Page last updated: 2024-10-24

regulation of cell migration involved in sprouting angiogenesis

Definition

Target type: biologicalprocess

Any process that modulates the frequency, rate or extent of cell migration involved in sprouting angiogenesis. Cell migration involved in sprouting angiogenesis is the orderly movement of endothelial cells into the extracellular matrix in order to form new blood vessels contributing to the process of sprouting angiogenesis. [GOC:BHF, GOC:dph, GOC:rl, GOC:tb]

Sprouting angiogenesis is a complex process that involves the coordinated migration and proliferation of endothelial cells, the cells that line blood vessels. This process is essential for the formation of new blood vessels, which is critical for tissue growth, repair, and development. The regulation of cell migration in sprouting angiogenesis is a tightly controlled process that involves a number of signaling pathways and molecular interactions.

One of the key steps in sprouting angiogenesis is the activation of endothelial cells by growth factors such as vascular endothelial growth factor (VEGF). VEGF binds to its receptor on endothelial cells, triggering a cascade of intracellular signaling events that lead to the activation of transcription factors and the expression of genes involved in cell migration, proliferation, and survival.

Activated endothelial cells then undergo a process called "tip cell selection," where a subset of endothelial cells become specialized to lead the sprout. Tip cells are characterized by their highly motile behavior and the expression of specific signaling molecules, such as Delta-like ligand 4 (Dll4) and vascular endothelial growth factor receptor 2 (VEGFR2), which are involved in cell-cell communication and the regulation of sprouting.

Tip cells migrate towards the source of VEGF, following a chemotactic gradient. This migration is driven by the coordinated action of the cytoskeleton, which provides structural support and propels the cell forward, and integrins, which mediate cell adhesion to the extracellular matrix. Tip cells also secrete proteolytic enzymes, such as matrix metalloproteinases (MMPs), that degrade the extracellular matrix, allowing the sprout to penetrate surrounding tissues.

As the sprout extends, it undergoes a process called "stalk cell formation." Stalk cells are endothelial cells that follow behind the tip cell and contribute to the formation of the lumen of the new blood vessel. Stalk cells are less motile than tip cells and express lower levels of VEGFR2 and Dll4. They are also more sensitive to signals that promote proliferation and differentiation, which allows them to contribute to the formation of the vascular tube.

The formation of new blood vessels requires the coordination of cell migration, proliferation, and differentiation. These processes are tightly regulated by a complex network of signaling pathways and molecular interactions, including:

- VEGF signaling
- Notch signaling
- Wnt signaling
- Hedgehog signaling
- TGF-beta signaling

These pathways interact with each other to ensure that the correct balance of cell behavior is achieved during angiogenesis. In addition to these signaling pathways, other factors also contribute to the regulation of cell migration in sprouting angiogenesis, including:

- Extracellular matrix composition
- Cell-cell interactions
- Mechanical forces

Dysregulation of angiogenesis is associated with a number of diseases, including cancer, diabetic retinopathy, and arthritis. Understanding the complex processes that regulate cell migration in sprouting angiogenesis is essential for developing new therapies to treat these diseases.
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Proteins (2)

ProteinDefinitionTaxonomy
Nuclear receptor subfamily 2 group E member 1A nuclear receptor subfamily 2 group E member 1 that is encoded in the genome of human. [PRO:DNx, UniProtKB:Q9Y466]Homo sapiens (human)
Fibroblast growth factor 2A fibroblast growth factor 2 that is encoded in the genome of human. [PRO:DNx, UniProtKB:P09038]Homo sapiens (human)

Compounds (9)

CompoundDefinitionClassesRoles
propafenonepropafenone : An aromatic ketone that is 3-(propylamino)propane-1,2-diol in which the hydrogen of the primary hydroxy group is replaced by a 2-(3-phenylpropanoyl)phenyl group. It is a class 1C antiarrhythmic drug with local anesthetic effects, and is used as the hydrochloride salt in the management of supraventricular and ventricular arrhythmias.

Propafenone: An antiarrhythmia agent that is particularly effective in ventricular arrhythmias. It also has weak beta-blocking activity.
aromatic ketone;
secondary alcohol;
secondary amino compound
anti-arrhythmia drug
propranololpropranolol : A propanolamine that is propan-2-ol substituted by a propan-2-ylamino group at position 1 and a naphthalen-1-yloxy group at position 3.

Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
naphthalenes;
propanolamine;
secondary amine
anti-arrhythmia drug;
antihypertensive agent;
anxiolytic drug;
beta-adrenergic antagonist;
environmental contaminant;
human blood serum metabolite;
vasodilator agent;
xenobiotic
dexpropranololpropranolol
tryptolinetryptoline: neurotoxic factor that may be involved in development of Parkinson's disease; enzymatic prep from human brain converts tryptamine to tryptoline; RN given refers to parent cpd; structurebeta-carbolines
tadalafilbenzodioxoles;
pyrazinopyridoindole
EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
n-desisopropylpropranololN-desisopropylpropranolol: RN given refers to parent cpd
tivozanibN-(2-chloro-4-((6,7-dimethoxy-4-quinolyl)oxy)phenyl)-N'-(5-methyl-3-isoxazolyl)urea: KNR-951 is the HCl, monohydrate salt; an antineoplastic agent; structure in first sourcearomatic ether
phosphomannopentaose sulfatephosphomannopentaose sulfate: structure in first source
pg 545PG 545: an anti-angiogenesis agent with heparanase inhibitory activity; structure in first source