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Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia
Published on: June 8, 2019
Endoglin haplo-insufficiency modifies the inflammatory response in irradiated mouse hearts without affecting
Ingar Seemann1, Johannes A M Te Poele, Sophia J Luikinga
1Division of Biological Stress Response, The Netherlands Cancer Institute, Amsterdam, the Netherlands.
Plos One
|July 30, 2013
Summary
Mice with reduced endoglin (Eng+/-) showed less inflammation and fibrosis after heart irradiation. However, this did not significantly alter microvascular damage or cardiac function compared to normal mice (Eng+/+).
Area of Science:
- Cardiovascular Biology
- Radiation Oncology
- Molecular Medicine
Background:
- Radiotherapy for thoracic tumors increases long-term cardiovascular damage risk, with microvascular damage implicated.
- Endoglin, an accessory TGF-β1 receptor, is upregulated in damaged endothelial cells and may influence heart tissue repair.
- The specific role of endoglin in radiation-induced cardiac microvascular damage and repair requires further investigation.
Purpose of the Study:
- To investigate the role of endoglin in the development of microvascular damage and repair following cardiac irradiation.
- To compare the inflammatory and fibrotic responses in the irradiated hearts of mice with differing endoglin levels.
Main Methods:
- Adult mice with normal (Eng+/+) or reduced (Eng+/-) endoglin expression were subjected to a single 16 Gy cardiac irradiation dose.
- Cardiac geometry and function were assessed using gated single-photon emission computed tomography (gSPECT) at 4, 20, and 40 weeks post-irradiation.
- Histo-morphology, microvascular damage markers (e.g., alkaline phosphatase, von-Willebrand-Factor), and gene expression were analyzed.
Main Results:
- Irradiated Eng+/- mice exhibited attenuated upregulation of inflammatory, immunological, and fibrosis-related genes (e.g., TGF-β1, ALK 5, PDGF) compared to Eng+/+ littermates.
- Collagen deposition was significantly increased in Eng+/+ mice during the early fibrotic phase (20 weeks) but not in Eng+/- mice.
- Despite gene expression differences, inflammatory cell invasion and microvascular damage markers were similar in both mouse strains.
Conclusions:
- Reduced endoglin levels in Eng+/- mice led to impaired early inflammatory and fibrotic responses to high-dose cardiac irradiation.
- These molecular and cellular differences did not translate into significant variations in microvascular damage or overall cardiac function between the endoglin genotypes.
