies of nodules from 14 LAM patients (cases) are compared with cultured cell lines (controls) with similar properties.
2008-12-30 | E-GEOD-12027 | biostudies-arrayexpress
Project description:Lymphangioleiomyomatosis (LAM) is a debilitating, progressive lung disease with few therapeutic options, largely due to a paucity of mechanistic knowledge of disease pathogenesis. Lymphatic endothelial cells (LECs) are known to envelope and invade clusters of LAM-cells, comprising of smooth muscle α-actin and/or HMB-45 positive "smooth muscle-like cells” however the role of LECs in LAM pathogenesis is still unknown. To address this critical knowledge gap, we investigated wether LECs interact with LAM-cells to augment their metastatic behaviour of LAM-cells. We performed in situ spatialomics and identified a core of transcriptomically related cells within the LAM nodules. Pathway analysis highlights wound and pulmonary healing, VEGF signaling, extracellular matrix/actin cytoskeletal regulating and the HOTAIR regulatory pathway enriched in the LAM Core cells. We developed an organoid co-culture model combining primary LAM-cells with LECs and applied this to evaluate invasion, migration, and the impact of Sorafenib, a multi-kinase inhibitor. LAM-LEC organoids had significantly higher extracellular matrix invasion, decreased solidity and a greater perimeter, reflecting increased invasion compared to non-LAM control smooth muscle cells. Sorafenib significantly inhibited this invasion in both LAM spheroids and LAM-LEC organoids compared to their respective controls. We identified TGFβ1ι1, a molecular adapter coordinating protein-protein interactions at the focal adhesion complex and known to regulate VEGF, TGFβ and Wnt signalling, as a Sorafenib-regulated kinase in LAM-cells. In conclusion we have developed a novel 3D co-culture LAM model and have demonstrated the effectiveness of Sorafenib to inhibit LAM-cell invasion, identifying new avenues for therapeutic intervention.
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