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Deletion of smooth muscle alpha‐actin alters blood‐retina barrier permeability and retinal function
Author(s) -
Tomasek James J,
Haaksma Carol J,
Ma Jianxing
Publication year - 2007
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.21.5.a232-b
Subject(s) - pericyte , retinal , retina , vascular permeability , vascular smooth muscle , mural cell , microbiology and biotechnology , blood–retinal barrier , blood vessel , chemistry , biology , anatomy , endothelial stem cell , biochemistry , endocrinology , smooth muscle , diabetic retinopathy , neuroscience , in vitro , diabetes mellitus
Vascular smooth muscle (SM) cells and pericytes are essential for normal vascular development. We have used SM α‐actin (SMAA) null mice to determine whether normal vascular SM and pericyte contractile function is necessary for vascular development, blood‐retina barrier (BRB) permeability and retinal function. Deletion of SMAA did not result in any alterations in retinal morphology, vascular pattern, or SM cell and pericyte ensheathment of vessels; however, retinal vascular permeability was significantly increased in SMAA null mice at both P50 and P75 (p<0.05 and p<0.001, respectively) and rod and cone function was significantly reduced in SMAA null mice at P22, P45, and P75 (p<0.01 at all ages). Experiments are underway to determine whether lack of SMAA increases susceptibility of the retina to neovascularization in the oxygen‐induced retinopathy model. These results demonstrate that SMAA in SM cells and pericytes is not necessary for the formation of a normal retinal vascular pattern; however, SMAA is necessary for SM cells and pericytes to interact with endothelial cells to form a fully functional BRB. (Supported by NEI grant EY014435)