GO:0060981 cell migration involved in coronary angiogenesis: Vascular Remodeling, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0060981 describes the directed movement of cells that contributes to the formation of new coronary blood vessels from pre-existing ones.
• This process is essential for restoring blood flow to the ischemic myocardium after acute myocardial infarction.
• Key cell types involved include endothelial cells, smooth muscle cells, and pericytes, which migrate and assemble into new vessel structures.
• Dysregulation of coronary angiogenesis contributes to heart failure, hypertension, and atherosclerosis.
• Studying GO:0060981 requires models that capture cell migration, proliferation, and vessel assembly in the heart.
• CRISPR-based knockout, knock-in, and overexpression models enable causal testing of genes driving this process.
Description
Coronary angiogenesis is the biological process by which new blood vessels form from pre-existing ones in the heart, a critical response to ischemic injury and a key determinant of cardiac repair. The Gene Ontology term GO:0060981, cell migration involved in coronary angiogenesis, specifically refers to the orderly movement of cells that contributes to this vessel formation. This process is distinct from general angiogenesis because it is spatially and temporally restricted to the coronary vasculature and involves coordinated migration of endothelial and mural cells. Understanding GO:0060981 is essential for researchers studying cardiac regeneration, ischemic heart disease, and therapeutic angiogenesis. The migration of endothelial cells is a rate-limiting step in coronary vessel growth, and its dysregulation is linked to impaired healing after myocardial infarction and to pathological vascular remodeling in hypertension and atherosclerosis. Moreover, single-cell studies have revealed cell-type-specific roles for RNA modifications in atherosclerosis, highlighting the complexity of migratory regulation in vascular disease. This article synthesizes current knowledge on the mechanisms, genes, and research methods relevant to GO:0060981, providing a resource for experimental design and therapeutic targeting.
cell migration involved in coronary angiogenesis At A Glance
| GO ID | GO:0060981 |
|---|---|
| GO term | cell migration involved in coronary angiogenesis |
| Ontology | biological_process |
| Synonym | None |
| Definition | The orderly movement of a cell from one site to another that will contribute to the formation of new blood vessels in the heart from pre-existing blood vessels. |
| Major function | Coordinated cell migration for coronary vessel formation |
| Related process | Angiogenesis after acute myocardial infarction |
| Cell types involved | Endothelial cells, smooth muscle cells, pericytes |
| Disease relevance | Myocardial infarction, hypertension, atherosclerosis [1,3] |
What Is GO:0060981?
GO:0060981 is defined as the orderly movement of a cell from one site to another that will contribute to the formation of new blood vessels in the heart from pre-existing blood vessels. In simpler terms, it is the directed migration of cells, such as endothelial cells, that is required for building new coronary arteries and capillaries after they sprout from existing vessels.
Why Is cell migration involved in coronary angiogenesis Important in Cell Biology?
GO:0060981 is critically important because coronary angiogenesis is the primary mechanism by which the heart restores blood flow to ischemic tissue after myocardial infarction. Without efficient migration of endothelial cells and supporting mural cells, the myocardium cannot be revascularized, leading to adverse remodeling and heart failure. Furthermore, dysregulated cell migration in coronary vessels contributes to pathological vascular remodeling in hypertension and atherosclerosis, where aberrant migration can promote plaque instability and arterial stiffening. Understanding the molecular drivers of this process is therefore essential for developing pro-angiogenic therapies and for predicting patient outcomes after cardiac injury.
• Essential for cardiac repair after myocardial infarction.
• Determines the extent of revascularization and functional recovery of the heart.
• Dysregulation contributes to heart failure and adverse remodeling.
• Plays a role in hypertension-associated vascular remodeling.
• Involved in atherosclerosis progression through cell-type-specific mechanisms.
• Target for therapeutic angiogenesis in ischemic heart disease.
• Requires coordinated migration of endothelial and mural cells.
• Regulated by metabolic and inflammatory signals.
• Can be studied using single-cell technologies to resolve cell heterogeneity.
• Provides a basis for CRISPR-based gene function studies in cardiovascular biology.
What Happens During cell migration involved in coronary angiogenesis?
Initiation and Sprouting
In simple terms: Existing blood vessels in the heart start to grow new branches.
After ischemic injury, pro-angiogenic factors such as VEGF are released, activating endothelial cells in pre-existing coronary vessels. These cells acquire a migratory phenotype, degrade the basement membrane, and form sprouts that extend toward the ischemic region. This initial step is dependent on the coordinated action of matrix metalloproteinases and integrins.
Directed Endothelial Cell Migration
In simple terms: Endothelial cells move in a coordinated direction to form new vessel tubes.
Endothelial cells at the tip of sprouts migrate through the extracellular matrix, guided by chemotactic gradients. This migration requires dynamic actin cytoskeleton remodeling and focal adhesion turnover. The process is tightly regulated by signaling pathways including PI3K/Akt and MAPK, which are activated downstream of growth factor receptors.
Mural Cell Recruitment and Vessel Stabilization
In simple terms: Supporting cells wrap around new vessels to make them stable.
Once endothelial tubes are formed, pericytes and smooth muscle cells migrate along the new vessels and invest them, providing structural support and regulating perfusion. This recruitment is mediated by PDGF-B and Angiopoietin-1 signaling. Without proper mural cell coverage, new vessels are unstable and prone to regression.
Remodeling and Maturation
In simple terms: New vessels are refined into a functional network.
The newly formed coronary vessels undergo remodeling, including pruning of excess branches and deposition of a mature basement membrane. This phase involves the migration of additional endothelial cells to optimize vessel diameter and connectivity. Maturation is essential for long-term vessel stability and function.
Resolution and Quiescence
In simple terms: The growth stops once enough blood vessels are formed.
After adequate revascularization, endothelial cells return to a quiescent state, and migration ceases. This transition is regulated by anti-angiogenic factors and cell-cell contact inhibition. Failure to resolve angiogenesis can lead to pathological vascular overgrowth.
Key Genes Involved in GO:0060981 cell migration involved in coronary angiogenesis
The following genes and proteins are central to the regulation and execution of cell migration involved in coronary angiogenesis, based on published literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| VEGFA | Primary pro-angiogenic factor; induces endothelial cell migration | Target for therapeutic angiogenesis after myocardial infarction |
| KDR (VEGFR2) | Receptor for VEGF; mediates migratory signaling | Key node in endothelial cell chemotaxis |
| PDGFB | Recruits mural cells to nascent vessels | Essential for vessel stabilization |
| ANGPT1 | Promotes vessel maturation and stability | Regulates endothelial-pericyte interactions |
| CD44 | Cell surface receptor involved in cell migration and metabolism | Potential modulator of vascular cell behavior |
| FUNDC1 | Mitophagy receptor; protects against endothelial senescence | Exercise-induced coronary endothelial protection |
| STAT3 | Transcription factor mediating inflammatory and proliferative signals | Involved in hypoxia-induced vascular remodeling |
| ITGA2 | Integrin subunit mediating cell-matrix adhesion | Promotes vascular remodeling through enhancer-associated lncRNA |
| ANXA2 | Membrane protein involved in cell migration and signaling | EP4/ANXA2 axis in pulmonary arterial hypertension |
| EP4 (PTGER4) | Prostaglandin E2 receptor; regulates vascular tone and remodeling | Therapeutic target in pulmonary hypertension |
| m6A RNA modification machinery | Regulates RNA stability and translation in vascular cells | Cell-type-specific roles in atherosclerosis |
| MMP2 | Matrix metalloproteinase; degrades extracellular matrix for migration | Facilitates endothelial sprouting |
| MMP9 | Matrix metalloproteinase; involved in matrix remodeling | Contributes to cell migration during angiogenesis |
| CXCR4 | Chemokine receptor; guides endothelial cell migration | Regulates homing to ischemic tissue |
| SDF1 (CXCL12) | Chemokine ligand for CXCR4; promotes migration | Enhances coronary angiogenesis |
| NOS3 (eNOS) | Endothelial nitric oxide synthase; regulates vascular tone and migration | Modulates angiogenic response |
| HIF1A | Hypoxia-inducible factor; drives pro-angiogenic gene expression | Master regulator of ischemic response |
How Is cell migration involved in coronary angiogenesis Regulated?
The process of cell migration involved in coronary angiogenesis is regulated by a complex interplay of growth factors, chemokines, and metabolic signals. VEGF-A is the primary driver, activating VEGFR2 and downstream PI3K/Akt and MAPK pathways to promote endothelial cell migration. Hypoxia-inducible factor 1-alpha (HIF1A) upregulates VEGF and other pro-angiogenic genes in response to low oxygen. Inflammatory mediators, such as STAT3 signaling, can modulate migration in the context of pulmonary hypertension. Metabolic regulators, including the mitophagy receptor FUNDC1, protect against endothelial senescence and preserve migratory capacity in aged mice. Additionally, RNA modifications such as m6A can influence vascular cell behavior in atherosclerosis, adding another layer of regulation. The EP4/ANXA2 axis has been implicated in pulmonary arterial hypertension, suggesting that prostaglandin signaling can affect vascular remodeling.
cell migration involved in coronary angiogenesis and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| VEGFA | Myocardial infarction; impaired angiogenesis | Knockout or overexpression in endothelial cells |
| FUNDC1 | Aged heart; endothelial senescence | Knockout mice subjected to exercise |
| STAT3 | Pulmonary hypertension; vascular remodeling | Inhibitor studies in hypoxia models |
| ITGA2 | Vascular remodeling; atherosclerosis | Enhancer-associated lncRNA knockout |
| EP4/ANXA2 | Pulmonary arterial hypertension | Pharmacological inhibition in animal models |
Myocardial Infarction and Heart Failure
After acute myocardial infarction, the heart attempts to restore blood flow through coronary angiogenesis, a process that depends on efficient cell migration. Insufficient or dysregulated migration leads to poor revascularization, adverse ventricular remodeling, and progression to heart failure. Therapeutic strategies aimed at enhancing endothelial cell migration are therefore of great interest.
Hypertension and Vascular Remodeling
Hypertension is associated with pathological vascular remodeling, in which aberrant cell migration contributes to arterial stiffening and increased peripheral resistance. Oxidative stress and inflammation are key drivers of these changes, and they can alter the migratory behavior of vascular cells. Understanding how GO:0060981 is dysregulated in hypertension may reveal new targets for therapy.
Atherosclerosis
Atherosclerosis involves the migration of smooth muscle cells and endothelial cells into the intima, contributing to plaque formation and instability. Single-cell studies have uncovered cell-type-specific roles for RNA m6A modification in atherosclerosis, highlighting the complexity of migratory regulation in this disease. Targeting these pathways could modulate plaque progression.
Pulmonary Arterial Hypertension
Pulmonary arterial hypertension is characterized by vascular remodeling in the lung, but shared mechanisms with coronary angiogenesis exist, including the EP4/ANXA2 axis. This axis regulates cell migration and proliferation, and its inhibition attenuates disease in experimental models. These findings suggest that molecules involved in coronary cell migration may also be relevant to pulmonary vascular disease.
From cell migration involved in coronary angiogenesis-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does gene X drive endothelial cell migration in coronary angiogenesis? | Endothelial-specific knockout (e.g., Cdh5-Cre; X fl/fl) |
| Does a point mutation in gene Y alter its pro-migratory function? | Knock-in of point mutant (e.g., X Y123F) |
| Can overexpression of gene Z enhance coronary angiogenesis after MI? | Endothelial-specific overexpression (e.g., Tie2-driven) |
| What is the role of gene W in mural cell recruitment? | Smooth muscle cell-specific knockout |
| How does gene V affect vessel stabilization? | Inducible knockout in adult mice |
| Does a tagged version of protein U localize to migrating cells? | Knock-in of fluorescent tag (e.g., GFP) |
How to Study the cell migration involved in coronary angiogenesis Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Transwell migration assay | Number of cells migrating through a membrane | In vitro screening of pro-migratory genes |
| Scratch wound assay | Rate of cell migration into a gap | Quantifying endothelial cell motility |
| Lineage tracing | Origin and fate of migrating cells | Tracking endothelial cells in coronary angiogenesis |
| Single-cell RNA-seq | Transcriptomic profiles of individual cells | Identifying migratory cell states |
| Confocal microscopy | Vascular morphology and cell position | Visualizing new vessel formation |
| CRISPR knockout screen | Genes essential for migration | Discovery of novel regulators |
| Western blot | Protein expression and phosphorylation | Validating signaling pathways |
| Immunohistochemistry | Protein localization in tissue | Assessing vessel density and cell recruitment |
Lineage Tracing and Migration Assays
To study cell migration in coronary angiogenesis, lineage tracing using Cre-lox systems can label endothelial cells and track their movement into the ischemic zone. In vitro scratch and transwell assays can quantify migratory capacity of isolated coronary endothelial cells. These methods are essential for linking gene function to migratory behavior.
Single-Cell RNA Sequencing
Single-cell RNA sequencing (scRNA-seq) allows unbiased profiling of cell types and states in the heart during angiogenesis. It can identify migratory subpopulations and cell-type-specific gene expression programs. This approach has been used to uncover RNA m6A modification roles in atherosclerosis.
Imaging of Vascular Morphology
Confocal and two-photon microscopy of fluorescently labeled vessels (e.g., lectin perfusion) enables visualization of new coronary vessels and migrating cells. Time-lapse imaging in zebrafish or mouse models can capture dynamic migration events. These techniques provide spatial and temporal resolution of GO:0060981.
CRISPR Screening and Functional Genomics
Pooled CRISPR knockout screens in endothelial cells can identify genes required for migration and tube formation. Such screens are powerful for discovering novel regulators of coronary angiogenesis. Validation in vivo using conditional knockout mice is then necessary to confirm physiological relevance.
How CRISPR Can Be Used to Study GO:0060981 cell migration involved in coronary angiogenesis
Knockout
CRISPR knockout of candidate genes in endothelial cells or mice can determine whether they are required for cell migration involved in coronary angiogenesis. For example, endothelial-specific knockout of VEGFA or its receptor KDR abolishes migration and vessel formation. Such models are essential for causal inference.
Point Mutation
Knock-in of point mutations can dissect specific phosphorylation sites or binding interfaces critical for migratory signaling. For instance, mutating a key tyrosine in a receptor can block downstream activation without affecting expression. This approach provides mechanistic insight beyond simple knockout.
Knock-in
Knock-in of reporter genes (e.g., GFP) or tags allows visualization and tracking of specific proteins during migration. It can also be used to express mutant proteins under endogenous regulatory elements. This is valuable for studying protein dynamics in vivo.
Overexpression
CRISPR activation (CRISPRa) or transgenic overexpression can test whether increasing a gene's activity enhances coronary angiogenesis. Overexpression of VEGFA in the heart promotes angiogenesis and improves function after myocardial infarction. Such gain-of-function models complement loss-of-function studies.
How EDITGENE Supports cell migration involved in coronary angiogenesis Research
Researchers studying cell migration involved in coronary angiogenesis-related genes often need to determine whether a candidate gene is causally involved in endothelial or mural cell migration, and whether its manipulation can enhance or impair vessel formation. EDITGENE provides a comprehensive suite of CRISPR-based services to address these questions, from gene knockout to precise point mutations and overexpression, enabling rigorous functional validation in cardiovascular models.
Contact EDITGENE today to design your custom CRISPR model for cell migration involved in coronary angiogenesis research.
Frequently Asked Questions About cell migration involved in coronary angiogenesis
What is GO:0060981?
GO:0060981 is the Gene Ontology term for cell migration involved in coronary angiogenesis, defined as the orderly movement of a cell that contributes to the formation of new blood vessels in the heart from pre-existing vessels.
What genes are involved in cell migration involved in coronary angiogenesis?
Key genes include VEGFA, KDR, PDGFB, ANGPT1, CXCR4, and HIF1A, among others, which regulate endothelial and mural cell migration.
Why is coronary angiogenesis important after a heart attack?
After myocardial infarction, coronary angiogenesis restores blood flow to ischemic tissue, and efficient cell migration is required for this revascularization to prevent heart failure.
How is cell migration in coronary angiogenesis regulated?
It is regulated by growth factors like VEGF, chemokines, metabolic signals such as FUNDC1-dependent mitophagy, and inflammatory pathways including STAT3 [1,7,8].
What diseases are associated with dysregulated coronary angiogenesis?
Dysregulation is linked to heart failure, hypertension, atherosclerosis, and pulmonary arterial hypertension [1,3,4,5].
What research methods are used to study GO:0060981?
Methods include transwell migration assays, lineage tracing, single-cell RNA-seq, confocal imaging, and CRISPR screens [1,4].
Can CRISPR be used to study coronary angiogenesis?
Yes, CRISPR knockout, knock-in, and overexpression models allow causal testing of genes in endothelial and mural cell migration [1,4].
What is the role of endothelial cells in coronary angiogenesis?
Endothelial cells are the primary migratory cells that sprout from existing vessels and form new tubes in response to pro-angiogenic signals.
How do pericytes and smooth muscle cells contribute to coronary angiogenesis?
They migrate along nascent vessels to stabilize them and regulate perfusion, a process mediated by PDGF-B and Angiopoietin-1.
What is the clinical relevance of targeting cell migration in coronary angiogenesis?
Enhancing migration could improve revascularization after myocardial infarction, while inhibiting pathological migration may treat atherosclerosis and hypertension [1,3].
Conclusion
GO:0060981, cell migration involved in coronary angiogenesis, is a fundamental biological process that underlies cardiac repair and vascular homeostasis. Its dysregulation contributes to major cardiovascular diseases, making it a prime target for therapeutic intervention. Advances in CRISPR-based models and single-cell technologies are accelerating the discovery of molecular drivers and will inform future strategies to modulate coronary angiogenesis for clinical benefit [1,4].
References
- 1. Wu X et al.. 2021. Angiogenesis after acute myocardial infarction.. Cardiovasc Res 117(5):1257-1273 PMID: 33063086
- 2. Weng X et al.. 2022. The membrane receptor CD44: novel insights into metabolism.. Trends Endocrinol Metab 33(5):318-332 PMID: 35249813
- 3. Totoń-Żurańska J et al.. 2024. Vascular remodelling in cardiovascular diseases: hypertension, oxidation, and inflammation.. Clin Sci (Lond) 138(13):817-850 PMID: 38920058
- 4. Ping X et al.. 2025. Deciphering single-cell landscape unravels cell-type-specific functional roles of RNA m(6)A modification in atherosclerosis.. Theranostics 15(10):4785-4807 PMID: 40225569
- 5. Xu H et al.. 2026. EP4/ANXA2 axis in pulmonary arterial hypertension: therapeutic implications.. Eur Heart J 47(10):1199-1217 PMID: 40996819
- 6. Guo X et al.. 2025. Enhancer-Associated LncRNA-ITGA2 Promotes Vascular Remodeling Through ITGA2.. Circ Res 136(12):1610-1628 PMID: 40321134
- 7. Ma L et al.. 2023. Exercise protects aged mice against coronary endothelial senescence via FUNDC1-dependent mitophagy.. Redox Biol 62:102693 PMID: 37030149
- 8. Yao Y et al.. 2024. Parthenolide attenuates hypoxia-induced pulmonary hypertension through inhibiting STAT3 signaling.. Phytomedicine 134:155976 PMID: 39265445
