Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibiting endothelial Rhoj blocks pro-fibrotic vascular intussusception and angiocrine factors to sustain lung regeneration

ABSTRACT: Inhibiting endothelial Rhoj blocks pro-fibrotic vascular intussusception and angiocrine factors to sustain lung regeneration

PROVIDER: PRJNA1150179 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Inhibiting endothelial Rhoj blocks pro-fibrotic vascular intussusception and angiocrine factors to sustain lung regeneration

Project description:Proliferation of vascular endothelial cells (ECs) is critical for providing sufficient cells lining the neo-vascular lumen. Moreover, expanding ECs need to undergo multiple steps to line new lumen, functionalizing anti-thrombotic and anti-inflammatory interface that prevents extravasation of inflammatory cells, maintains blood perfusion, and facilitates cellular crosstalk. Therefore, productive angiogenesis in regeneration requires formation of endothelial tight junction, arrangement of endothelial apical lumen, and alignment of basolateral side juxtaposed with alveolar epithelial cells. As a result, we used single cell RNA sequencing (scRNA-seq) to detect the function of diverse EC clusters.

2025-08-01 | GSE275285 | GEO

Endothelial H2S-AMPK dysfunction upregulates the angiocrine factor PAI-1 and contributes to lung fibrosis

Project description:Dysfunction of the vascular angiocrine system is critically involved in regenerative defects and fibrosis of injured organs. Previous studies have identified various angiocrine factors and found that risk factors such as aging and metabolic disorders can disturb the vascular angiocrine system in fibrotic organs. One existing key gap is what sense the fibrotic risk to modulate the vascular angiocrine system in organ fibrosis. Here, using human and mouse data, we discovered that the metabolic pathway hydrogen sulfide (H2S)-AMP-activated protein kinase (AMPK) is a sensor of fibrotic stress and serves as a key mechanism upregulating the angiocrine factor plasminogen activator inhibitor-1 (PAI-1) in endothelial cells to participate in lung fibrosis.

2024-01-31 | GSE250474 | GEO

Expression gene (angiocrine) profile of various activated endothelial cells

Project description:Endothelial cells were transduced with different genes modulating signaling pathways and compared to GFP transduced control group to identify changes in the expression of the angiocrine factors. The experiment compared endothelial genetic changes upon Akt, MAP kinase and PymT activation.

2011-12-31 | E-GEOD-24093 | biostudies-arrayexpress

Angiocrine Bmp2 signaling in murine liver controls normal iron homeostasis

Project description:Microvascular endothelial cells (EC) display a high degree of phenotypic and functional heterogeneity among different organs. Organ-specific EC control their tissue microenvironment by angiocrine factors in health and disease. Liver sinusoidal EC (LSEC) are uniquely differentiated to fulfil important organ-specific functions in development, under homeostatic conditions, and in regeneration and liver pathology. Recently, Bmp2 has been identified by us as an organ-specific angiokine derived from LSEC. To study angiocrine Bmp2 signaling in the liver, we conditionally deleted Bmp2 in LSEC using EC subtype-specific Stab2-Cre mice. Genetic inactivation of hepatic angiocrine Bmp2 signaling in Stab2-Cre;Bmp2fl/fl (Bmp2LSECKO) mice caused massive iron overload in the liver, and increased serum iron levels and iron deposition in several organs similar to classic hereditary hemochromatosis. Iron overload was mediated by decreased hepatic expression of hepcidin, a key regulator of iron homeostasis. Thus, angiocrine Bmp2 signaling within the hepatic vascular niche represents a constitutive pathway indispensable for iron homeostasis in vivo that is non-redundant with Bmp6. Notably, we demonstrate that organ-specific angiocrine signaling is essential not only for the homeostasis of the respective organ, but also for the homeostasis of the whole organism.

2017-01-31 | GSE90506 | GEO

Supinoxin Blocks Small Cell Lung Cancer Progression by Inhibiting Mitochondrial Respiration through DDX5

Project description:Supinoxin Blocks Small Cell Lung Cancer Progression by Inhibiting Mitochondrial Respiration through DDX5

| PRJNA1076252 | ENA

Expression gene (angiocrine) profile of various activated endothelial cells

2011-12-31 | GSE24093 | GEO

Endothelial-derived angiocrine signals induce and sustain regenerative lung alveolarization.

Project description:To identify pathways involved in adult lung regeneration, we employ a unilateral pneumonectomy (PNX) model that promotes regenerative alveolarization in the remaining intact lung. We show that PNX stimulates pulmonary capillary endothelial cells (PCECs) to produce angiocrine growth factors that induce proliferation of epithelial progenitor cells supporting alveologenesis. Endothelial cells trigger expansion of cocultured epithelial cells, forming three-dimensional angiospheres reminiscent of alveolar-capillary sacs. After PNX, endothelial-specific inducible genetic ablation of Vegfr2 and Fgfr1 in mice inhibits production of MMP14, impairing alveolarization. MMP14 promotes expansion of epithelial progenitor cells by unmasking cryptic EGF-like ectodomains that activate the EGF receptor (EGFR). Consistent with this, neutralization of MMP14 impairs EGFR-mediated alveolar regeneration, whereas administration of EGF or intravascular transplantation of MMP14(+) PCECs into pneumonectomized Vegfr2/Fgfr1-deficient mice restores alveologenesis and lung inspiratory volume and compliance function. VEGFR2 and FGFR1 activation in PCECs therefore increases MMP14-dependent bioavailability of EGFR ligands to initiate and sustain alveologenesis.

| S-EPMC3228268 | biostudies-literature

Identification of myeloid-derived growth factor as a mechanically-induced, growth-promoting angiocrine signal for human hepatocytes

Project description:Recently, we have shown that after partial hepatectomy (PHx), an increased hepatic blood flow initiates liver growth in mice by vasodilation and mechanically-triggered release of angiocrine signals. Here, we use mass spectrometry to identify a mechanically-induced angiocrine signal in human hepatic endothelial cells, that is, myeloid-derived growth factor (MYDGF). We show that it induces proliferation and promotes survival of primary human hepatocytes derived from different donors in two-dimensional cell culture, via activation of mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription 3 (STAT3). MYDGF also enhances proliferation of human hepatocytes in three-dimensional organoids. In vivo, genetic deletion of MYDGF decreases hepatocyte proliferation in the regenerating mouse liver after PHx; conversely, adeno-associated viral delivery of MYDGF increases hepatocyte proliferation and MAPK signaling after PHx. We conclude that MYDGF represents a mechanically-induced angiocrine signal and that it triggers growth of, and provides protection to, primary mouse and human hepatocytes

2023-12-28 | PXD033942 | Pride

Endothelial cells control muscle regeneration through angiocrine lactate

Project description:Endothelial cells control muscle regeneration through angiocrine lactate

| PRJNA625078 | ENA

Endothelial Jak3 expression enhances pro-hematopoietic angiocrine function

Project description:Endothelial Jak3 expression enhances pro-hematopoietic angiocrine function

| PRJNA670425 | ENA