Single cell RNA sequencing for normal and lymphangiogenesis-inhibiting vascular allografts
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA871906 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21152745_1.fastq.gz | Fastqsanger.gz | |||
| SRR21152745_2.fastq.gz | Fastqsanger.gz | |||
| SRR21152746_1.fastq.gz | Fastqsanger.gz | |||
| SRR21152746_2.fastq.gz | Fastqsanger.gz | |||
| SRR21152747_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 104 |
Similar Datasets
Project description:Transplant arteriosclerosis is a major limitation to long-term survival of patients with solid organ transplantation. Although lymphatic vessels have been recently reported to possess organ-specific features in allograft transplantation, the relationship between lymphangiogensis and transplant arteriosclerosis remains unknown.
2024-04-12 | GSE211731 | GEO
Project description:Prostate cancer is the most common cancer in men and is often associated with distant metastasis in its later stages. Lymphangiogenesis has been identified as a critical factor in cancer metastasis, and the adipokine apelin has been implicated in cancer progression and metastasis. However, researchers have yet to elucidate the mechanisms by which apelin regulates the key lymphangiogenic factor, Vascular Endothelial Growth Factor-C (VEGF-C), to promote distant metastasis in prostate cancer. This study identified a strong positive correlation between apelin levels and prostate cancer metastasis. Apelin stimulation was shown to upregulate VEGF-C expression, promoting the formation of new lymphatic vessels. Apelin treatment was also shown to downregulate miR-196a-5p expression via the proto-oncogene tyrosine kinase c-Src (c-Src) and Signal transducer and activator of transcription 3 (STAT3) signaling pathways, which regulates VEGF-C expression and lymphangiogenesis in prostate cancer cell lines. In an orthotopic mouse model, apelin inhibition prevented lymphangiogenesis and distant metastasis. These findings suggest that targeting apelin could be a promising therapeutic approach to preventing prostate cancer metastasis and lymphangiogenesis
2024-11-09 | GSE281393 | GEO
Project description:Arianna Bianchi, Kevin J. Painter & Jonathan A. Sherratt. A mathematical model for lymphangiogenesis in normal and diabetic wounds. Journal of Theoretical Biology 383 (2015).
Several studies suggest that one possible cause of impaired wound healing is failed or insufficient lymphangiogenesis, that is the formation of new lymphatic capillaries. Although many mathematical models have been developed to describe the formation of blood capillaries (angiogenesis) very few have been proposed for the regeneration of the lymphatic network. Moreover, lymphangiogenesis is markedly distinct from angiogenesis, occurring at different times and in a different manner. Here a model of five ordinary differential equations is presented to describe the formation of lymphatic capillaries following a skin wound. The variables represent different cell densities and growth factor concentrations, and where possible the parameters are estimated from experimental and clinical data. The system is then solved numerically and the results are compared with the available biological literature. Finally, a parameter sensitivity analysis of the model is taken as a starting point for suggesting new therapeutic approaches targeting the enhancement of lymphangiogenesis in diabetic wounds. The work provides a deeper understanding of the phenomenon in question, clarifying the main factors involved. In particular, the balance between TGF-β and VEGF levels, rather than their absolute values, is identified as crucial to effective lymphangiogenesis. In addition, the results indicate lowering the macrophage-mediated activation of TGF-β and increasing the basal lymphatic endothelial cell growth rate, inter alia, as potential treatments. It is hoped the findings of this paper may be considered in the development of future experiments investigating novel lymphangiogenic therapies.
2024-09-02 | BIOMD0000000722 | BioModels
Project description:During development, lymphatic vasculature forms as a second and distinct network that derives from embryonic blood vessels. Transdifferentiation of venous endothelial cells into specified lymphatic endothelial cells (LECs) is the first step in this process. Transdifferentiation and specification of LEC fate requires Prox1, but how Prox1 regulates transdifferentiation and differentiation is not fully understood. We present a single cell transcriptomic atlas of lymphangiogenesis spanning four key developmental stages that reveals new markers and functional regulators of lymphatic development. We extend this to comprehensively profile single cell transcriptomic and chromatin changes controlled by Prox1 using zygotic prox1a mutants, which form lymphatics that then dedifferentiate. Combining this with single cell analysis of Prox1-null, double prox1a/prox1b maternal zygotic mutants, we reveal in depth the role of Prox1 in control of LEC fate specification and differentiation. This resource reveals dual and progressive functions for Prox1, blocking blood vascular and hematopoietic fate while simultaneously up-regulating a small number of early acting genes that include tspan18a/b and lgals3a/b which are essential for lymphangiogenesis. This embryonic developmental resource will serve as a baseline to better understand both developmental and pathological lymphangiogenesis in the future. [Citations in sample metadata correspond to reference numbers in the associated publication.]
2023-04-27 | GSE188341 | GEO
Project description:During development, lymphatic vasculature forms as a second and distinct network that derives from embryonic blood vessels. Transdifferentiation of venous endothelial cells into specified lymphatic endothelial cells (LECs) is the first step in this process. Transdifferentiation and specification of LEC fate requires Prox1, but how Prox1 regulates transdifferentiation and differentiation is not fully understood. We present a single cell transcriptomic atlas of lymphangiogenesis spanning four key developmental stages that reveals new markers and functional regulators of lymphatic development. We extend this to comprehensively profile single cell transcriptomic and chromatin changes controlled by Prox1 using zygotic prox1a mutants, which form lymphatics that then dedifferentiate. Combining this with single cell analysis of Prox1-null, double prox1a/prox1b maternal zygotic mutants, we reveal in depth the role of Prox1 in control of LEC fate specification and differentiation. This resource reveals dual and progressive functions for Prox1, blocking blood vascular and hematopoietic fate while simultaneously up-regulating a small number of early acting genes that include tspan18a/b and lgals3a/b which are essential for lymphangiogenesis. This embryonic developmental resource will serve as a baseline to better understand both developmental and pathological lymphangiogenesis in the future. [Citations in sample metadata correspond to reference numbers in the associated publication.]
2023-04-27 | GSE188340 | GEO
Project description:Progressive Decline of Function in Renal Allografts with Normal One Year Biopsies
| PRJNA753311 | ENA
Project description:Lymphangiogenesis plays a pivotal role in the pathogenesis of various vascular disorders, including ocular vascular diseases and cancers. Deregulation of N6-methyladenosine (m6A) modification has been identified as a key contributor to human diseases. However, the specific involvement of m6A modification in lymphatic remodeling remains poorly understood. In this study, we demonstrate that inflammatory stimulation and corneal sutures induce elevated levels of METTL3-mediated m6A modification. METTL3 knockdown inhibits lymphatic endothelial viability, proliferation, migration, and tube formation in vitro. METTL3 knockdown attenuates corneal sutures-induced lymphangiogenesis and intratumoral lymphangiogenesis initiated by subcutaneous grafts, consequently restraining corneal neovascularization, tumor growth, and tumor neovascularization in vivo. Mechanistically, METTL3 knockdown upregulates prostaglandin-endoperoxide synthase 2 (PTGS2) expression through an m6A-YTHDF2-dependent pathway, enhancing the synthesis of cyclopentenone prostaglandins (CyPGs). Aberrant CyPG production in lymphatic endothelial cells impairs mitochondrial oxidative phosphorylation, contributing to pathological lymphangiogenesis. Moreover, selective inhibition of METTL3 with STM2457 reduces m6A levels in lymphatic endothelial cells, effectively suppressing pathological lymphangiogenesis. This study provides compelling evidence that lymphatic-specific METTL3 plays a critical role in vascular patterning through prostaglandin metabolism reprogramming. Thus, METTL3 emerges as a promising target for treating pathological lymphangiogenesis.
2024-10-15 | GSE273930 | GEO
Project description:Angiogenesis and lymphangiogenesis have important roles in cancer progression and chronic inflammatory diseases, but efficient therapies against these diseases have been hampered by the lack of identified vascular lineage-specific markers and growth factors. Using transcriptional profiling of matched pairs of human dermal blood vascular and lymphatic endothelial cells, we first identified 236 lymphatic and 342 blood vascular signature genes. In silico analyses of the biologic pathways associated with these genes revealed lineage-specific functions for each cell type. Using a selection of 85 identified vascular lineage-specific genes, we developed a TaqMan RT-PCR-based, microfluidic card-formatted low-density microvascular differentiation array (LD-MDA) that was used to reliably identify and quantify the degree of lineage-specific differentiation in different types of endothelial cells, and to detect admixture of lymphatic endothelial cells in commercial preparations of microvascular endothelial cells. Application of Prediction Relevance Ranking and analysis of variance of LD-MDA expression profiles of 43 lesional skin samples obtained from patients with the chronic inflammatory disease psoriasis led to identification of cytokines which are significantly associated with angiogenesis or lymphangiogenesis in vivo. In particular, interleukin-7 and fibroblast growth factor-12 were identified as novel (lymph)angiogenic factors. This technology provides a novel tool to quantify lineage-specific vascular differentiation and to characterize (lymph)angiogenesis in clinical samples obtained from angiogenic diseases. This SuperSeries is composed of the following subset Series: GSE11306: Quantification of vascular lineage-specific differentiation (cell type comparison) GSE11307: Quantification of vascular lineage-specific differentiation, psoriasis (chronic inflammation) study Keywords: SuperSeries Refer to individual Series
2008-10-04 | E-GEOD-11308 | biostudies-arrayexpress
Project description:Paraspeckle protein NONO attenuates vascular calcification by inhibiting BMP2 transcription
| PRJNA1058999 | ENA