April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Suppression of transient receptor potential canonical (TRPC) channel 4 inhibits retinal neovascularization in the mouse model of oxygen induced retinopathy
Author Affiliations & Notes
  • Hyun Beom Song
    Fight against Angiogenesis-Related Blindness (FARB) Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
    Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea
  • Hyoung Oh Jun
    Fight against Angiogenesis-Related Blindness (FARB) Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
  • Jin Hyoung Kim
    Fight against Angiogenesis-Related Blindness (FARB) Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
  • Jeong Hun Kim
    Fight against Angiogenesis-Related Blindness (FARB) Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Republic of Korea
    Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships Hyun Beom Song, None; Hyoung Oh Jun, None; Jin Hyoung Kim, None; Jeong Hun Kim, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 5409. doi:
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    • Get Citation

      Hyun Beom Song, Hyoung Oh Jun, Jin Hyoung Kim, Jeong Hun Kim; Suppression of transient receptor potential canonical (TRPC) channel 4 inhibits retinal neovascularization in the mouse model of oxygen induced retinopathy. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5409.

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

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Abstract

Purpose: The aim of this study is to investigate whether suppression of transient receptor potential canonical (TRPC) channel 4 inhibits retinal neovascularization in the mouse model of oxygen induced retinopathy.

Methods: The expressions of TRP channel isoforms on mouse retina and human renal microvascular endothelial cells (HRMECs) were evaluated by RT-PCR. The anti-angiogenic activity of TRPC channel inhibitors and siRNA against TRPC4 was evaluated by vascular endothelial growth factor (VEGF)-induced migration and in vitro tube formation assay of HRMECs. In the mouse model of oxygen induced retinopathy, retinal neovascularization was evaluated after intraocular injection of TRP channel inhibitors and siRNA against TRPC4.

Results: TRP channel 1, 3, 4 and 6 were strongly expressed on mouse retina and HRMECs. TRP channel inhibitor, SKF 96365, and siRNA against TRPC4, effectively suppressed VEGF-induced in vitro angiogenesis of HRMECs including migration and tube formation, respectively. In the mouse model of oxygen induced retinopathy, intraocular injection of TRP channel inhibitor, SKF 96365 and siRNA against TRPC4, significantly inhibited retinal neovascularization. In addition, VEGF-induced activation of p38 MAPK and ERK was inhibited by treatment with siRNA against TRPC4 in HRMECs.

Conclusions: TRPC channel 4 is required for retinal neovascularization in the mouse model of oxygen induced retinopathy. Furthermore, inhibition of retinal neovascularization by suppressing TRPC4 could be extensively applied to variable vaso-proliferative retinopathies.

Keywords: 700 retinal neovascularization • 569 ion channels • 439 calcium  
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