Our laboratory has previously shown that AGEs in extracellular matrix (ECM) proteins promote TGFβ2 (transforming growth factor-beta 2)-mediated epithelial-to-mesenchymal transition (EMT) of lens epithelial cells (LECs), which could play a role in fibrosis associated with posterior capsule opacification.
Expression of connective tissue growth factor (CTGF) mRNA in plaques of human anterior subcapsular cataracts and membranes of posterior capsule opacification.
In addition, upregulation of MALAT1 and downregulation of miR-26a were detected in human posterior capsule opacification (PCO) attached LECs and the LECs obtained from patients with anterior polar cataracts by quantitative RT-PCR (qRT-PCR).
Furthermore, overexpression of miR-34a downregulated the levels of phosphorylated Akt, phosphorylated ERK1/2 and other cell cycle regulators. miR-34a expression was significantly reduced in posterior capsule opacification (PCO) clinical samples.
Furthermore, overexpression of miR-34a downregulated the levels of phosphorylated Akt, phosphorylated ERK1/2 and other cell cycle regulators. miR-34a expression was significantly reduced in posterior capsule opacification (PCO) clinical samples.
Mammalian target of rapamycin (mTOR) serves a central role in regulating cell growth and survival, and has been demonstrated to be involved in the pathological progression of posterior capsule opacification (PCO).
The previous study has demonstrated that epidermal growth factor (EGF) and EGF receptor (EGFR) signaling plays a critical role in the development of posterior capsule opacification (PCO) through regulating lens epithelial cells (LECs) proliferation.
Our laboratory has previously shown that AGEs in extracellular matrix (ECM) proteins promote TGFβ2 (transforming growth factor-beta 2)-mediated epithelial-to-mesenchymal transition (EMT) of lens epithelial cells (LECs), which could play a role in fibrosis associated with posterior capsule opacification.
Fibronectin-exposed cultures also showed increased TGFβ signaling-dependent differentiation into the two cell types responsible for posterior capsule opacification after cataract surgery, namely myofibroblasts and lens fiber cells.
In this cross sectional study, where posterior capsule opacification (PCO) was used as a comparator, patients were consented for one photograph with SLC and two with DCC (DCC1 and DCC2), with a slit lamp adaptor.
Our study lays the foundation for future research in lncRNAs related to EMT in HLE B-3 cells and could provide new avenues for the prevention and treatment of posterior capsule opacification (PCO).
P(MPC-MAA) modification significantly reduced postoperative inflammation and anterior capsule opacification (ACO), and did not affect posterior capsule opacification (PCO).
These data reveal that miR-181a can inhibit the proliferation, migration, and EMT of LECs and suggest that the restoration of miRNA-181a expression may be a potential novel therapeutic target for the prevention and treatment of posterior capsule opacification.
These data reveal that miR-26b can inhibit the proliferation, migration, and EMT of lens epithelial cells, and restoration of miRNA-26b may be a potential, novel therapeutic target for the prevention and treatment of posterior capsule opacification.
To investigate the correlation between connective tissue growth factor (CTGF) mRNA expression and immunohistochemical characteristics of anterior subcapsular cataract (ASC) formation as well as posterior capsule opacification (PCO) development (expression of type I collagen, alpha-smooth muscle actin and tenascin) under in vivo and under in vitro conditions in human and porcine lens epithelial cells.
To investigate the correlation between connective tissue growth factor (CTGF) mRNA expression and immunohistochemical characteristics of anterior subcapsular cataract (ASC) formation as well as posterior capsule opacification (PCO) development (expression of type I collagen, alpha-smooth muscle actin and tenascin) under in vivo and under in vitro conditions in human and porcine lens epithelial cells.