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The Suppression of Kallistatin on High-Glucose-Induced Proliferation of Retinal Endothelial Cells in Diabetic Retinopathy.

Abstract：

BACKGROUND:Diabetic retinopathy (DR) is a severe ocular complication of diabetes. Kallistatin has multiple biological functions including anti-inflammation and antiangiogenesis. Our aim was to detect the level of kallistatin in the vitreous of proliferative DR (PDR) and its effect on proliferation, migration, and tube formation of human retinal endothelial cells (HRECs) under high glucose in an in vitro model. METHODS:Vitreous humor samples were obtained through pars plana vitrectomy from 7 nondiabetic patients with idiopathic macular holes or idiopathic preretinal membranes and 10 PDR patients. The vitreous levels of kallistatin were measured by ELISA. HRECs were cultured with different concentrations of glucose and 1,000 nM kallistatin. The proliferation of HRECs was evaluated by a Cell Counting Kit-8 assay. Cell migration was assessed by using Transwell chambers. Cell sprouting was detected by tube formation assay. The RNA interference technique was used to create the knockdown of the kallistatin gene in HRECs for evaluating its effect on the proliferation, migration, and tube formation of HRECs. RESULTS:The vitreous levels of kallistatin were significantly lower in PDR patients in comparison with nondiabetic control patients (p < 0.05). Compared with 5 mM of normal glucose treatment, high glucose (30 mM) in culture significantly increased the proliferation and migration of HRECs, which was attenuated by 1,000 nM kallistatin. In addition, 1,000 nM kallistatin was shown to suppress high-glucose-induced tube formation and the expression of vascular endothelial growth factor of HRECs. Furthermore, the knockdown of kallistatin enhanced the proliferation, migration, and tube formation of HRECs. CONCLUSIONS:Our data indicated that kallistatin might be a potent inhibitory factor for PDR. The molecule plays its role by inhibiting high-glucose-induced proliferation of HRECs. The findings suggest that the upregulation of kallistatin might be an effective strategy for PDR prevention.

journal_name

Ophthalmic Res

journal_title

Ophthalmic research

authors

Xing Q,Zhang G,Kang L,Wu J,Chen H,Liu G,Zhu R,Guan H,Lu P

doi

10.1159/000447776

subject

Has Abstract

pub_date

2017-01-01 00:00:00

pages

141-149

issue

eissn

0030-3747

issn

1423-0259

pii

000447776

journal_volume

pub_type

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The Suppression of Kallistatin on High-Glucose-Induced Proliferation of Retinal Endothelial Cells in Diabetic Retinopathy.