June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Identification of a dual inhibitor of SRPK1 and CK2 that attenuates pathological angiogenesis of macular degeneration in mice
Author Affiliations & Notes
  • Satoshi Morooka
    Ophthalmology and Visual Sciences, Kyoto University, Kyoto, Japan
    Anatomy and Developmental Biology, Kyoto University, Kyoto, Japan
  • Isao Kii
    Anatomy and Developmental Biology, Kyoto University, Kyoto, Japan
  • Yukiko Okuno
    Medical Research Support Center, Kyoto University, Kyoto, Japan
  • Nobutoshi Ito
    Laboratory of Structural Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan
  • Masatoshi Hagiwara
    Anatomy and Developmental Biology, Kyoto University, Kyoto, Japan
  • Nagahisa Yoshimura
    Ophthalmology and Visual Sciences, Kyoto University, Kyoto, Japan
  • Footnotes
    Commercial Relationships Satoshi Morooka, None; Isao Kii, None; Yukiko Okuno, None; Nobutoshi Ito, None; Masatoshi Hagiwara, None; Nagahisa Yoshimura, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2304. doi:
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      Satoshi Morooka, Isao Kii, Yukiko Okuno, Nobutoshi Ito, Masatoshi Hagiwara, Nagahisa Yoshimura; Identification of a dual inhibitor of SRPK1 and CK2 that attenuates pathological angiogenesis of macular degeneration in mice. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2304.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract
 
Purpose
 

We found that SRPIN340, a specific inhibitor of SR protein kinase 1 (SRPK1) which phosphorylates Serine-arginine-rich (SR) proteins and regulates splicing and transcription, suppressed the expression of vascular endothelial growth factor (VEGF) and choroidal neovascularization (CNV). Here we screened for more active SRPK1 inhibitors which suppressed CNV effectively than SRPIN340.

 
Methods
 

Crystallographic study; Crystals of the kinase fragment of SRPK1 (residues 42-255 and 474-655) were obtained according to a previously reported method with some modifications. The SRPIN340 complex was obtained by soaking crystals of apo-SRPK1 in mother liquor containing the inhibitor.<br /> In-silico screening; Structure-based virtual screening (SBVS) was applied against the general chemical library, which include 71955 compounds.<br /> In vitro kinase assay; The reaction mixture was incubated at 30 °C for 15 min and detected the residual ATP was measured by Kinase Glow following the manufacturer’s instruction.<br /> VEGF ELISA; We added 10μM compounds or control (0.1% DMSO) to ARPE-19 cells. The medium was collected 72 hours after the addition of the compounds. We evaluated the VEGF protein level in the culture medium by ELISA with manufacturer’s instruction.<br /> In vivo examination; The compound was intravitreally injected to laser CNV model mice immediately after laser photocoagulation. Seven days after laser injury, the mice were perfused with 1mL of 0.5% fluorescein-isothiocyanate (FITC)-labeled dextran. Flat mounts of retinal pigment epithelium (RPE)-choroid complex were obtained and the area of CNV was measured by fluorescence microscopy.

 
Results
 

We solved the structure of SRPK1 bound to SRPIN340 by X-ray crystallography. Using pharmacophore docking models followed by in vitro kinase assays, we screened a large-scale chemical library, and thus identified a new inhibitor of SRPK1 named as SRPIN803. SRPIN803 inhibited Casein kinase 2 (CK2) as well as SRPK1. SRPIN803 decreased the VEGF protein levels most effectively as measured by VEGF ELISA. In a laser-induced mouse model, topical administration of eye ointment containing SRPIN803 significantly inhibited CNV.

 
Conclusions
 

We obtained a new anti-angiogenic drug, SRPIN803, which inhibits SRPK1 and CK2 activity.

 
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