Browse
Submit Data
Databases
API
Help

Dataset Information

30 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The sinus venosus contributes to coronary vasculature through VEGFC-stimulated angiogenesis.

ABSTRACT: Identifying coronary artery progenitors and their developmental pathways could inspire novel regenerative treatments for heart disease. Multiple sources of coronary vessels have been proposed, including the sinus venosus (SV), endocardium and proepicardium, but their relative contributions to the coronary circulation and the molecular mechanisms regulating their development are poorly understood. We created an ApjCreER mouse line as a lineage-tracing tool to map SV-derived vessels onto the heart and compared the resulting lineage pattern with endocardial and proepicardial contributions to the coronary circulation. The data showed a striking compartmentalization to coronary development. ApjCreER-traced vessels contributed to a large number of arteries, capillaries and veins on the dorsal and lateral sides of the heart. By contrast, untraced vessels predominated in the midline of the ventral aspect and ventricular septum, which are vessel populations primarily derived from the endocardium. The proepicardium gave rise to a smaller fraction of vessels spaced relatively uniformly throughout the ventricular walls. Dorsal (SV-derived) and ventral (endocardial-derived) coronary vessels developed in response to different growth signals. The absence of VEGFC, which is expressed in the epicardium, dramatically inhibited dorsal and lateral coronary growth but left vessels on the ventral side unaffected. We propose that complementary SV-derived and endocardial-derived migratory routes unite to form the coronary vasculature and that the former requires VEGFC, revealing its role as a tissue-specific mediator of blood endothelial development.

SUBMITTER: Chen HI

PROVIDER: S-EPMC4302936 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

The sinus venosus myocardium contributes to the atrioventricular canal: potential role during atrioventricular node development?

Project description:The presence of distinct electrophysiological pathways within the atrioventricular node (AVN) is a prerequisite for atrioventricular nodal reentrant tachycardia to occur. In this study, the different cell contributions that may account for the anatomical and functional heterogeneity of the AVN were investigated. To study the temporal development of the AVN, the expression pattern of ISL1, expressed in cardiac progenitor cells, was studied in sequential stages performing co-staining with myocardial markers (TNNI2 and NKX2-5) and HCN4 (cardiac conduction system marker). An ISL1+/TNNI2+/HCN4+ continuity between the myocardium of the sinus venosus and atrioventricular canal was identified in the region of the putative AVN, which showed a pacemaker-like phenotype based on single cell patch-clamp experiments. Furthermore, qPCR analysis showed that even during early development, different cell populations can be identified in the region of the putative AVN. Fate mapping was performed by in ovo vital dye microinjection. Embryos were harvested and analysed 24 and 48 hrs post-injection. These experiments showed incorporation of sinus venosus myocardium in the posterior region of the atrioventricular canal. The myocardium of the sinus venosus contributes to the atrioventricular canal. It is postulated that the myocardium of the sinus venosus contributes to nodal extensions or transitional cells of the AVN since these cells are located in the posterior region of the AVN. This finding may help to understand the origin of atrioventricular nodal reentrant tachycardia.

| S-EPMC4459851 | biostudies-other

Chemokine-guided angiogenesis directs coronary vasculature formation in zebrafish.

Project description:Interruption of the coronary blood supply severely impairs heart function with often fatal consequences for patients. However, the formation and maturation of these coronary vessels is not fully understood. Here we provide a detailed analysis of coronary vessel development in zebrafish. We observe that coronary vessels form in zebrafish by angiogenic sprouting of arterial cells derived from the endocardium at the atrioventricular canal. Endothelial cells express the CXC-motif chemokine receptor Cxcr4a and migrate to vascularize the ventricle under the guidance of the myocardium-expressed ligand Cxcl12b. cxcr4a mutant zebrafish fail to form a vascular network, whereas ectopic expression of Cxcl12b ligand induces coronary vessel formation. Importantly, cxcr4a mutant zebrafish fail to undergo heart regeneration following injury. Our results suggest that chemokine signaling has an essential role in coronary vessel formation by directing migration of endocardium-derived endothelial cells. Poorly developed vasculature in cxcr4a mutants likely underlies decreased regenerative potential in adults.

| S-EPMC4448080 | biostudies-literature

Cavopulmonary window: an extreme form of sinus venosus defect.

Project description:We present an unusual variant of the sinus venosus defect in which an obvious window is formed between a single pulmonary vein and the superior vena cava, the pulmonary vein retaining its connection to the left atrium. Two patients were operated on via right anterior minithoracotomy. A large single right pulmonary vein was found connecting to the left atrium. There was a large side-to-side communication between the superior vena cava and the pulmonary vein resulting in partially anomalous pulmonary venous drainage. A side-biting clamp was applied in the superior vena cava and the pulmonary vein at both sides of the communication, and the vein was divided. The incision in both veins was closed with a running suture.

| S-EPMC3895076 | biostudies-literature

Anatomy of a wrong diagnosis: false sinus venosus atrial septal defect.

Project description:In contrast with transthoracic echocardiography, transesophageal echocardiography provides a sure way to make the diagnosis of sinus venosus atrial septal defect; on the other hand this abnormality is more complex than that seen with the secundum atrial septal defect, and inexperienced operators may fail to recognize properly the defect. In front of a high reported sensitivity using transesophageal echocardiography, specificity is difficult to assess, due to possible underreporting of diagnostic errors. We describe a false positive diagnosis of sinus venosus atrial septal defect, in the setting of enlarged right chambers of the heart because of pressure overload. Modified anatomy of the heart, together with the presence of a prominent linear structure(probably Eustachian Valve) and an incomplete examination in this case made image interpretation very prone to misinterpretation. In this anatomical setting transesophageal longitudinal "bicaval" view may be sub-optimal for examining the atrial septum, potentially showing false images that need to be known for correct image interpretation. Nonetheless, a scan plane taken more accurately at the superior level would have demonstrated/excluded the pathognomonic feature of sinus venosus atrial septal defect in the high atrial septum, between the fatty limbus and the inferior aspect of the right pulmonary artery; moreover TEE allows morphological information about the posterior structures of the heart that need to be investigated in detail for a complete diagnosis.

| S-EPMC270092 | biostudies-literature

Rspo1/Wnt signaling promotes angiogenesis via Vegfc/Vegfr3.

Project description:Here, we show that a novel Rspo1-Wnt-Vegfc-Vegfr3 signaling pathway plays an essential role in developmental angiogenesis. A mutation in R-spondin1 (rspo1), a Wnt signaling regulator, was uncovered during a forward-genetic screen for angiogenesis-deficient mutants in the zebrafish. Embryos lacking rspo1 or the proposed rspo1 receptor kremen form primary vessels by vasculogenesis, but are defective in subsequent angiogenesis. Endothelial cell-autonomous inhibition of canonical Wnt signaling also blocks angiogenesis in vivo. The pro-angiogenic effects of Rspo1/Wnt signaling are mediated by Vegfc/Vegfr3(Flt4) signaling. Vegfc expression is dependent on Rspo1 and Wnt, and Vegfc and Vegfr3 are necessary to promote angiogenesis downstream from Rspo1-Wnt. As all of these molecules are expressed by the endothelium during sprouting stages, these results suggest that Rspo1-Wnt-VegfC-Vegfr3 signaling plays a crucial role as an endothelial-autonomous permissive cue for developmental angiogenesis.

| S-EPMC3201658 | biostudies-literature

Unanticipated complication of transcatheter correction of superior sinus venosus atrial septal defect.

Project description:Transcatheter correction of superior sinus venosus atrial septal defect (SVASD) is being considered as an alternative to surgery in selected patients. We present the case of a 42-year-old woman with SVASD and partial anomalous venous connection of the right upper pulmonary vein (RUPV), who underwent transcatheter correction with self-expanding aortic stent graft, following feasibility assessment by balloon occlusion. Hemodynamic parameters and angiography demonstrated successful closure of the SVASD without any residual shunt and unobstructed return of RUPV to the left atrium. She developed cardiac tamponade after a few hours despite pericardial drain and underwent emergency exploratory thoracotomy. This revealed leak from a small rent in the ascending aortic wall adjacent to superior vena cava (SVC) caused by barbs of the stent protruding from SVC, without any leak in SVC. This was repaired with suture and further Teflon was placed around the barbs in SVC to prevent further injury. We also discuss the possible reason for this complication, considering our successful previous two cases with the same stents. This case highlights the importance of assessing the relationship between SVC and aorta to decide about the cranial placement of the aortic stent either by computed tomography prior or by contrast aortogram during the procedure. <Learning objective: Transcatheter correction of superior sinus venosus atrial septal defect is becoming an appropriate alternative option for cardiac surgery. There are multiple reports of this technique in the literature - mostly with balloon expandable stents, and few with self-expanding stents placed in superior vena cava (SVC). We present an unanticipated complication of self-expanding aortic stent in this situation and its management, highlighting the need for assessing the relationship between SVC and aorta to decide about the appropriate placement of stent.>.

| S-EPMC8766320 | biostudies-literature

Mesenchymal stromal cells pretreated with pro-inflammatory cytokines promote skin wound healing through VEGFC-mediated angiogenesis.

Project description:Skin is the largest organ of the human body. Skin wound is one of the most common forms of wound. Mesenchymal stromal cells (MSCs) have been used to aid skin wound healing via their paracrine factors. Because the secretome of MSCs can be greatly enriched and amplified by treatment with IFN-γ and TNF-α (IT), we here tested whether supernatant derived from MSCs pretreated with IT, designated as S-MSCs-IT, possesses improved wound healing effect by using a murine model of cutaneous excision, S-MSCs-IT was found to be more potent in promoting angiogenesis, constricting collagen deposition and accelerating wound closure than control supernatant (S-MSCs) during the healing of skin wound. VEGFC, but not VEGFA, was greatly upregulated by IT and was found to be a key factor in mediating the improved wound healing effect of S-MSCs-IT. Our results indicate that the beneficial paracrine effect of MSCs on wound healing can be enhanced by pretreatment with inflammatory cytokines. IT treatment may represent a new strategy for optimizing the therapeutic effect of MSCs on skin injuries.

| S-EPMC7519767 | biostudies-literature

Pitx2 confers left morphological, molecular, and functional identity to the sinus venosus myocardium.

Project description:AimsThe sinus venous myocardium, comprising the sinoatrial node (SAN) and sinus horns (SH), is a region subject to congenital malformations and cardiac arrhythmias. It differentiates from symmetric bilateral mesenchymal precursors, but morphological, molecular, and functional left/right differences are progressively established through development. The role of the laterality gene Pitx2 in this process is unknown. We aimed to elucidate the molecular events driving left/right patterning in the sinus venosus (SV) myocardium by using a myocardial Pitx2 knockout mouse.Methods and resultsWe generated a myocardial specific Pitx2 knockout model (cTP mice). cTP embryos present several features of Pitx2 null, including right atrial isomerism with bilateral SANs and symmetric atrial entrance of the systemic veins. By in situ hybridization and optical mapping analysis, we compared throughout development the molecular and functional properties of the SV myocardium in wt and mutant embryos. We observed that Pitx2 prevents the expansion of the left-SAN primordium at the onset of its differentiation into myocardium; Pitx2 promotes expansion of the left SH through development; Pitx2 dose-dependently represses the autorhythmic properties of the left SV myocardium at mid-gestation (E14.5); Pitx2 modulates late foetal gene expression at the left SH-derived superior caval vein.ConclusionPitx2 drives left/right patterning of the SV myocardium through multiple developmental steps. Overall, Pitx2 plays a crucial functional role by negatively modulating a nodal-type programme in the left SV myocardium.

| S-EPMC3258653 | biostudies-literature

Multimodality Imaging of Sinus Venosus Atrial Septal Defect: A Challenging Diagnosis in Adults.

Project description: Not available

| S-EPMC9120852 | biostudies-literature

Angiogenesis stimulated by elevated PDGF-BB in subchondral bone contributes to osteoarthritis development.

Project description:Increased subchondral bone angiogenesis with blood vessels breaching the tidemark into the avascular cartilage is a diagnostic feature of human osteoarthritis. However, the mechanisms that initiate subchondral bone angiogenesis remain unclear. We show that abnormally increased platelet-derived growth factor-BB (PDGF-BB) secretion by mononuclear preosteoclasts induces subchondral bone angiogenesis, contributing to osteoarthritis development. In mice after destabilization of the medial meniscus (DMM), aberrant joint subchondral bone angiogenesis developed during an early stage of osteoarthritis, before articular cartilage damage occurred. Mononuclear preosteoclasts in subchondral bone secrete excessive amounts of PDGF-BB, which activates platelet-derived growth factor receptor-? (PDGFR-?) signaling in pericytes for neo-vessel formation. Selective knockout of PDGF-BB in preosteoclasts attenuates subchondral bone angiogenesis and abrogates joint degeneration and subchondral innervation induced by DMM. Transgenic mice that express PDGF-BB in preosteoclasts recapitulate pathological subchondral bone angiogenesis and develop joint degeneration and subchondral innervation spontaneously. Our study provides the first evidence to our knowledge that PDGF-BB derived from preosteoclasts is a key driver of pathological subchondral bone angiogenesis during osteoarthritis development and offers a new avenue for developing early treatments for this disease.

| S-EPMC7205438 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data