Related Experiment Video
Updated: Aug 9, 2026
Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model
Published on: September 7, 2013
Molecular regulation of UVB-induced cutaneous angiogenesis
D R Bielenberg1, C D Bucana, R Sanchez
1Department of Cell Biology, The University of Texas MD Anderson Cancer Center, Houston 77030, USA.
Abstract:
We determined whether cutaneous angiogenesis induced by exposure of mice to ultraviolet-B (UVB) radiation is associated with an imbalance between positive and negative angiogenesis-regulating molecules. Unshaved C3H/HeN mice were exposed to a single dose (15 kJ per m2) of UVB. At various times, the mice were killed, and their external ears were processed for routine histology and immunohistochemistry. Antibodies against proliferating cell nuclear antigen and bromodeoxyuridine identified dividing cells. Antibodies against CD31/ PECAM-1 identified endothelial cells, and antibodies against basic fibroblast growth factor (bFGF), vascular endothelial growth factor/vascular permeability factor, and interferon-beta (IFN-beta) identified angiogenesis-regulating molecules. Epidermal hyperplasia was documented by 48 h and reached a maximum on day 7 after exposure to UVB. The expression of bFGF increased by 24 h, whereas the expression of IFN-beta decreased by 72 h after exposure to UVB. The expression of vascular endothelial growth factor/vascular permeability factor increased slightly after irradiation. The altered balance between bFGF and IFN-beta was associated with increased endothelial cell proliferation (bromodeoxyuridine + CD31 + cells) within existing blood vessels, leading to telangiectasia and new blood vessels. UV-induced epidermal hyperplasia and cutaneous angiogenesis were highest in IFN-alpha/beta receptor knockout mice. These results demonstrate that in response to UVB radiation, dividing keratinocytes produce a positive angiogenic molecule (bFGF) but not a negative angiogenic molecule (IFN-beta), and that this altered balance is associated with enhanced cutaneous angiogenesis.
Insights
Exposure to ultraviolet-B (UVB) radiation causes skin to produce more basic fibroblast growth factor (bFGF) and less interferon-beta (IFN-beta). This imbalance promotes new blood vessel growth in the skin.
Area of Science:
- Dermatology
- Angiogenesis Research
- Molecular Biology
Background:
- Cutaneous angiogenesis, or new blood vessel formation in the skin, is a complex process.
- Ultraviolet-B (UVB) radiation is known to induce changes in skin, including inflammation and potential damage.
- The regulation of angiogenesis involves a balance between pro-angiogenic and anti-angiogenic factors.
Purpose of the Study:
- To investigate the relationship between UVB-induced cutaneous angiogenesis and the expression of key angiogenesis-regulating molecules.
- To determine if an imbalance between positive and negative regulators of angiogenesis occurs after UVB exposure.
- To explore the role of specific molecules like basic fibroblast growth factor (bFGF) and interferon-beta (IFN-beta) in UVB-induced skin responses.
Main Methods:
- Mice (C3H/HeN) were exposed to a single dose of UVB radiation.
- Skin tissues were collected at various time points post-exposure for histological and immunohistochemical analysis.
- Antibodies were used to identify proliferating cells (proliferating cell nuclear antigen, bromodeoxyuridine), endothelial cells (CD31/PECAM-1), and angiogenesis regulators (bFGF, vascular endothelial growth factor/vascular permeability factor, IFN-beta).
- Expression levels of these molecules were analyzed in relation to epidermal hyperplasia and angiogenesis.
Main Results:
- UVB exposure led to epidermal hyperplasia, peaking around day 7.
- Basic fibroblast growth factor (bFGF) expression increased within 24 hours, while interferon-beta (IFN-beta) expression decreased by 72 hours post-UVB.
- Vascular endothelial growth factor/vascular permeability factor showed a slight increase after irradiation.
- An altered balance favoring bFGF over IFN-beta correlated with increased endothelial cell proliferation and formation of new blood vessels (telangiectasia).
- UV-induced skin changes and angiogenesis were more pronounced in mice lacking the IFN-alpha/beta receptor.
Conclusions:
- UVB radiation disrupts the balance of angiogenesis regulators in the skin.
- Dividing keratinocytes in response to UVB produce more bFGF (a positive regulator) and less IFN-beta (a negative regulator).
- This shift in molecular balance is a key mechanism driving UVB-induced cutaneous angiogenesis and epidermal hyperplasia.
Related Concept Videos
01:35Mutations
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
01:10Mechanism of Angiogenesis
01:24Regulation of Angiogenesis and Blood Supply
01:23Role of Skin in Vitamin D Synthesis
The solar UV B rays (290-315 nm) are absorbed by the skin, and 7-dehydrocholesterol (provitamin D3) photolyzes it to previtamin D3, which undergoes a rapid transformation to vitamin D3(cholecalciferol).
01:30Skin Cancer
Basal Cell Carcinoma (BCC): BCC is the most common type of skin cancer, accounting for about 80% of cases. It typically develops in...