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Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

Mechanism of Angiogenesis

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...

Overview of Cell-Matrix Interactions

Overview of Cell-Matrix Interactions

The extracellular matrix or ECM holds cells together to form a tissue and allows the cells within the tissue to communicate. ECM comprises proteins such as fibronectin, collagen, laminin, etc. The most abundant protein in this space is collagen. Collagen fibers are interwoven with carbohydrate-containing protein molecules called proteoglycans. ECM allows cell migration and provides a structural scaffold at cell adhesion that anchors the cell when the extracellular matrix proteins interact with...

The Tumor Microenvironment

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...

Role of Matrix Metalloproteases in Degradation of ECM

Role of Matrix Metalloproteases in Degradation of ECM

Matrix metalloproteases (MMPs) are enzymes involved in the hydrolysis of proteins and glycoproteins of the extracellular matrix. MMPs are essential for the migration and proliferation of cells through the dense matrix network, throughout embryonic development, and throughout morphogenesis. The first MMP activity discovered was a collagenase in a tadpole's tail undergoing metamorphosis. The active collagen deposition and modifications lead to the morphogenesis of tadpoles into the adult body.
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Chronic Inflammation: Introduction

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...

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Related Experiment Video

Updated: Jun 18, 2026

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Published on: June 30, 2023

Perivascular Matrix Densification Dysregulates Angiogenesis and Activates Pro-Inflammatory Endothelial Cells.

Jingyi Xia¹, William Y Wang¹, Kyle A Jacobs²

¹Department of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan, USA.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|June 17, 2026

Summary

Fibrosis development is linked to endothelial cell (EC) behavior. Increased matrix fiber density drives ECs toward a pro-inflammatory phenotype, promoting fibrotic progression and aberrant cell invasion.

Keywords:

TGF‐β signaling adherens junctions angiogenesis bleomycin cell migration endothelial cells endothelial‐mesenchymal transition extracellular matrix fibrosis microphysiologic systems

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Related Experiment Videos

Last Updated: Jun 18, 2026

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Published on: June 30, 2023

In Vivo Study of Human Endothelial-Pericyte Interaction Using the Matrix Gel Plug Assay in Mouse

In Vivo Study of Human Endothelial-Pericyte Interaction Using the Matrix Gel Plug Assay in Mouse

Published on: December 19, 2016

Rat Mesentery Exteriorization: A Model for Investigating the Cellular Dynamics Involved in Angiogenesis

Rat Mesentery Exteriorization: A Model for Investigating the Cellular Dynamics Involved in Angiogenesis

Published on: May 20, 2012

Area of Science:

Cell Biology
Vascular Biology
Tissue Engineering

Background:

Fibrosis, a common fibrotic condition, affects many organs and is linked to wound healing and vascular endothelium.
Endothelial cells (ECs) and angiogenesis play roles in fibrotic diseases, but their specific contribution to fibrosis versus healing is unclear.

Purpose of the Study:

To investigate how endothelial cell phenotype influences tissue healing and fibrosis.
To elucidate the mechanisms by which extracellular matrix density affects endothelial cell behavior in fibrotic conditions.

Main Methods:

Utilized a murine lung injury model with endothelial cell (EC) lineage tracing.
Developed a microphysiological system of human microvessels in a tunable stromal matrix.
Analyzed endothelial cell to mesenchymal transition, aberrant tip EC (ATEC) invasion, and pro-inflammatory factor secretion.

Main Results:

Observed invasion of aberrant ECs from bronchial microvasculature post-injury, with concurrent extracellular matrix fiber densification.
Demonstrated that heightened fiber density induces ECs to undergo endothelial to mesenchymal transition, promoting ATEC invasion.
Identified that ATECs adhere to fibrotic matrix, exhibit a pro-inflammatory phenotype, secrete TGF-β2, and involve VE-cadherin and TGF-βR2 interactions.

Conclusions:

Enhanced matrix fiber density in fibrogenesis regulates EC phenotype, generating pro-inflammatory ATECs.
This study reveals novel contributions of ECs to fibrotic progression, highlighting ECs as potential therapeutic targets.