June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Downregulation of Syndecan-4 prevent injury-induced capsule opacification in mouse
Author Affiliations & Notes
  • Yingyan Qin
    The State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
  • Furong Luo
    The State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
  • Min Hou
    The State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
  • Xuan Bao
    The State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
  • Yi Zhu
    The State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
  • Mingxing Wu
    The State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China
  • Footnotes
    Commercial Relationships   Yingyan Qin, None; Furong Luo, None; Min Hou, None; Xuan Bao, None; Yi Zhu, None; Mingxing Wu, None
  • Footnotes
    Support  National Natural Science Foundation of China Grant 81270982
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 3191. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to Subscribers Only
      Sign In or Create an Account ×
    • Get Citation

      Yingyan Qin, Furong Luo, Min Hou, Xuan Bao, Yi Zhu, Mingxing Wu; Downregulation of Syndecan-4 prevent injury-induced capsule opacification in mouse. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3191.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose : The proliferation, migration, adhesion and epithelial-to-mesenchymal transition of lens epithelium cells (LECs) are the typical pathological changes during posterior capsule opacification (PCO), the most common complication after cataract surgery worldwide. Syndecan-4 (SDC-4) serves as a co-receptor for both basic fibroblast growth factor (bFGF) and integrin, which might play an important role in formation of PCO. However, the role of SDC-4 in capsular opacification development has not been characterized. The present study aimed to investigate the role of SDC-4 in an injury-induced anterior capsule opacification model in vivo.

Methods : 6 to 8 weeks old SDC-4 deficient mice and age-matched wild-type (WT) mice were used in the study. Mice were anesthetized with 0.2ml 5% Cholrali Hydras. After mydriatic with tropicamide eyedrop, a 26-gauge hypodermic needle was used to make a puncturation in central anterior capsule of the right eye through cornea. Mice were photographed by slit lamp and killed 3 days after surgery. The anterior capsules were isolated for immunofluorescence and the expression of Ki67 was measured. Lenses were isolated for western blot. The expression of p-FAK, PKCα, p-Akt, p-ERK, p-S6RP, total FAK, total Akt, total ERK and total S6RP were detected by western blot.

Results : 3 days after surgery, WT mice developed an obvious anterior capsule opacities while the opacities remained much smaller in SDC-4-/- mice. Immunofluorescent staining of lens capsules showed extensive multilayer of cells forming plaques beneath the anterior lens capsules in WT mice. By contrast, the volumes of subcapsular plaques and expression of Ki67, which is a marker of proliferation, were obviously decreased in anterior capsules of SDC-4-/- mice. In addition, SDC-4-/- mice showed reduced activation of FAK at Thr397, PKCα, ERK1/2, Akt at Thr308, Akt at Ser473 and S6RP at Ser235/236 in lens.

Conclusions : Downregulation of SDC-4 might inhibit capsule opacification formation. The possible mechanism may be insufficient activation of bFGF and integrin pathway effectors, including PKCα, ERK1/2, PI3K/Akt/mTOR and FAK.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×