HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Kornberg, L. J. Articles by Grant, M. B. Search for Related Content PubMed PubMed Citation Articles by Kornberg, L. J. Articles by Grant, M. B.

Focal Adhesion Kinase Overexpression Induces Enhanced Pathological Retinal Angiogenesis

¹From the Departments of Otolaryngology and ²Pharmacology and Therapeutics, College of Medicine, University of Florida, Gainesville, Florida.

PURPOSE. Focal adhesion kinase (FAK) is involved in processes integral to angiogenesis, such as cell growth, survival, and migration. FAK is activated by angiogenic growth factors, such as insulin-like growth factor (IGF)-I, vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF). The study was conducted to determine whether overexpression of FAK or FAK-related nonkinase (FRNK), an inhibitor of FAK, could influence human retinal endothelial cell (HREC) migration and in vivo angiogenesis.

METHODS. Migration in response to a combination of growth factors was examined in transfected HRECs overexpressing FAK or FRNK. The effect of FAK or FRNK overexpression on preretinal neovascularization was examined in a mouse model of oxygen-induced retinopathy.

RESULTS. Overexpression of FAK in HRECs resulted in a 102% ± 13% increase (P = 1.4 x 10^–4) in cell migration, whereas overexpression of FRNK resulted in a 20% ± 8% decrease (P = 0.01). Overexpression of FAK in mouse eyes led to formation of numerous large vascular tufts resembling glomeruli and a 57% ± 7% increase in preretinal neovascularization (P = 3 x 10^–9), whereas FRNK resulted in a 55% ± 15% reduction (P = 5 x 10^–5).

CONCLUSIONS. Modulating the FAK/FRNK system may provide a novel approach to inhibiting pathologic retinal angiogenesis.

This article has been cited by other articles:

				J. Halder, A. A. Kamat, C. N. Landen Jr., L. Y. Han, S. K. Lutgendorf, Y. G. Lin, W. M. Merritt, N. B. Jennings, A. Chavez-Reyes, R. L. Coleman, et al. Focal Adhesion Kinase Targeting Using In vivo Short Interfering RNA Delivery in Neutral Liposomes for Ovarian Carcinoma Therapy. Clin. Cancer Res., August 15, 2006; 12(16): 4916 - 4924. [Abstract] [Full Text] [PDF]

				V. Shukla, X. Coumoul, L. Cao, R.-H. Wang, C. Xiao, X. Xu, S. Ando, S. Yakar, D. LeRoith, and C. Deng Absence of the full-length breast cancer-associated gene-1 leads to increased expression of insulin-like growth factor signaling axis members. Cancer Res., July 15, 2006; 66(14): 7151 - 7157. [Abstract] [Full Text] [PDF]