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Antiangiogenic and Antineuroinflammatory Effects of Kallistatin Through Interactions With the Canonical Wnt Pathway

Liu, Xiaochen, Zhang, Bin, McBride, Jeffrey D., Zhou, Kevin, Lee, Kyungwon, Zhou, Yueping, Liu, Zuguo, Ma, Jian-xing·2013·Diabetes
DOI 10.2337/db12-1710PMC PMC3837048
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Abstract

Kallistatin is a member of the serine proteinase inhibitor superfamily. Kallistatin levels have been shown to be decreased in the vitreous while increased in the circulation of patients with diabetic retinopathy (DR). Overactivation of the Wnt pathway is known to play pathogenic roles in DR. To investigate the role of kallistatin in DR and in Wnt pathway activation, we generated kallistatin transgenic (kallistatin-TG) mice overexpressing kallistatin in multiple tissues including the retina. In the oxygen-induced retinopathy (OIR) model, kallistatin overexpression attenuated ischemia-induced retinal neovascularization. In diabetic kallistatin-TG mice, kallistatin overexpression ameliorated retinal vascular leakage, leukostasis, and overexpression of vascular endothelial growth factor and intracellular adhesion molecule. Furthermore, kallistatin overexpression also suppressed Wnt pathway activation in the retinas of the OIR and diabetic models. In diabetic Wnt reporter (BAT-gal) mice, kallistatin overexpression suppressed retinal Wnt reporter activity. In cultured retinal cells, kallistatin blocked Wnt pathway activation induced by high glucose and by Wnt ligand. Coprecipitation and ligand-binding assays both showed that kallistatin binds to a Wnt coreceptor LRP6 with high affinity (Kd = 4.5 nmol/L). These observations suggest that kallistatin is an endogenous antagonist of LRP6 and inhibitor of Wnt signaling. The blockade of Wnt signaling may represent a mechanism for its antiangiogenic and antineuroinflammatory effects.

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Metadata

Authors
Liu, X., Zhang, B., McBride, J. D., Zhou, K., Lee, K., Zhou, Y., Liu, Z., & Ma, J.-X.
Affiliations
  • Eye Institute of Xiamen University, Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Xiamen, China
  • Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas
  • Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
  • Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
Venue
Diabetes
Publisher
American Diabetes Association
Published
2013-11-16
Volume
62
Issue
12
Pages
4228-4238
ISSN
  • 0012-1797
  • 1939-327X
DOI
10.2337/db12-1710
PMC
PMC3837048
Cited by
53
References
1
Language
en
Licence
creativecommons.org/licenses/by-nc-nd/3.0/ (vor, 2844 d)

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