July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Effects of Interleukin-6 on Posterior Capsular Opacification
Author Affiliations & Notes
  • Bo Ma
    Ophthalmology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China
  • Ruihua Jing
    Ophthalmology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China
  • Cheng Pei
    Ophthalmology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China
  • Footnotes
    Commercial Relationships   Bo Ma, None; Ruihua Jing, None; Cheng Pei, None
  • Footnotes
    Support  National Natural Science Foundation of China (No. 81470614)
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 1603. doi:https://doi.org/
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    • Get Citation

      Bo Ma, Ruihua Jing, Cheng Pei; Effects of Interleukin-6 on Posterior Capsular Opacification. Invest. Ophthalmol. Vis. Sci. 2018;59(9):1603. doi: https://doi.org/.

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

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Abstract

Purpose : The effects of Interleukin-6 (IL-6) on the development of posterior capsular opacification (PCO) was investigated in vitro and in vivo.

Methods : Western-blot and Real-time PCR were used to test IL-6-induced epithelial-mesenchymal transition (EMT) marker α-smooth muscle actin (α-SMA), extracellular matrix (ECM) markers fibronectin (Fn) and type I collagen (COL-1), transforming growth factor β2 (TGF-β2), the activation and the role of the JAK/STAT3 signaling pathway in human lens epithelial cells (HLECs). Immunocytofluorescense staining was performed to detect the expression of gp130 and IL-6Rα in HLECs. Capsular bag models were established to examine the proliferation of LECs by using JAK/STAT3 signaling pathway’s inhibitor WP1066. Rat PCO models were then established to examine the impact of STAT3 knockdown by shRNA adeno-associated virus on PCO development and Immunohistochemical staining was performed to detect the expression of Fn in the anterior and posterior capsule in vivo.

Results : We found that IL-6 promotes the expression of Fn, COL-1, TGF-β2, p-JAK2 and p-STAT3 in HLECs but exerts little effect on α-SMA. The JAK/STAT3 inhibitor WP1066 effectively suppressed the IL-6-induced cell proliferation and expression of Fn and COL-1 in LECs. STAT3 knockdown effectively inhibited the development of PCO in rats and significantly reduced the expression of Fn in the anterior and posterior capsule.

Conclusions : IL-6 contributed to the development of PCO by promoting TGF-β2 activation, ECM synthesis and LEC proliferation through a JAK/STAT3 signaling-dependent mechanism. Furthermore, inhibiting JAK/STAT3 signaling effectively impaired both PCO development in a rat and ECM synthesis in the lens capsule.

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

 

Proposed mechanism of IL-6 regulation of ECM protein expression in LECs and the implications of its interaction with TGF-β2 in PCO. The expression of IL-6 was increased in the aqueous humor after cataract surgery. IL-6 promoted ECM synthesis through activating JAK/STAT3 signalling pathway and activity of TGF-β2. IL-6 and TGF-β2 interacted with each other and lead to LECs proliferation and expression a large number of EMT and ECM proteins. EMT and ECM proteins accumulated continually result in PCO.

Proposed mechanism of IL-6 regulation of ECM protein expression in LECs and the implications of its interaction with TGF-β2 in PCO. The expression of IL-6 was increased in the aqueous humor after cataract surgery. IL-6 promoted ECM synthesis through activating JAK/STAT3 signalling pathway and activity of TGF-β2. IL-6 and TGF-β2 interacted with each other and lead to LECs proliferation and expression a large number of EMT and ECM proteins. EMT and ECM proteins accumulated continually result in PCO.

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