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Deletion of smooth muscle alpha‐actin in mice alters neovascularization response to oxygen‐induced retinopathy
Author(s) -
Tomasek James J,
Haaksma Carol J,
Hu Yang,
Ma Jianxing
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.524.4
Subject(s) - neovascularization , pericyte , diabetic retinopathy , retina , retinopathy of prematurity , hyperoxia , retinal , contractility , retinopathy , blood vessel , medicine , endocrinology , angiogenesis , chemistry , biology , ophthalmology , diabetes mellitus , endothelial stem cell , biochemistry , neuroscience , lung , in vitro , pregnancy , genetics , gestational age
Retinal neovascularization, growth of new abnormal blood vessels, is part of proliferative diabetic retinopathy resulting in blindness. Neovascularization can be mimicked using the oxygen‐induced retinopathy (OIR) model; neonatal mice are placed into hyperoxia (P7‐12) resulting in avascularization of the central retina with rapid and abnormal neovascularization upon return to normoxia. Smooth muscle α‐actin (SMAA) null mice were used to determine effects reduction in contractile function of pericytes and smooth muscle cells (SMC) have upon neovascularization. Lack of SMAA significantly enhances increased retinal vascular permeability observed in response to OIR. WT mice exposed to OIR have significantly greater pre‐retinal tufts, a measure of neovascularization, compared to SMAA null mice. Similarly, SMAA null mice have reduced vessels in the central avascular zone after return to normoxia compared with WT mice. These results suggest that reduced contractility in pericytes and SMCs may reduce OIR‐induced neovascularization due to a reduced response to or reduced levels of angiogenic factors which are critical in diabetic retinopathy. Supported by the Juvenile Diabetes Research Foundation