Matricellular protein thrombospondins: influence on ocular angiogenesis, wound healing and immuneregulation
Open accessAbstract
Thrombospondins are a family of large multi-domain glycoproteins described as matricelluar proteins based on their ability to interact with a broad range of receptors, matrix molecules, growth factors or proteases, and to modulate array of cellular functions including intracellular signaling, proliferation and migration. Two members of the thrombospondin family, thrombospondin 1 (TSP-1) and thrombospondin 2 (TSP-2) are studied extensively to determine their structure and function. While expressed at low levels in normal adult tissues, their increased expression is seen predominantly in response to cellular perturbations. Despite structural similarities, a notable functional difference between TSP-1 and TSP-2 includes the ability of former to activate of latent TGF-β and its competitive inhibition by the latter. Both these thrombospondins are reported to play important roles in TGF-β rich ocular environment with most reports related to TSP-1. They are expressed by many ocular cell types and detectable in the aqueous and vitreous humor. TSP-1 and TSP-2 influence many cellular interactions in the eye such as angiogenesis, cell migration, wound healing, TGF-β activation and regulation of inflammatory immune responses. Together, these processes are known to contribute to the immune privilege status of the eye. Emerging roles of TSP-1 and TSP-2 in ocular functions and pathology are reviewed here.
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In the eye, TSP1 regulates ocular surface inflammation (dry eye disease).
“In the eye it regulates ocular surface inflammation (dry eye disease) [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 [43]
This 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 [43]
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Self-citation
- Authors
- Masli, S., Sheibani, N., Cursiefen, C., & Zieske, J.
- Affiliations
- Boston University (US)
- University of Wisconsin–Madison (US)
- University of Cologne (DE)
- Massachusetts Eye and Ear Infirmary (US)
- Corresponding author
- Masli, Sharmila
- Venue
- Current Eye Research
- Publisher
- Informa UK Limited
- Published
- 2014-02-21
- Volume
- 39
- Issue
- 8
- Pages
- 759-774
- ISSN
- 0271-3683 (ISSN-L)
- 1460-2202
- PMC
- PMC4278647
- OpenAlex
- W2157167110
- Cited by
- 54
- References
- 113
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 3 · 2023: 3 · 2022: 7 · 2021: 7 · 2020: 3 · 2019: 6 · 2018: 7 · 2017: 3 · 2016: 2 · 2015: 7
- FWCI
- 0.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Eye Research (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1rc4ey021357-01)
- National Eye Institute (RC4-EY021357, R24EY022883, P30EY016665, P30EY003790)
- National Cancer Institute (P30CA014520)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Rheumatology › Bone and Dental Protein Studies
- Keywords
- thrombospondin-1, thrombospondin-2, matricellular proteins, ocular angiogenesis, wound healing, immune regulation, TGF-beta activation, TGF-beta inhibition, immune privilege, ocular inflammation, cell migration, aqueous humor, vitreous humor
- MeSH terms
- Animals, Eye, Eye Diseases, Humans, Immunity, Cellular, Neovascularization, Pathologic, Wound Healing, Signal Transduction, Thrombospondins
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