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Updated: May 20, 2026
In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
Differential expression of vascular endothelial growth factor isoforms and receptor subtypes in the infarcted heart
Tieqiang Zhao1, Wenyuan Zhao, Yuanjian Chen
1Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, United States.
Insights
Vascular endothelial growth factor (VEGF) and its receptor (VEGFR) expressions change after myocardial infarction (MI). Increased VEGF-C and VEGF-D suggest roles in cardiac repair and remodeling post-MI.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Regenerative Medicine
Background:
- The vascular endothelial growth factor (VEGF) family plays a crucial role in angiogenesis.
- Understanding VEGF and VEGFR expression post-myocardial infarction (MI) is vital for cardiac repair research.
Purpose of the Study:
- To investigate the temporal and spatial expression patterns of VEGF isoforms and their receptor subtypes in the infarcted rat heart.
- To elucidate the roles of specific VEGFs and VEGFRs in cardiac repair and remodeling following MI.
Main Methods:
- Examined temporal and spatial expression of VEGF isoforms and VEGFR subtypes in rat hearts post-MI.
- Utilized sham-operated rats as controls for comparison.
- Analyzed expression changes over a 42-day observation period.
Main Results:
- VEGF-A showed transient increase in the border zone early post-MI, then decreased.
- VEGF-B expression was suppressed, while VEGF-C and VEGF-D were markedly increased in the infarcted heart.
- VEGFR-1 and VEGFR-2 decreased, whereas VEGFR-3 significantly increased, particularly in blood vessels and myofibroblasts.
Conclusions:
- VEGF isoforms and VEGFR subtypes exhibit differential expression patterns following MI.
- Increased VEGF-C and VEGF-D, along with VEGFR-3, suggest a significant role in regulating cardiac repair and remodeling processes.
- VEGF-A's early increase may initiate angiogenesis, while suppressed VEGF-B indicates a lesser role in cardiac repair post-MI.
Aims:
The vascular endothelial growth factor (VEGF) family contains four major isoforms and three receptor subtypes. The expressions of each VEGF isoform and receptor subtype in cardiac repair/remodeling after myocardial infarction (MI) remain uncertain and are investigated in the current study.
Methods And Results:
Temporal and spatial expressions of VEGF isoforms and VEGFR subtypes were examined in the infarcted rat heart. Sham-operated rats served as controls. We found that the normal myocardium expressed all VEGF isoforms. Following MI, VEGF-A was only increased in the border zone at day 1 and was significantly decreased in the infarcted heart during the 42 day observation period afterwards. VEGF-B was significantly suppressed in the infarcted heart. VEGF-C and VEGF-D were markedly increased in the infarcted heart in both early and late stages of MI. VEGFR-1 and 2 were significantly decreased in the infarcted heart, while VEGFR-3 was significantly increased, which was primarily expressed in blood vessels and myofibroblasts (myoFb).
Conclusions:
VEGF isoforms and VEGFR subtypes are differentially expressed in the infarcted heart. Increased VEGF-A in the very early stage of MI suggests the potential role in initiating the cardiac angiogenic response. Suppressed cardiac VEGF-B postMI suggests that it may not be critical to cardiac repair. The presence of enhanced VEGF-C and VEGF-D along with its receptor, VEGFR-3, in various cell types of the infarcted heart suggest that these isoforms may regulate multiple responses during cardiac repair/remodeling.
