High-Mobility Group Box-1 and Endothelial Cell Angiogenic Markers in the Vitreous from Patients with Proliferative Diabetic Retinopathy

Mediators of Inflammation - Tập 2012 - Trang 1-7 - 2012
Ahmed M. Abu El‐Asrar1,2, Mohd Imtiaz Nawaz1, Dustan Kangave1, Marwan A. Abouammoh1, Ghulam Mohammad1
1Department of Ophthalmology, College of Medicine, King Saud University, Riyadh 11411, Saudi Arabia
2Department of Ophthalmology, King Abdulaziz University Hospital, Old Airport Road, P.O. Box 245, Riyadh 11411, Saudi Arabia

Tóm tắt

The aim of this study was to measure the levels of high-mobility group box-1 (HMGB1) in the vitreous fluid from patients with proliferative diabetic retinopathy (PDR) and to correlate its levels with clinical disease activity and the levels of vascular endothelial growth factor (VEGF), the angiogenic cytokine granulocyte-colony-stimulating factor (G-CSF), the endothelial cell angiogenic markers soluble vascular endothelial-cadherin (sVE-cadherin), and soluble endoglin (sEng). Vitreous samples from 36 PDR and 21 nondiabetic patients were studied by enzyme-linked immunosorbent assay. HMGB1, VEGF, sVE-cadherin, and sEng levels were significantly higher in PDR patients than in nondiabetics (P=0.008; <0.001; <0.001; 0.003, resp.). G-CSF was detected in only 3 PDR samples. In the whole study group, there was significant positive correlation between the levels of HMGB1, and sVE-cadherin (r=0.378,P=0.007). In PDR patients, there was significant negative correlation between the levels of sVE-cadherin and sEng (r=−0.517,P=0.0005). Exploratory regression analysis identified significant associations between active PDR and high levels of VEGF (odds ratio = 76.4; 95% confidence interval = 6.32–923) and high levels of sEng (odds ratio = 6.01; 95% confidence interval = 1.25–29.0). Our findings suggest that HMGB1, VEGF, sVE-cadherin and sEng regulate the angiogenesis in PDR.

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10.1055/s-2001-18601

10.1096/fj.03-1476fje

10.1073/pnas.96.19.10836

2006, European Cytokine Network, 17, 155

10.1136/bjo.2008.142182

10.1007/s10456-008-9093-5

10.1046/j.1365-2796.2003.01204.x

10.1182/blood-2002-05-1300

10.1016/j.imbio.2009.11.001

10.1038/onc.2012.49

2006, Journal of Immunology, 176, 12, 10.4049/jimmunol.176.1.12

2005, American Journal of Pathology, 166, 1259, 10.1016/S0002-9440(10)62344-9

10.1161/01.RES.0000257774.55970.f4

10.1182/blood-2006-02-004291

2011, Molecular Vision, 17, 508

2011, Molecular Vision, 17, 1829

10.1161/ATVBAHA.107.158014

10.1016/j.ceb.2010.07.006

10.1111/j.1365-2257.2006.00756.x

10.1158/0008-5472.CAN-04-0265

10.1002/art.33336

10.1253/circj.68.1

10.1007/s10165-009-0246-1

10.1093/humrep/dem429

2002, American Journal of Pathology, 161, 35, 10.1016/S0002-9440(10)64154-5

10.1007/s10456-008-9101-9

10.1096/fj.02-0634rev

2000, International Journal of Cancer, 86, 122

10.1210/jc.2006-2349

10.1158/0008-5472.CAN-09-4466

10.1074/jbc.M111.260133

10.1016/j.brainres.2005.07.076

10.1096/fj.04-3496fje

10.1016/S0006-291X(02)02335-5

10.1056/NEJM199412013312203

10.1167/iovs.06-1358

10.2337/db07-1808

10.1159/000317023

10.2337/db09-0801

10.1530/EJE-11-0662

10.1111/j.0300-9475.2004.01518.x

10.1111/j.1365-2559.2005.02104.x

10.1210/jc.2006-1231

10.2337/db06-1694

10.1186/1741-7015-8-86

10.1007/s00380-011-0163-z

10.1007/s10792-007-9053-x

10.1038/labinvest.3700251

10.1038/nm1429

10.1371/journal.pone.0005149