Abstract
Purpose :
The effects of Connective tissue growth factor (CTGF) on the development of posterior capsule opacification (PCO) were investigated both in vitro and in vivo.
Methods :
In the pig capsular bag model, immunofluorescence was performed to determine expression of epithelialto-mesenchymal transition (EMT) markers. After induced with 60μg/l CTGF for different times, the expressions of p-ERK, t-ERK, p-p38, t-p38, p-JNK and JNK1/2 proteins were detected with Western-blot in HLECs. The expressions of α-SMA, Fn and COL-1 in HLECs induced by 60μg/l CTGF for 24h were detected by Real-time PCR and Western-blot after blocking ERK’s signaling pathway by U0126, and a scratch assay was used to determine cell migration. To build the rat PCO model, blocking the expression of CTGF by shRNA with AAV (adeno-associated virus) vector was injected into the anterior chamber. PCO was observed under slit lamp and the expression of CTGF and α-smooth muscle actin(α-SMA) in posterior capsule were tested with immunohistochemical.
Results :
CTGF promoted EMT, proliferation, migration and the expression of p-ERK1/2 protein in LECs but exerted little effect on the expression of p-p38 and p-JNK1/2 proteins. MEK inhibitor U0126 effectively restrained the CTGF-induced expression of α-smooth muscle actin (α-SMA), fibronectin (Fn) and type I collagen (COL-1) in HLECs. CTGF knockdown effectively postponed the onset of PCO in the rats and significantly reduced the expression of α-SMA in the capsule.
Conclusions :
CTGF contributed to the development of PCO presumably by promoting proliferation, migration of LECs, EMT and ECM synthesis in HLECs, which is dependent on ERK signalling. Furthermore, blocking CTGF effectively inhibited PCO in the rats and the EMT 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.