Page last updated: 2024-10-24

blood vessel endothelial cell delamination

Definition

Target type: biologicalprocess

The process of negative regulation of cell adhesion that results in blood vessel endothelial cells splitting off from an existing endothelial sheet. [GOC:dgh, PMID:23698350]

Blood vessel endothelial cell delamination is a complex process involving the detachment of endothelial cells from the underlying basement membrane and the formation of gaps between adjacent endothelial cells. This process is essential for normal vessel development, tissue repair, and angiogenesis, but it can also contribute to pathological conditions such as atherosclerosis, tumor growth, and inflammation.

The delamination process can be initiated by a variety of stimuli, including:

- **Mechanical stress:** Shear stress from blood flow or mechanical injury can disrupt cell-cell and cell-matrix adhesions, leading to delamination.
- **Cytokines and growth factors:** Inflammatory mediators like TNF-alpha and VEGF can trigger signaling pathways that promote endothelial cell delamination.
- **Extracellular matrix (ECM) degradation:** Proteolytic enzymes like MMPs can degrade the basement membrane, weakening the attachment of endothelial cells.

Once delamination is initiated, endothelial cells undergo a series of morphological and molecular changes:

- **Loss of cell-cell junctions:** Adherens junctions and tight junctions between endothelial cells are disrupted, allowing cells to separate from each other.
- **Downregulation of cell-matrix adhesion molecules:** Integrins and other adhesion molecules that mediate the attachment of endothelial cells to the basement membrane are downregulated.
- **Actin cytoskeleton reorganization:** The actin cytoskeleton undergoes remodeling, promoting cell rounding and detachment.
- **Cell migration:** Delaminated endothelial cells migrate away from the vessel wall, contributing to vessel growth or repair.

The delamination process is tightly regulated by a complex interplay of signaling pathways and molecular mechanisms. This includes:

- **Rho GTPase signaling:** Rho GTPases, particularly RhoA, regulate actin cytoskeleton reorganization and cell adhesion.
- **MAPK signaling:** MAPK pathways mediate the effects of cytokines and growth factors on endothelial cell delamination.
- **VEGF signaling:** VEGF is a key regulator of angiogenesis and promotes endothelial cell delamination.

Overall, blood vessel endothelial cell delamination is a dynamic and multifaceted process that plays a crucial role in both physiological and pathological processes. Understanding the molecular mechanisms underlying this process is important for developing therapeutic strategies for vascular diseases and promoting tissue regeneration.'
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Proteins (1)

ProteinDefinitionTaxonomy
Transient receptor potential cation channel subfamily V member 4A transient receptor potential cation channel TRPV4 that is encoded in the genome of human. [PRO:CNA, UniProtKB:Q9HBA0]Homo sapiens (human)

Compounds (9)

CompoundDefinitionClassesRoles
cannabinolCannabinol: A physiologically inactive constituent of Cannabis sativa L.dibenzopyran
cannabichromene1-benzopyran
(6ar-trans)-isomer of tetrahydrocannabivarin 9
hc 0300312-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl)acetamide: a TRPA1 channel blocker
hc-067047HC-067047: a TRPA1 antagonist; structure in first source
rn 1734RN 1734: a TRPV4 antagonist; structure in first source
cannabigerolcannabigerol : A member of the class of resorcinols that is resorcinol which is substituted by a (2E)-3,7-dimethylocta-2,6-dien-1-yl group at position 2 and by a pentyl group at position 5. It is a natural product found in Cannabis sativa and Helichrysum species.

cannabigerol: RN given refers to (E)-isomer; structure given in first source
phytocannabinoid;
resorcinols
anti-inflammatory agent;
antibacterial agent;
antioxidant;
appetite enhancer;
cannabinoid receptor agonist;
neuroprotective agent;
plant metabolite
cannabidivarincannabidivarin: from Cannabis sativamonoterpenoid
gsk 1016790aGSK1016790A : A tertiary carboxamide that is piperazine in which one of the amino groups has undergone condensation with the carboxy group of N-[(2,4-dichlorophenyl)sulfonyl]-L-serine, while the other has undergone condensation with the carboxy group of N-(1-benzothiophen-2-ylcarbonyl)-L-leucine. It is a cell-permeable, potent and selective agonist of the TRPV4 (transient receptor potential vanilloid 4) channel.1-benzothiophenes;
aromatic primary alcohol;
dichlorobenzene;
N-acylpiperazine;
sulfonamide;
tertiary carboxamide
TRPV4 agonist