July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Conditional deletion of VEGFR-1 in smooth muscle cells causes decreased retinal vessel growth and reduced alveolarisation in mice
Author Affiliations & Notes
  • Xiangke Yin
    Zhongshan Ophthalmic Center Sun Yat-Sen University , Guangzhou, China
  • Yuxiang Du
    Zhongshan Ophthalmic Center Sun Yat-Sen University , Guangzhou, China
  • Zhimin Ye
    Zhongshan Ophthalmic Center Sun Yat-Sen University , Guangzhou, China
  • Qishan Chen
    Zhongshan Ophthalmic Center Sun Yat-Sen University , Guangzhou, China
  • Lijuan Huang
    Zhongshan Ophthalmic Center Sun Yat-Sen University , Guangzhou, China
  • Liu Lixian
    Zhongshan Ophthalmic Center Sun Yat-Sen University , Guangzhou, China
  • Xuri Li
    Zhongshan Ophthalmic Center Sun Yat-Sen University , Guangzhou, China
  • Rong Ju
    Zhongshan Ophthalmic Center Sun Yat-Sen University , Guangzhou, China
  • Footnotes
    Commercial Relationships   Xiangke Yin, None; Yuxiang Du, None; Zhimin Ye, None; Qishan Chen, None; Lijuan Huang, None; Liu Lixian, None; Xuri Li, None; Rong Ju, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 581. doi:
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    • Get Citation

      Xiangke Yin, Yuxiang Du, Zhimin Ye, Qishan Chen, Lijuan Huang, Liu Lixian, Xuri Li, Rong Ju; Conditional deletion of VEGFR-1 in smooth muscle cells causes decreased retinal vessel growth and reduced alveolarisation in mice. Invest. Ophthalmol. Vis. Sci. 2018;59(9):581.

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

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Abstract

Purpose : Vascular endothelial growth factor receptor-1(VEGFR-1) plays a key role in the control of cell proliferation and differentiation during vascular development. Vascular smooth muscle cell (VSMC) which expresses VEGFR-1 abundantly constitutes the majority of the wall of blood vessels, but the functional role of VEGFR-1 in the VSMC remains less explored. The purpose of this study is to investigate the impacts of VEGFR1 deletion specifically in SMC.

Methods : VEGFR-1 in VSMC-specific cKO mice were generated by crossing floxed VEGFR1 f /f mice with SM22-Cre mice. VEGFR1 f/f mice were used as littermate controls to VEGFR-1 cKO mice. Mouse pups were sacrificed at postnatal day 4 (P4). Retina whole mount were stained with Isolectin B4 (IB4), and the retinal vessel area was quantified area. The alveolar histological structure was observed by pulmonary paraffin section stained with hematoxylin-eosin.

Results : The area of the retinal vessel in VEGFR-1 in VSMC-specific cKO mice was significantly decreased compared to the VEGFR1 f/f mice. The alveolar diameter was significantly increased in VSMC-specific cKO mice compared to the VEGFR1 f/f mice.

Conclusions : Our results reveal that VEGFR-1 is necessary to keep VSMC in normal physiology. Loss of the VEGFR-1 in VSMC delays the vascular development in retina and induces alveolar morphology abnormity.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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