Lack of thrombospondin 1 and exacerbation of choroidal neovascularization
Open accessAbstract
OBJECTIVES: To assess the impact of thrombospondin 1(TSP1) deficiency on choroidal neovascularization (CNV)and to determine whether administration of a TSP1 antiangiogenic mimetic peptide attenuates CNV. METHODS: The impact of TSP1 deficiency on laser induced CNV was assessed using wild-type (TSP1 +/+) and TSP1-deficient (TSP1 −/−) mice. Three laser burns were placed in each eye of TSP1 +/+ and TSP1 −/− mice to induce CNV. Intravitreal injection of the TSP1 mimetic peptide was performed on days 1 and 7 postlaser in the mice.For quantitative measurements of neovascularization, intercellular adhesion molecule 2 staining was performed at 14 days postlaser of the choroidal-sclera flat mounts. The recruitment of macrophages to the sites of damage was investigated by immunohistochemistry. The CNV area was measured by intercellular adhesion molecule 2 staining and use of ImageJ software. RESULTS: The TSP1 −/− mice exhibited significantly larger areas of neovascularization on choroidal flat mounts compared with TSP1 +/ mice. This was consistent with enhanced recruitment of macrophages in TSP1 −/− mice compared with TSP1 +/+ mice 3 days postlaser. The development of CNV was significantly attenuated in mice receiving the TSP1 antiangiogenic mimetic peptide compared with those receiving vehicle alone. CONCLUSIONS: Deficiency of TSP1 contributes to enhanced choroidal neovascularization. This is consistent with the anti-inflammatory and antiangiogenic activity of TSP1. The TSP1 antiangiogenic peptide was effective in attenuation of CNV. CLINICAL RELEVANCE: Intravitreal injection of TSP1 antiangiogenic mimetic peptides may provide alternative treatment for CNV.
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Decreased TSP1 expression exacerbates ocular neovascularization.
“Decreased TSP1 expression exacerbates ocular neovascularization [12].”
From Thrombospondin-1, BIM and CFH polymorphisms and response to anti-VEGF treatment in neovascular age- related macular degeneration patients (2024) · cites this paper as [12]
The Results section (‘TSP1-deficiency results in increased areas of CNV’) reports substantially larger laser-induced choroidal neovascular lesions in mice lacking TSP1. The claim extends that finding from complete TSP1 deficiency to decreased expression generally, and from choroidal neovascularization to ocular neovascularization broadly; those extensions were not tested here. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThis study correlates with preclinical studies showing that mice lacking TSP1 have increased inflammation and CNV in laser-induced model of nAMD.
“This study correlates with preclinical studies showing that mice lacking TSP1 have increased inflammation and CNV in laser-induced model of nAMD [12, 43].”
From Thrombospondin-1, BIM and CFH polymorphisms and response to anti-VEGF treatment in neovascular age- related macular degeneration patients (2024) · cites this paper as [12]
TSP1 mimetic peptides effectively inhibit CNV in preclinical studies.
“TSP1 is touted for having an anti-inflammatory and anti-angiogenic role in the eye impacting inflammation and angiogenesis with TSP1 mimetic peptides effectively inhibiting CNV in our preclinical studies [12].”
From Thrombospondin-1, BIM and CFH polymorphisms and response to anti-VEGF treatment in neovascular age- related macular degeneration patients (2024) · cites this paper as [12]
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Self-citation
- Authors
- Wang, S., Sorenson, C. M., & Sheibani, N.
- Affiliations
- University of Wisconsin–Madison (US)
- Corresponding author
- Sheibani, Nader
- Venue
- Archives of Ophthalmology
- Publisher
- American Medical Association (AMA)
- Published
- 2012-05-01
- Volume
- 130
- Issue
- 5
- Pages
- 615-20
- ISSN
- 0003-9950 (ISSN-L)
- PMC
- PMC3404202
- OpenAlex
- W2062675409
- Cited by
- 61
- References
- 48
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 5 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 8 · 2019: 2 · 2018: 6 · 2017: 5 · 2016: 2 · 2015: 6 · 2014: 3 · 2013: 5
- FWCI
- 4.19
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Archives of Ophthalmology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1rc4ey021357-01)
- National Eye Institute (RC4-EY021357, EY-18179, P30-EY-16665, EY21357, R01EY018179, EY16995, P30EY016665)
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
- Keywords
- thrombospondin-1, choroidal neovascularization, laser-induced CNV, macrophage recruitment, ICAM-2, anti-inflammatory activity, intravitreal injection
- MeSH terms
- Animals, Disease Models, Animal, Female, Macrophages, Mice, Inbred C57BL, Microscopy, Fluorescence, Oligopeptides, Mice, Knockout, Thrombospondin 1, Choroidal Neovascularization, Angiogenesis Inhibitors, Biomimetics, Mice, Intravitreal Injections
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